Mortality experience of haematite mine workers in China

The mortality risk of iron ore (haematite) miners between 1970 and 1982 was investigated in a retrospective cohort study of workers from two mines, Longyan and Taochong, in China. The cohort was limited to men and consisted of 5406 underground miners and 1038 unexposed surface workers. Among the 490 underground miners who died, 205 (42%) died of silicosis and silicotuberculosis and 98 (20%) of cancer, including 29 cases (5.9%) of lung cancer. The study found an excess risk of non-malignant respiratory disease and of lung cancer among haematite miners. The standardised mortality ratio for lung cancer compared with nationwide male population rates was significantly raised (SMR = 3.7), especially for those miners who were first employed underground before mechanical ventilation and wet drilling were introduced (SMR = 4.8); with jobs involving heavy exposure to dust, radon, and radon daughters (SMR = 4.2); with a history of silicosis (SMR = 5.3); and with silicotuberculosis (SMR = 6.6). No excess risk of lung cancer was observed in unexposed workers (SMR = 1.2). Among current smokers, the risk of lung cancer increased with the level of exposure to dust. The mortality from all cancer, stomach, liver, and oesophageal cancer was not raised among underground miners. An excess risk of lung cancer among underground mine workers which could not be attributed solely to tobacco use was associated with working conditions underground, especially with exposure to dust and radon gas and with the presence of non-malignant respiratory disease. Because of an overlap of exposures to dust and radon daughters, the independent effects of these factors could not be evaluated.     

Mortality of Sardinian lead and zinc miners: 1960-88.

The mortality of 4740 male workers of two lead and zinc mines was followed up from 1960 to 1988. Exposure to respirable dust was comparable in the two mines, but the median concentration of silica in respirable dust was 10-fold higher in mine B (12.8%) than in mine A (1.2%), but the mean annual exposure to radon daughters in underground workplaces differed in the opposite direction (mine A: 0.13 working levels (WL), mine B: 0.011 WL). Total observed deaths (1205) were similar to expected figures (1156.3) over a total of 119 390.5 person-years at risk. Underground workers of mine B had significant increases in risk of pulmonary tuberculosis (SMR 706, 95% confidence interval (95% CI) 473-1014) and non-malignant respiratory diseases (SMR 518; 95% CI 440-1606), whereas the only significant excess at mine A was for non-malignant respiratory diseases (SMR 246; 95% CI 191-312). Total cancer and lung cancer mortality did not exceed the expectation in the two mines combined. A 15% excess mortality for lung cancer, increased up to an SMR 204 (95% CI 89-470) for subjects employed > or = 26 years, was, however, found among underground workers in mine A who on the average experienced an exposure to radon daughters 10-fold higher than those of mine B. By contrast, despite their higher exposure to silica, mine B underground workers experienced a lower than expected lung cancer mortality. A ninefold increase in risk of peritoneal and retroperitoneal cancer combined was also found among underground workers of mine A (SMR 917; 95% CI 250-2347; based on four deaths). A causal association with workplace exposures is unlikely, however, as the SMR showed an inverse trend by duration of employment. These findings are consistent with low level exposure to radon daughters as a risk factor for lung cancer among metal miners. Exposure to silica at the levels estimated for the mine B underground environment did not increase the risk of lung cancer.     

Mortality of a cohort of tin miners 1941-86.

The mortality patterns of United Kingdom tin miners were examined in relation to calendar period and duration of underground work with particular attention to lung cancer and exposure to radon. Subjects were all men who had worked for at least one year between 1941 and 1984 at one of two United Kingdom tin mines and for whom a complete work history could be constructed from mine records. Standardised mortality ratios (SMRs) were calculated using national (England and Wales) rates. The pattern of SMRs in relation to potential explanatory variables was analysed using Poisson regression methods. Mortalities from lung cancer and silicosis (including silicotuberculosis) were significantly raised and showed a significant relation with duration of underground work (mortality from stomach cancer was raised in both underground and surface workers, but not significantly). Excess mortality from silica related disease declined steeply from 35% among workers first exposed before 1920 to 1% among those first exposed after 1950. Thirteen surface workers with known exposure to arsenic had high rates of lung and stomach cancer. The SMR for lung cancer showed a consistent pattern in relation to duration of underground exposure, rising from 83 (observed/expected = 8/9.6) for surface workers (without exposure to arsenic) to 447 (15/3.4) for workers with more than 30 years underground exposure. Examination of the SMR for lung cancer by total underground exposure, age, and time since last exposure gave rise to a model for the expression of risk which depends only on total exposure and time since exposure. The fitted model implies that the effect of exposure to radon in a given year has no effect on risk for 10 years, then rapidly rises to a maximum from which the excess risk then declines, halving every 4.3 years. There were no direct measurements of historic radon levels. A conservative estimate based on measurements taken since 1969 by the National Radiological Protection Board and the Mines and Quarries Inspectorate is that the annual dose to an underground worker was about 10 working level months (WLM). Given this assumption, the risk/exposure slope implied by the present data, and the model fitted to it, was somewhat lower than that given in the fourth Committee on the Biological Effects of Ionisation Radiation (BEIR IV) report (about 40% lower for lifetime exposures). The present data also imply different risks depending on the age at exposure, with relatively higher lifetime risks for exposure at older ages, and relatively lower risks for exposures at younger ages. In conclusion, there was a clear relation between exposure to radon and death from lung cancer. The relative risk of lung cancer due to exposure to radon was not constant in cessation of exposure. The lifetime excess risk of lung cancer implied by these data for 40 years exposure at the current statutory limit of four WLM a year starting at age 20, was about 8% (79 excess deaths per 1000 exposed), assuming average smoking habits among the exposed workers. Control of dust concentrations in the mines has substantially reduced--and may have eliminated--direct mortality from silica related disease.     

Mortality of a cohort of tin miners 1941-86

The mortality patterns of United Kingdom tin miners were examined in relation to calendar period and duration of underground work with particular attention to lung cancer and exposure to radon. Subjects were all men who had worked for at least one year between 1941 and 1984 at one of two United Kingdom tin mines and for whom a complete work history could be constructed from mine records. Standardised mortality ratios (SMRs) were calculated using national (England and Wales) rates. The pattern of SMRs in relation to potential explanatory variables was analysed using Poisson regression methods. Mortalities from lung cancer and silicosis (including silicotuberculosis) were significantly raised and showed a significant relation with duration of underground work (mortality from stomach cancer was raised in both underground and surface workers, but not significantly). Excess mortality from silica related disease declined steeply from 35% among workers first exposed before 1920 to 1% among those first exposed after 1950. Thirteen surface workers with known exposure to arsenic had high rates of lung and stomach cancer. The SMR for lung cancer showed a consistent pattern in relation to duration of underground exposure, rising from 83 (observed/expected = 8/9.6) for surface workers (without exposure to arsenic) to 447 (15/3.4) for workers with more than 30 years underground exposure. Examination of the SMR for lung cancer by total underground exposure, age, and time since last exposure gave rise to a model for the expression of risk which depends only on total exposure and time since exposure. The fitted model implies that the effect of exposure to radon in a given year has no effect on risk for 10 years, then rapidly rises to a maximum from which the excess risk then declines, halving every 4.3 years. There were no direct measurements of historic radon levels. A conservative estimate based on measurements taken since 1969 by the National Radiological Protection Board and the Mines and Quarries Inspectorate is that the annual dose to an underground worker was about 10 working level months (WLM). Given this assumption, the risk/exposure slope implied by the present data, and the model fitted to it, was somewhat lower than that given in the fourth Committee on the Biological Effects of Ionisation Radiation (BEIR IV) report (about 40% lower for lifetime exposures). The present data also imply different risks depending on the age at exposure, with relatively higher lifetime risks for exposure at older ages, and relatively lower risks for exposures at younger ages. In conclusion, there was a clear relation between exposure to radon and death from lung cancer. The relative risk of lung cancer due to exposure to radon was not constant in cessation of exposure. The lifetime excess risk of lung cancer implied by these data for 40 years exposure at the current statutory limit of four WLM a year starting at age 20, was about 8% (79 excess deaths per 1000 exposed), assuming average smoking habits among the exposed workers. Control of dust concentrations in the mines has substantially reduced--and may have eliminated--direct mortality from silica related disease.     

Lung cancer mortality and airways obstruction among metal miners exposed to silica and low levels of radon daughters

Starting from a cross-sectional survey in 1973, the mortality of two cohorts of Sardinian metal miners was followed through December 31, 1988. In mine A, the quartz concentration in respirable dust ranged between 0.2% and 2.0% and the exposure to radon daughters averaged 0.13 working level (WL), with the highest estimated cumulative exposure around 80–120 WLM. In mine B, the silica content was much higher (6.5–29%), but exposure to radon daughters was significantly lower than in mine A. More than 98% of the overall work force in 1973 (1,741 miners) entered the cohort, providing 25,842.5 person-years. Smoking, occupational history, chest radiographs, and lung function tests were available for the cohort members at admission. Mortality for all causes was slightly lower than expected. A significant excess for nonmalignant chronic respiratory diseases was noticed in both mines. Twenty-four subjects died of lung cancer, 17 from mine A (SMR: 128; 95% confidence interval [CI]: 75–205) and 7 from mine B (SMR: 85; 95% CI: 34–175). The SMR for lung cancer was highest among the underground workers from mine A (SMR: 148; 95% CI: 74–265), with a significant upward trend by duration of employment in underground jobs. Mine B underground miners showed lung cancer SMRs close to 100 without a significant trend by duration of employment. Among underground miners with spirometric airways obstruction in 1973, those from mine A showed the highest risk (SMR: 316; 95% CI: 116–687). The relationship did not change after adjusting for age and smoking. Based on the present findings, crystalline silica per se does not appear to affect lung cancer mortality. A slight association between lung cancer mortality and exposure to radon daughters, though within relatively low levels, may be considered for underground miners from mine A. Impaired pulmonary function may be an independent predictor of lung cancer and an important risk factor enhancing the residence time of inhaled carcinogens, i.e., alpha particles or PAHs, by impairing their bronchial and alveolar clearance. © 1994 Wiley-Liss, Inc.     

Mortality from lung cancer among silicotic patients in Sardinia: an update study with 10 more years of follow up

OBJECTIVES—To evaluate the association between silica, silicosis and lung cancer, the mortality of 724 patients with silicosis, first diagnosed by standard chest x ray film between 1964 and 1970, has been analysed by a cohort study extended to 31 December 1997.METHODS—Smoking and detailed occupational histories were available for each member of the cohort as well as the estimated lifetime exposure to respirable silica dust and radon daughters. Two independent readers blindly classified standard radiographs according to the 12 point International Labour Organisation (ILO) scale. Lung function tests meeting the American Thoracic Society''s criteria were available for 665 patients. Standardised mortality ratios (SMRs) for selected causes of death were based on the age specific Sardinian regional death rates.RESULTS—The mortality for all causes was significantly higher than expected (SMR 1.35, 95% confidence interval (95% CI) 1.24 to 1.46) mainly due to tuberculosis (SMR 22.0) and to non-malignant chronic respiratory diseases (NMCRD) (SMR 6.03). All cancer deaths were within the expected numbers (SMR 0.93; 95% CI 0.76 to 1.14). The SMR for lung cancer was 1.37 (95% CI 0.98 to 1.91, 34 observed), increasing to 1.65 (95% CI 0.98 to 2.77) allowing for 20 years of latency since the first diagnosis of silicosis. Although mortality from NMCRD was strongly associated to the severity of radiological silicosis and to the extent of the cumulative exposure to silica, SMR for lung cancer was weakly related to the ILO categories and to the cumulative exposure to silica dust only after 20 years of lag interval. A significant excess of deaths from lung cancer (SMR 2.35) was found among silicotic patients previously employed in underground metal mines characterised by a relatively high airborne concentration of radon daughters and among ever smokers who showed an airflow obstruction at the time of the first diagnosis of silicosis (SMR 3.29). Mortality for lung cancer related to exposure was evaluated with both the Cox''s proportional hazards modelling within the entire cohort and a nested case-control study (34 cases of lung cancer and 136 matched controls). Both multivariate analyses did not show any significant association with cumulative exposure to silica or severity of silicosis, but confirmed the association between mortality for lung cancer and relatively high exposure to radon, smoking, and airflow obstruction as significant covariates.CONCLUSIONS—The findings indicate that the slightly increased mortality for lung cancer in this cohort of silicotic patients was significantly associated with other risk factors—such as cigarette smoking, airflow obstruction, and estimated exposure to radon daughters in underground mines—rather than to the severity of radiological silicosis or to the cumulative exposure to crystalline silica dust itself.     

Mortality of iron miners in Lorraine (France): relations between lung function and respiratory symptoms and subsequent mortality.

An increased mortality from lung and stomach cancer was found in previous studies on Lorraine iron miners. A detailed analysis, however, was not possible due to the lack of data for survivors. In this study the cohort included 1178 workers selected at random from all the 5300 working miners aged between 35 and 55 at the start of the follow up period, which ranged from 1975 to 1985. Occupational exposures and tobacco consumption, lung function tests, and respiratory symptoms were assessed for each subject in 1975, 1980, and 1985. This study confirmed the excess of lung cancer (standardised mortality ratio (SMR) = 389, p < 0.001) and of stomach cancer (SMR = 273, p < 0.05). There was no excess of lung cancer in non-smokers and moderate smokers (< 20 pack-years) or the miners who worked only at the surface or underground for less than 20 years. A significant excess (SMR = 349, p < 0.001) was found in moderate smokers when they worked underground for between 20 and 29 years. Heavy smokers (over 30 pack-years) or subjects who worked underground for more than 30 years experienced a high risk: SMR = 478 (p < 0.001) for moderate smokers who worked underground for over 30 years; 588 (p < 0.001) for heavy smokers who worked underground for between 20 and 29 years; and 877 (p < 0.001) for heavy smokers who worked underground for over 30 years. This showed an interaction between smoking and occupational exposure. The excess mortality from lung cancer was because there were some subjects who died young (from 45 years old). Comparison with the results of a previous study showed that additional hazards produced by diesel engines and explosives increased the mortality from lung cancer. The SMR was higher than 400 (p < 0.001) from 45 years old instead of from 56 years. A relation was found between a decrease in vital capacity (VC), forced expiratory volume in one second (FEV1) and of FEV1/VC and mortality from all causes and from lung cancer in heavy smokers or men who had worked underground for more than 20 years. Respiratory symptoms were related to mortality from lung cancer among smokers (moderate and heavy) who worked underground for more than 20 years. It is considered that the risk of lung cancer in the Lorraine iron miners was mainly due to dust, diesel engines, and explosives although the role of low exposure to radon daughters could not be totally excluded.     

Mortality among workers at a talc mining and milling facility

BACKGROUND: This study evaluated mortality among workers at a talc mining and milling facility. METHODS: Subjects were white men actively employed between 1948 and 1989 and known to have been alive in or after 1950. Analyses assessed cancer mortality during the period 1950-89 (809 subjects) and non-cancer mortality during 1960-89 (782 subjects). RESULTS: Comparisons with regional general population death rates for 1960-89 indicated that the workers had more than expected deaths from all causes combined [209 observed/160 expected, standardized mortality ratio (SMR) = 131, 95% confidence interval (CI) = 114-150], due mainly to increased mortality from lung cancer (31/13, SMR = 232, CI = 157-329) and non-malignant respiratory disease (NMRD) (28/13, SMR = 221, CI = 147-320). The lung cancer excess was concentrated in miners (18/4.6, SMR = 394, CI = 233-622); millers had only a small increase (7/5.5, SMR = 128, CI = 51-263). An excess of NMRD occurred both in miners (10/4.2, SMR = 241, CI = 116-444) and in millers (11/4.8, SMR = 227, CI = 113-407). The median estimated exposure to respirable dust was 511 mg/m(3)-days for all exposed employees, 739 mg/m(3)-days for mine workers and 683 mg/m(3)-days for mill workers. Employees with high, compared with low, estimated exposure to dust had a rate ratio of 0.5 (CI = 0.2-1.3) for lung cancer and of 11.8 (CI = 3.1-44.9) for pulmonary fibrosis. CONCLUSIONS: Exposure to talc ore dust may not have been responsible for the lung cancer excess among these workers but probably contributed to the elevated rate of NMRD, particularly pulmonary fibrosis.     

云母矿工人肺癌的流行病学调查

对内蒙古某云母矿井下男性矿工进行了肺癌回顾性队列调查。对生产环境中某些有害因素进行了测定。以全国及内蒙古男性人群肺癌死亡率作参比人群，标化死亡比（ＳＭＲ）分别为４．０５和６．６２，具有统计学意义。肺癌标化死亡率为８７．６１／１０５。有矽肺和无矽肺者肺癌发病有显著差异（Ｐ＜０．０５）。肺癌患者皆为尘肺患者。对肺癌高发原因，初步认为肺癌高发与长期高浓度接尘有关。很难排除矿尘中ＳｉＯ２和云母的作用。井下空气中存在的３，４－苯并芘，氡及其子体浓度极低，不足以构成本矿肺癌的原因。本次调查未见肺癌与吸烟有关。     

Mortality from lung cancer among copper miners.

A cohort mortality study of lung cancer in 7088 copper miners was made from 1 January 1969 to 31 December 1988. There was an excess of deaths from lung cancer in the copper miners. The standardised mortality ratio (SMR) was 147 (p < 0.01). The SMR increased with calendar period. There was a higher risk of deaths from lung cancer in the miners employed in the 1950s. Age at the start of exposure had no effect on the risk of lung cancer. The risk of death from lung cancer increased with the duration of exposure and the time since first exposure. The SMR for lung cancer was 173 in underground miners and 193 for drilling miners (both p < 0.01). These data show that exposure to dust is associated with an excess of deaths from lung cancer in copper miners whereas exposure to radiation does not seem to carry such risk.     

A cohort study of uranium millers and miners of Grants, New Mexico, 1979-2005

A cohort mortality study of workers engaged in uranium milling and mining activities near Grants, New Mexico, during the period from 1955 to 1990 was conducted. Vital status was determined through 2005 and standardised mortality ratio (SMR) analyses were conducted for 2745 men and women alive after 1978 who were employed for at least six months. Overall, mortality from all causes (SMR 1.15; 95% CI 1.07-1.23; n = 818) and all cancers (SMR 1.22; 95% CI 1.07-1.38; n = 246) was greater than expected on the basis of US mortality rates. Increased mortality, however, was seen only among the 1735 underground uranium miners and was due to malignant (SMR 2.17; 95% CI 1.75-2.65; n = 95) and non-malignant (SMR 1.64; 95% CI 1.23-2.13; n = 55) respiratory diseases, cirrhosis of the liver (SMR 1.79; n = 18) and external causes (SMR 1.65; n = 58). The lung cancer excess likely is attributable to the historically high levels of radon in uranium mines of the Colorado Plateau, combined with the heavy use of tobacco products. No statistically significant elevation in any cause of death was seen among the 904 non-miners employed at the Grants uranium mill. Among 718 mill workers with the greatest potential for exposure to uranium ore, no statistically significant increase in any cause of death of a priori interest was seen, i.e., cancers of the lung, kidney, liver, or bone, lymphoma, non-malignant respiratory disease, renal disease or liver disease. Although the population studied was relatively small, the follow-up was long (up to 50 yrs) and complete. In contrast to miners exposed to radon and radon decay products, for uranium mill workers exposed to uranium dusts and mill products there was no clear evidence of uranium-related disease.     

Radon and lung cancer risk: an extension of the mortality follow-up of the Newfoundland fluorspar cohort

Radon is a well-recognized cause of lung cancer, and studies of underground miners have provided invaluable insights on the mechanisms of radon carcinogenesis. Given the dramatic decreases in occupational exposures and the latent interval between the time of exposure and the development of lung cancer, continued follow-up of these cohorts is needed to address uncertainties in risk estimates. Here, we report on the relationship between radon and lung cancer mortality in a cohort of 1,742 Newfoundland fluorspar miners between 1950 and 2001; follow-up has been extended 11 y from previous analyses. The standardized mortality ratio (SMR) was used to compare the mortality experience of the cohort to similarly aged Newfoundland males. Poisson regression methods were used to characterize the radon-lung cancer relationship with respect to: age at first exposure, attained age, time since last exposure, interactions with cigarette smoking, and exposure rate. In total, 191 lung cancers were observed among underground miners (SMR = 3.09; 95% CI = 2.66, 3.56). ERR/WLMs decreased with attained age and time since last exposure. An inverse dose-rate effect was observed, while age at first exposure was not associated with lung cancer risk. An important strength of this study is that the effects of gamma radiation, thoron, and radioactive dust, common exposures in other miner studies, can be ruled out because the source of radon was from water running through the mine. However, the results should be interpreted cautiously due to uncertainties associated with the estimation of radon exposure levels before ventilation was introduced into the mine, and the relatively small number of lung cancer deaths that precluded joint modeling of multiple risk factors.     

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.     

Lung cancer risk and talc not containing asbestiform fibres: a review of the epidemiological evidence

A literature search was done and all epidemiological cancer studies mentioning talc as a risk factor were selected. The talc exposed populations were divided into three groups: (1) populations in which no other occupational carcinogen was mentioned (only talc millers satisfied this criterion); (2) populations of talc miners exposed to talc, quartz, and/or radon; and (3) other industrial populations in which talc is associated with quartz, nitrosamines, and asbestos depending on the study. No excess lung cancer mortality was found for the populations of talc millers exposed to high levels of talc but without any other potential carcinogen (SMR = 0.92, 42 cases) while the summary of mortality of talc miners exposed to quartz and/or radon was in excess (fixed effect SMR = 1.20, random effect RR = 1.85, 40 cases). Six studies in other industrial settings were identified. All reported increased lung cancer mortality among talc exposed workers but the talc exposure was confounded with other carcinogens and only one study was able to adjust on them. In conclusion, no increased lung cancer mortality was observed among talc millers despite their high exposure experience. In populations in which talc was associated with other potential carcinogens, some lung cancer excesses were observed.     

Exposures and mortality among chrysotile asbestos workers. Part II: mortality

A retrospective cohort mortality study was conducted among a cohort of 1,261 white males employed one or more months in chrysotile asbestos textile operations and followed between 1940 and 1975. Statistically significant excess mortality was observed for all causes combined (standardized mortality ratio [SMR] = 150), lung cancer (SMR = 135), diseases of the circulatory system (SMR = 125), nonmalignant respiratory diseases (SMR = 294), and accidents (SMR = 134). Using estimated fiber exposure levels in conjunction with detailed worker job histories, exposure-response relationships were investigated. Strong exposure-response relationships for lung cancer and asbestos related non-malignant respiratory diseases were observed. Compared with data for chrysotile miners and millers, chrysotile textile workers were found to experience significantly greater lung cancer mortality at lower lifetime cumulative exposure levels. Factors such as differences in airborne fiber characteristics may partially account for the large differences in exposure response between textile workers and miners and millers.     

Radon daughter exposure to uranium miners

Radon exposures to U.S. uranium miners under present conditions average about 1.3 WLM per year approximately or equal to 60 WLM per full working lifetime. This is intermediate between (a) the lowest exposures for which there have been excess lung cancers reported among U.S. miners (120-240 WLM) and (b) average environmental radon exposures (16 WLM), so models based on these two situations are used to estimate expected effects on present uranium miners. In Model A, the loss of life expectancy is 45 days, the SMR (standardized mortality ratio) for lung cancer is 1.10, and the SMR for all causes between ages 18 and 65 is 1.013. In Model B these are 10 days, 1.03 and 1.002 respectively. It is shown that the radon exposures to miners are similar to those to millions of Americans from environmental exposure, and that miner health risks are comparable to those of other radiation workers. Their lung cancer risk from radon is 7-50 times less than their job-related accident mortality risk, and represents 0.7-4% of their total risk in mining. Miners suffer from many diseases with SMR very much larger than that for radon-induced lung cancer, and there are many other occupations and industries with far higher SMR for lung cancer than that from radon exposure to miners.     

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     

Cancer incidence among workers exposed to radon and thoron daughters at a niobium mine

The aim of this study was to investigate the incidence of cancer among 318 male employees of a niobium mining company which was only operated between 1951 and 1965. Many of the workers, especially underground miners, were exposed to the daughters of radon and thoron and also to thorium. The accumulated doses to the workers from short-lived radon and thoron daughters in the mine atmosphere were assessed to be relatively low; up to 300 working-level months. During the follow-up period 1953-1981, 24 new cases of cancer were observed compared to an expected number of 22.8. Twelve cases of lung cancer had occurred versus 3.0 expected. Among the 77 miners, 9 cases of lung cancer were observed against 0.8 expected. Associations between the occurrence of lung cancer and exposure to alpha radiation and smoking were found. For the radon and thoron daughter exposure, about 50 excess cases per million person-years at risk per working-level month were observed.     

Carcinoma of the lung in Ontario gold miners: possible aetiological factors.

A cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.