Mortality of middle aged white South African gold miners

A cohort of 3971 white miners in South Africa, born between 1 January 1916 and 31 December 1930 who were alive on 1 January 1970 and currently working in the East Rand-Central Rand-West Rand mining areas, was followed up for nine years, when the 3426 survivors were aged from 48 to 62. Fifteen (0.4%) had been lost to view and 530 had died (13.4% of the 3956 whose vital status was determined). Based on the occupational histories of a 30% sample of the cohort it was known that the vast majority were gold miners. An estimated 93% had worked more than 85% of their mining service in gold mines. Standardised mortality ratios were calculated as the ratios of the deaths observed in the cohort to those expected on the basis of concurrent mortality in the reference population--the total white male population in the Republic of South Africa. There was little sign of a "healthy worker effect"; of several possible reasons, one is that the white miner in South Africa had adopted certain unhealthy life styles, another is that the reference population was otherwise inappropriate. The SMR for all causes of death (117.6) was raised because of excess mortality due to the following causes: lung cancer (161.2), chronic respiratory diseases (165.6), and acute and chronic nephritis (381.0). A case-referent analysis was carried out on those miners in the cohort who had spent at least 85% of their service in gold mines. For lung cancer, smoking was the main contributory factor towards disease. For chronic respiratory diseases bronchitis, emphysema, asthma, pneumoconiosis, and pulmonary heart disease), smoking was also the main risk factor, but there was an association wih cumulative dust exposure. Raised blood pressure, smoking, and adiposity were associated with ischaemic heart disease as was the duration of service underground. Study of comprehensive medical histories in all 530 deaths, including necropsy in most cases, showed that none was directly due to pneumoconiosis or to tuberculosis.     

Mortality of middle aged white South African gold miners.

A cohort of 3971 white miners in South Africa, born between 1 January 1916 and 31 December 1930 who were alive on 1 January 1970 and currently working in the East Rand-Central Rand-West Rand mining areas, was followed up for nine years, when the 3426 survivors were aged from 48 to 62. Fifteen (0.4%) had been lost to view and 530 had died (13.4% of the 3956 whose vital status was determined). Based on the occupational histories of a 30% sample of the cohort it was known that the vast majority were gold miners. An estimated 93% had worked more than 85% of their mining service in gold mines. Standardised mortality ratios were calculated as the ratios of the deaths observed in the cohort to those expected on the basis of concurrent mortality in the reference population--the total white male population in the Republic of South Africa. There was little sign of a "healthy worker effect"; of several possible reasons, one is that the white miner in South Africa had adopted certain unhealthy life styles, another is that the reference population was otherwise inappropriate. The SMR for all causes of death (117.6) was raised because of excess mortality due to the following causes: lung cancer (161.2), chronic respiratory diseases (165.6), and acute and chronic nephritis (381.0). A case-referent analysis was carried out on those miners in the cohort who had spent at least 85% of their service in gold mines. For lung cancer, smoking was the main contributory factor towards disease. For chronic respiratory diseases bronchitis, emphysema, asthma, pneumoconiosis, and pulmonary heart disease), smoking was also the main risk factor, but there was an association wih cumulative dust exposure. Raised blood pressure, smoking, and adiposity were associated with ischaemic heart disease as was the duration of service underground. Study of comprehensive medical histories in all 530 deaths, including necropsy in most cases, showed that none was directly due to pneumoconiosis or to tuberculosis.     

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 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.     

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.     

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.     

Mortality from stomach cancer in Ontario miners.

An excess of mortality from stomach cancer has been found in Ontario gold miners (observed (obs) 104, standardised mortality ratio (SMR) 152, 95% confidence interval (95% CI) 125-185) and no excess of stomach cancer could be detected in other miners in Ontario (obs 74, SMR 102, 95% CI 80-128). The excess of stomach cancer appeared five to 19 years after the miners began gold mining in Ontario. In that interval, similar patterns of excess mortality from stomach cancer were found in miners born in north America (obs 14, SMR 268, CI 147-450) and in miners born outside north America (obs 12, SMR 280, 95% CI 145-489). Twenty or more years after the miners began mining gold, an excess of mortality from stomach cancer was found in gold miners born outside of north American (obs 41, SMR 160, 95% CI 115-218) but not in gold miners born in north America (obs 37, SMR 113, 95% CI 80-156). The excess of stomach cancer in gold miners under the age of 60 (obs 45, SMR 167, 95% CI 122-223) seems larger than the excess in gold miners between the ages of 60 and 74 (obs 59, SMR 143, 95% CI 109-184). Exposures to arsenic, chromium, mineral fibre, diesel emissions, and aluminium powder were considered as possible explanations of the excess of stomach cancer in Ontario gold miners. Exposure to diesel emissions and aluminium powder was rejected as gold miners and uranium miners were exposed to both agents but an excess of stomach cancer was noted only in gold miners. The association between the excess of stomach cancer and the time since the miner began mining gold suggested that duration of exposure to dust in gold mines ought to be weighted according to the time since the exposure to dust occurred and that an appropriate time weighting function would be one in the interval five to 19 years after each year of exposure to dust and zero otherwise. A statistically significant association between the relative risk of mortality from stomach cancer and the time weighted duration of exposure to dust in gold mines was found in miners under the age of 60. Time weighted indices of exposure to chromium and arsenic were formed for each gold miner by time weighting the product of the duration of exposure to dust in a gold mine and the percentages of arsenic and chromium in rocks in that gold mine. Exposure to mineral fibre was measured in terms of the time weighted duration of employment in those gold mines that contain mineral fibre. A statistically significant association between the excess of stomach cancer in gold miners under the age of 60 and the time weighted index of exposure to chromium occurred and not association was found between the excess of stomach cancer and either the time weighted duration of employment in mines containing mineral fibre. The excess of stomach cancer in gold miners under the age of 60 was better associated with the time weighted index of exposure to chromium than to the time weighted duration of exposure to dust in gold mines. Although the number of cases of gastric cancer that were classified according to the system of Lauren was small, the data suggest that for miners under the age of 60, exposure to chromium is associated with the development of the intestinal rather than the diffuse type of gastric cancer.     

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 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.     

Silicosis and lung cancer in U.S. metal miners

The association between silicosis and lung cancer mortality was estimated in 9,912 (369 silicotics and 9,543 nonsilicotics) white male metal miners. These miners were examined by the U.S. Public Health Service during 1959-1961 and were followed through 1975. Miners were excluded from this study if they were employed in a mine during 1959-1961 that used diesel equipment underground. The ores that were mined consisted of copper, lead-zinc, iron, mercury, lead silver, gold and gold-silver, tungsten, and molybenum. The standardized mortality ratio (SMR, U.S. white male rates) for lung cancer was 1.73 (95% CI: .94-2.90) in silicotics and 1.18 (95% CI: .98-1.42) in nonsilicotics. Additionally, SMRs were higher in silicotics than in nonsilicotics, even in most subgroups stratified by cigarette smoking habit, type of ore mined, years of service in an underground job, radon exposure group, or year of hire. When lung cancer mortality between silicotics and nonsilicotics was compared, the age-adjusted rate ratio (95% CI) was 1.56 (.91-2.68), and the age- and smoking-adjusted rate ratio was 1.96 (.98-3.67). Corresponding figures for miners who were employed in mines with low levels of radon exposure were 1.90 (.98-3.67) and 2.59 (1.44-4.68), respectively. These findings indicate that lung cancer mortality risk was increased in silicotics, and this probably did not result from chance or bias. However, confounding from radon exposure could not be ruled out. The findings indicate that further follow-up of this cohort is needed.     

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.     

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.     

Long-term mortality in miners with coal workers' pneumoconiosis in The Netherlands: a pilot study

In order to investigate whether the prolonged exposure to coal mine dust increases the cancer risk for coal miners, a pilot study in a selected cohort of 334 Dutch miners with coal workers' pneumoconiosis (CWP), followed from 1956 until 1983, was conducted. In total, 165 miners had died (49.4%); for 162 (98.2%) the cause of death was traced. In comparison to the general Dutch male population, total mortality in the cohort was statistically significantly increased (SMR: 153). This was in general due to the significantly higher than expected cancer mortality (SMR: 163), cancer of stomach and small intestine (SMR: 401) and nonmalignant respiratory disease (SMR: 426). The lung cancer mortality was within the expected range.     

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.     

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.     

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     

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 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.     

Mortality of Dutch coal miners in relation to pneumoconiosis, chronic obstructive pulmonary disease, and lung function.

OBJECTIVES: To analyse the mortality patterns of former Dutch coal miners, focusing on coal workers' pneumoconiosis (CWP) and chronic obstructive pulmonary diseases (COPD) in relation to pre-existing impairment of lung function. METHODS: 3790 selected miners, medically examined between 1952 and 1963, were followed up to the end of 1991 with the municipal population registries and the causes of death from the death certificates were ascertained and converted to the codes from the ninth revision of the international classification of diseases (ICD-9). Mortality comparisons were made with the male population in The Netherlands, resulting in standardised mortality ratios (SMRs). 3367 miners had radiological manifestation of CWP at medical examinations. RESULTS: 80% of the miners died during the follow up period. Excess mortalities from CWP (SMR 4523) and COPD (SMR 179) were found. Coal miners without CWP also showed an increased mortality from COPD (SMR 2913). A diminished lung function (forced expiratory volume in one second (FEV1), or FEV1/FVC (forced vital capacity) ratio) at medical examination resulted in a significantly increased SMR for COPD (322 and 212 respectively) whereas normal lung function yielded expected mortalities from COPD. A positive correlation also emerged between diminished lung function and the SMR due to CWP. The body mass index (BMI) at the moment of medical examination was correlated with the risk of dying of COPD and CWP: a decreasing BMI resulting in an increased SMR. CONCLUSIONS: Not only infectious diseases and CWP but also COPD is an important cause of occupational mortality in miners with extensive exposure to coal mine dust. No obvious connection between pre-existing CWP and the COPD mortality exists. Impaired FEV1 and FEV1/FVC ratios are predictors of an increased risk of COPD death. The BMI seems to indicate the severity of the COPD, resulting in premature death.     

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.