Vermont granite mortality study: an update with an emphasis on lung cancer

This mortality study extends the period of observation of an article published in 1988 of 5414 workers in Vermont granite sheds and quarries to assess whether previously reported reductions in silicosis and tuberculosis mortality were maintained. The relationship between lung cancer and quartz exposure is also examined by comparing mortality in workers hired before and after 1940, when dust controls were introduced and exposures were reduced by 80% to 90%. Before 1940, general stone shed air contained 20 million particles/cubic foot (mppcf) (approximately equivalent to 0.2 mg/m of quartz), and pneumatic chisel workers were exposed on average to 60 mppcf (approximately equivalent to 0.6 mg/m of quartz). Other workers had variable exposures. After 1940, a period of decline occurred in dust levels and then stabilized in approximately 1955, when average dust levels were 5 to 6 mppcf (equivalent to 0.05-.06 mg/m of quartz). Dust exposures in the Vermont industry is considered to be free of confounding occupational substances such as arsenic, although cigarette smoking was common. By the end of 1996, 2539 workers, or 46.9% of the cohort, had died. There were no silicosis deaths in workers hired after 1940 who were exposed only in the Vermont granite industry, illustrating the effect of lowering quartz exposures. Tuberculosis caused 2 deaths in those hired after 1940 (standardized mortality ratio [SMR] = 0.52; not significant). Overall lung cancer mortality was elevated in shed workers who had been exposed both to high levels of quartz before 1940 and to the lower levels prevailing after 1940 (SMR = 1.32; P < 0.01). Quarry workers did not show an excess of lung cancer (SMR = 0.73; not significant). When shed workers with high and low exposure histories (before and after 1940) but with comparable latency and tenure were contrasted, lung cancer mortality was similar. Differing levels of quartz exposure, which resulted in large differences in the mortality experience from silicosis, did not result in differences in lung cancer mortality. The results do not support the hypothesis that granite dust exposure has a causal association with lung cancer.     

Mortality from lung cancer among Sardinian patients with silicosis

The mortality of 724 subjects with silicosis, first diagnosed in 1964-70 in the Sardinia region of Italy, was followed up through to 31 December 1987. Smoking, occupational history, chest x ray films, and data on lung function were available from clinical records for each member of the cohort. The overall cohort accounted for 10,956.5 person-years. The standardised mortality ratios (SMRs) for selected causes of death (International Classification of Diseases (ICD) eighth revision) were based on the age specific regional death rates for each calendar year. An excess of deaths for all causes (SMR = 1.40) was found, mainly due to chronic obstructive lung disease, silicosis, and tuberculosis with an upward trend of the SMR with increasing severity of the International Labour Office (ILO) radiological categories. Twenty two subjects died from lung cancer (SMR = 1.29, 95% confidence interval (95% CI) = 0.8-2.0). The risk increased after a 10 and 15 year latency but the SMR never reached statistical significance. No correlation was found between lung cancer and severity of the radiological category, the type of silica (coal or metalliferous mines, quarries etc), or the degree of exposure to silica dust. A significant excess of deaths from lung cancer was found among heavy smokers (SMR = 4.11) and subjects with airflow obstruction (SMR = 2.83). A nested case-control study was planned to investigate whether the association between lung cancer and airway obstruction was due to confounding by smoking. No association was found with the ILO categories of silicosis or the estimated cumulative exposure to silica. The risk estimate for lung cancer by airflow obstruction after adjusting by cigarette consumption was 2.86 for a mild impairment and 7.23 for a severe obstruction. The results do not show any clear association between exposure to silica, severity of silicosis, and mortality from lung cancer. Other environmental or individual factors may act as confounders in the association between silicosis and lung cancer. Among them, attention should be given to chronic airways obstruction as an independent risk factor for lung cancer in patients with silicosis.     

Mortality from lung cancer among Sardinian patients with silicosis.

The mortality of 724 subjects with silicosis, first diagnosed in 1964-70 in the Sardinia region of Italy, was followed up through to 31 December 1987. Smoking, occupational history, chest x ray films, and data on lung function were available from clinical records for each member of the cohort. The overall cohort accounted for 10,956.5 person-years. The standardised mortality ratios (SMRs) for selected causes of death (International Classification of Diseases (ICD) eighth revision) were based on the age specific regional death rates for each calendar year. An excess of deaths for all causes (SMR = 1.40) was found, mainly due to chronic obstructive lung disease, silicosis, and tuberculosis with an upward trend of the SMR with increasing severity of the International Labour Office (ILO) radiological categories. Twenty two subjects died from lung cancer (SMR = 1.29, 95% confidence interval (95% CI) = 0.8-2.0). The risk increased after a 10 and 15 year latency but the SMR never reached statistical significance. No correlation was found between lung cancer and severity of the radiological category, the type of silica (coal or metalliferous mines, quarries etc), or the degree of exposure to silica dust. A significant excess of deaths from lung cancer was found among heavy smokers (SMR = 4.11) and subjects with airflow obstruction (SMR = 2.83). A nested case-control study was planned to investigate whether the association between lung cancer and airway obstruction was due to confounding by smoking. No association was found with the ILO categories of silicosis or the estimated cumulative exposure to silica. The risk estimate for lung cancer by airflow obstruction after adjusting by cigarette consumption was 2.86 for a mild impairment and 7.23 for a severe obstruction. The results do not show any clear association between exposure to silica, severity of silicosis, and mortality from lung cancer. Other environmental or individual factors may act as confounders in the association between silicosis and lung cancer. Among them, attention should be given to chronic airways obstruction as an independent risk factor for lung cancer in patients with silicosis.     

Mortality of a cohort of men in a silicosis register: further evidence of an association with lung cancer

Lung cancer mortality from 1980 to 1986 was studied in a cohort of 1,419 men in a silicosis register who had no previous exposure to asbestos and polyaromatic hydrocarbons. The 28 deaths from lung cancer were statistically in excess of expected (SMR 2.03; 95% CI 1.35-2.93). Excess risks of lung cancer were found in both underground workers (SMR 3.41; 95% CI 1.10-7.97; based on 5 deaths) and surface workers (SMR 1.87, 95% CI 1.18-2.81; based on 23 deaths). All lung cancer deaths were smokers. There was an increase in SMRs with longer latency periods and years of exposure, with the greatest risk found in those who had worked for 30 or more years after more than 30 years since first exposed (SMR 3.07, based on 16 deaths). The risk for lung cancer was higher in those with tuberculosis (SMR 2.52; 95% CI 1.52-3.94) and showed an increasing trend with severity of silicosis, from category 1 to 3 and from category A to C, with highest risk in those with tuberculosis and category 3 (SMR 4.44 based on 3 deaths) or tuberculosis and category C (SMR 7.63 based on 7 deaths). Most of the excess lung cancer risk in silicotics is due to smoking, but a synergistic effect between smoking and silica/silicosis on the risk of lung cancer is also likely. In particular, a possible role of silicosis and tuberculosis as the fibrotic seedbed for malignant growth in the lung is strongly supported.     

Mortality from lung and kidney disease in a cohort of North American industrial sand workers: an update

BACKGROUND: A previously published cohort study of some 2670 employees of the North American sand industry, followed through 1994, provided strong evidence of a causal relationship between quartz exposure and death from both silicosis and lung cancer, after allowance for cigarette smoking and in the absence of known occupational carcinogens. Unexpectedly, a significant excess mortality from chronic non-malignant renal disease [observed 16; expected 7.6; standardized mortality ratio (SMR) 212] was also found, whereas deaths from renal cancer at this stage were close to expectation (observed 6; expected 5.2). OBJECTIVES: Our primary aim was to discover whether death from chronic renal disease was related to the estimated intensity of crystalline silica exposure. A further aim was to determine whether or not our previous estimates of lung cancer and silicosis risk were confirmed by mortality in the cohort 6 years later. METHODS: With help from the US National Death Index, surviving members of the cohort, with the exception of employees of a small plant in Canada, were traced through 2000. The cause of death was determined for all who had died, for comparison against National and State mortality rates. Nested case-referent analyses were then undertaken, as previously, of deaths from lung cancer and silicosis, plus end-stage renal disease and kidney cancer, in relation to quantitative re-estimates of quartz exposure. RESULTS: The total number of deaths through 1994 was 990; there were 231 additional deaths during the period 1995-2000. The SMRs were significantly higher in the later than the earlier period, mainly due to a relative increase in heart disease and external causes. The updated odds ratios for lung cancer and silicosis were almost identical to those published previously, with lung cancer risk again related to average silica concentration and cumulative exposure, but not to length of employment. In contrast, risks of neither end-stage renal disease nor renal cancer were related to cumulative exposure, although now based on 19 cases (SMR 239), and 10 cases (SMR 202), respectively, in fact, opposite trends were apparent for both diseases. However, because of the small numbers there was only limited power to assess the statistical significance of these trends or of any separate relationship with the duration or intensity of exposure. CONCLUSIONS: Our findings support a causal relationship between lung cancer and quartz exposure after allowance for cigarette smoking, in the absence of other known carcinogens, but failed to find similar evidence to explain the excess mortality from either chronic renal disease or kidney cancer.     

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.     

Respiratory cancer and other chronic disease mortality among silicotics in california

Silicotics have increased mortality from tuberculosis (TB) and from nonmalignant respiratory diseases (NMRD), including silicosis and silicotuberculosis. Since the publication of the International Agency for Research on Cancer monograph in 1987 indicating that silica was a probable human carcinogen, there has been an extensive debate about the cancer risks among silicotics. The authors identified 590 claims for silicosis among a registry of lung diseases compiled from California Workers' Compensation cases from 1945 to 1975. Using state vital records, we determined the mortality risks from 1946 to 1991. Our findings confirmed that these claimants had a significantly elevated risk for all causes of death with a standardized mortality ratio (SMR) of 1.30 (95% confidence interval [CI] = 1.18, 1.43); TB had a SMR of 56.35 (95% CI = 41.10, 75.40) and NMRD a SMR of 3.80 (95% CI = 3.11, 4.60). Cancers of the trachea, bronchus, and lung had a SMR of 1.90 (95% CI = 1.35, 2.60). For malignancies of the large intestine, there was a previously unreported SMR of 2.08 (95% CI = 1.14, 3.50). Mortality from all diseases of the heart was significantly less than expected with a SMR of 0.68 (95% CI = 0.55, 0.83); cancers of the prostate and lymphatic system were also significantly low with SMRs of 0.26 (95% CI = 0.03, 0.94) and 0.17 (95% CI = 0.04, 0.97), respectively. Workers with silicosis should be warned about these chronic disease risks, and prevention efforts to control occupational silica dust exposure should become a higher priority.     

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.     

Epidemiologic study of cancer mortality among Israeli asphalt workers

BACKGROUND: We describe the results of a cancer mortality study among asphalt workers in Israel. METHODS: Personal identifiers and employment histories of 2,176 workers were extracted from company records. RESULTS: Mortality from all malignant neoplasms was significantly reduced in the whole cohort (SMR 0.68, 95% confidence interval (CI) 0.56-0.83). SMR for lung cancer was elevated in workers exposed to bitumen (SMR 1.05, 95% CI 0.62-1.66). No significant elevation or reduction in mortality was observed in relation to a specific site. SMRs for lung cancer was higher among ever exposed to bitumen than among unexposed. There was no association between lung cancer risk and estimated exposure to bitumen fume, and no dose-response was apparent. CONCLUSIONS: While the results of this cohort study indicate a slightly increased SMR for lung cancer, it did not produce evidence of a causal link between lung cancer and exposure to bitumen fume.     

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.     

10个钨矿职工死因分析

对中南地区10个钨矿1972—1974年入矿(工龄至少1年)的在册职工28453人进行了队列研究。队列成员追访至1989年,死亡2870人,比全国居民死亡率计算的期望值略高(SMR=1.15,95％CI=1.11—1.19);主要是非恶性呼吸道疾病,特别是尘肺(SMR=66.79,95％CI=59.65—73.68)以及与呼吸道疾病相关的肺心病明显超高(SMR=8.19,95％CI=7.42—9.02),比全国居民死亡率高5倍。癌症死亡数在全死因中虽占第一位,但仅鼻咽癌轻度超高(SMR=1.73,95％CI=1.23—2.37),而肺癌死亡率明显偏低(SMR=0.53)。研究结果不支持矽肺与肺癌病因学相关的假说。     

Mortality among employees of lead battery plants and lead-producing plants, 1947-1980

Two cohorts of male lead workers, 4 519 battery plant workers and 2 300 lead production workers, all of whom had been employed for at least one year during the period 1 January 1946 through 31 December 1970, were observed for mortality during the 34 years from 1 January 1947 through 31 December 1980. Vital status as of the closing date was determined for 94.7% of the former group and 91.6% of the latter. There were 1 718 deaths in the first cohort and 621 in the second. Mortality from all causes combined was significantly greater than expected in each cohort, the standardized mortality ratio (SMR) being 107 and 113, respectively. Among the battery plant workers the greater than expected mortality rate resulted in large part from a significant number of excess deaths from malignant neoplasms (SMR 113), other hypertensive disease (mainly renal) (SMR 320), chronic nephritis (SMR 222), and a group of ill-defined conditions (SMR 355). Among the lead production workers the pattern was similar, with a significant number of excess deaths from other hypertensive disease (SMR 475), hypertensive heart disease (SMR 203), chronic nephritis (SMR 265), and ill-defined conditions (SMR 214). There was also a significant excess of deaths from external causes (SMR 143). The SMR for total malignancies was 113, but this value was not significantly elevated at the 5% level. In neither cohort were deaths from cerebrovascular disease in significant excess, the SMR being 93 and 132, respectively. A proportionate mortality analysis showed that the excess deaths from cerebrovascular disease and from hypertensive heart disease among smelter workers were in part due to the high proportion of nonwhites in the smelter populations. The stomach, liver, and lungs were the sites responsible for most excess cancer deaths in both cohorts, but the elevated SMR values were statistically significant only for gastric and lung cancers in battery plant workers. There were no excess deaths from malignancies of the kidney, brain, or lymphopoietic system in either cohort. It is impossible to relate the observed mortality to levels of lead exposure; because of meager quantitative information prior to 1960. It is known that past exposures had been very high. Ethnicity, diet, alcohol, and cigarette smoking could not be ruled out as possible confounding etiologic factors for the cancer deaths.     

Cohort mortality study of North American industrial sand workers. I. Mortality from lung cancer, silicosis and other causes

BACKGROUND: In 1997 a Working Group of the International Agency for Research on Cancer changed an earlier classification of crystalline silica as a human carcinogen from Group 2A to Group 1, though commenting that the carcinogenicity might vary with industrial circumstances and depend on additional factors affecting biological activity, including the distribution of its polymorphs.Objective: We aimed to determine whether pure quartz exposure uncomplicated by the presence of other contaminating carcinogens, as experienced by workers in the production of high-grade industrial sand, was causally related to an increased risk of lung cancer. METHODS: A cohort of 2670 men employed before 1980 for 3 years or more in one of nine North American sand-producing plants and a large associated office complex was selected for study. Of the cohort, 2644 (99%) were traced through 1994, and certificated cause of death ascertained for 1025 (99%) of the 1039 men known to have died. Standardised mortality ratios (SMRs) were calculated for the main causes of death, using both US and state or provincial male mortality rates for reference. FINDINGS: The main analyses of deaths, 20 or more years after first employment against regional rates, gave the following SMRs: all causes 109, lung cancer 139, other malignancies 98, non-malignant respiratory disease 161, and nephritis/nephrosis 244. There were, in total, 37 deaths from silicosis or silico-tuberculosis, with one or more death at least in all nine production plants. Analyses failed to show any relation between lung cancer risk and duration of employment. The increased SMR for lung cancer was wholly due to high rates in four plants in two states, whereas no increase was found in the remainder of the cohort. CONCLUSION: In the absence of information on smoking histories and risk in relation to estimated exposure, the increased SMR for lung cancer (139), although statistically significant, cannot be attributed confidently to crystalline silica. An answer to the question of attributability must await the findings of the nested case-control study, in which level of exposure and smoking habits were ascertained for cases and matched controls. The strong indication in this cohort of excess mortality from non-malignant renal disease deserves further investigation.     

Carbon black and lung cancer: Testing a new exposure metric in a German cohort

BACKGROUND: A cohort mortality study of a large carbon black production plant in Germany showed an elevation in lung cancer mortality (SMR 1.81 (95% CI: 1.34-2.39)), although the elevation could not be linked to exposure to carbon black. METHODS: In follow up to a British study of carbon black production workers [Sorahan et al., 2007] in which risk of lung cancer progressively declined after cessation of employment-in contrast to an expected upward trend-we evaluated the German cohort with a similar methodology, that is, by focusing on the first 15 years after leaving employment in terms of lung cancer SMR. RESULTS: In our SMR analysis of the German cohort of 1,528 men and an inception cohort of 1,271 men, distinctly different results from the British cohort were observed. We observed a rising trend in lung cancer SMR, in contrast to the declining SMR trend noted in the British cohort. In fact, Cox models for lung cancer mortality with attained age as the basic time variable showed negative coefficients for the full and inception cohorts. CONCLUSIONS: Our analysis of a large German cohort of carbon black workers does not support the concept of a declining risk of lung cancer following cessation of employment.     

Follow-up study of chrysotile asbestos textile workers: Cohort mortality and case-control analyses

Previous studies of mortality among white males employed in a Charleston, South Carolina asbestos textile plant using chrysotile demonstrated significant excess mortality due to asbestos-related disease and a steep exposure-response relationship for lung cancer. This cohort was further studied by adding 15 years of follow-up and including mortality among white female and black male workers. Nested case-control analyses were undertaken to further explore possible differences in lung cancer risk by textile operation as well as possible confounding by mineral oil exposures. Preliminary data for white males have been previously published. White males experienced statistically significant excess mortality due to lung cancer (standardized mortality ratio [SMR] = 2.30; confidence interval [CI] = 1.88–2.79), all causes (SMR = 1.48; CI = 1.38–1.58), all cancers (SMR = 1.50; CI = 1.29–1.72), diabetes mellitus (SMR = 2.05; CI = 1.18–3.33), heart disease (SMR = 1.41; CI = 1.26–1.58), cerebrovascular disease (SMR = 1.50; CI = 1.08–2.02), pneumoconiosis and other respiratory diseases (SMR = 4.10; CI = 3.10–5.31), and accidents (SMR = 1.49; CI = 1.15–1.91). Among white females, statistically significant excesses occurred for lung cancer (SMR = 2.75; CI = 2.06–3.61), all causes (SMR = 1.21; CI = 1.11–1.32), pneumoconiosis and other respiratory diseases (SMR = 2.40; CI = 1.53–3.60), and other respiratory cancers (SMR = 14.98; CI = 4.08–38.7). Among the total cohort of black males, the only statistically significant excess observed was for pneumoconiosis (SMR = 2.19; CI = 1.23–3.62). Based on historical exposure measurements at the plant, there was a positive exposure-response relationship for both lung cancer and pneumoconiosis. Data for the entire cohort demonstrate an increase in the lung cancer relative risk of 2–3% for each fiber/cc-year of cumulative chrysotile exposure. This relationship was more consistent for the white male workers. The excess risk for lung cancer among white males and females appeared to occur at cumulative exposures lower than those for black males. Possible reasons for the lesser lung cancer risk among black males include less smoking and differences in airborne fiber characteristics experienced by black males as a result of plant job placement patterns. The case-control analysis found employment in preparation and carding operations (where most of the black males worked) to be associated with a slightly reduced lung cancer risk, although not statistically significant, whereas spinning and twisting employment was associated with a statistically significant increased lung cancer risk compared to other plant operations. Airborne fiber size data, determined by transmission electron microscopy, demonstrated slightly longer fibers in spinning and twisting compared to other textile operations. Case-control analyses demonstrated little effect of mineral oil exposures on the lung cancer exposure-response estimates. Two deaths due to mesothelioma were observed among this cohort.     

Mortality of lead smelter workers

To examine patterns of death in lead smelter workers, a retrospective analysis of mortality was conducted in a cohort of 1,987 males employed between 1940 and 1965 at a primary lead smelter in Idaho. Overall mortality was similar to that of the United States white male population (standardized mortality ratio (SMR) = 98). Excess mortality, however, was found from chronic renal disease (SMR = 192; confidence interval (CI) = 88-364), and the risk of death from renal disease increased with increasing duration of employment, such that after 20 years employment, the standardized mortality ratio reached 392 (CI = 107-1,004). Excess mortality was also noted for nonmalignant respiratory disease (SMR = 187, CI = 128-264). Eight of 32 deaths in this category were caused by silicosis; at least five workers who died of silicosis had been miners for a part of their lives. An additional 11 deaths resulted from tuberculosis (SMR = 139; CI = 69-249); in six of these cases, silicosis was a contributory cause of death. Cancer mortality was not increased overall (SMR = 95; CI = 78-114). An increase, however, was noted for deaths from kidney cancer (six cases; SMR = 204; CI = 75-444). Finally, excess mortality was noted for injuries (SMR = 138; CI = 104-179); 13 (23%) of the 56 deaths in this category were caused by mining injuries. The data from this study are consistent with previous reports of increased mortality from chronic renal disease in persons exposed occupationally to lead.     

Mortality in a cohort of asbestos cement workers in Bari

The study describes the mortality of 417 workers employed in a asbestos-cement plant, located in Bari, Puglia, Southern Italy. Follow up started on February 1st 1972. The vital status and cause of death were ascertained at 1995. The mortality experience of the Apulian population was used as comparison. Using 90% confidence limits (CLs), a significant increase in mortality was observed in our cohort from: all causes of death (SMR 118, CL 100-139), pneumoconiosis (SMR 14810, CL 10298-20683), all types of cancer (SMR 139, CL 105-181), lung (SMR 191, CL 126-277), pleural (SMR 1560 CL 431-4081) and peritoneum (SMR 1705, CL 303-5367) malignant neoplasms. In our cohort, the discrepancy between observed and expected mortality for lung and pleural cancer occurred 30 years after the first exposure, after 40 years for all neoplasms and peritoneum cancer. Under the Cox regression model, lung cancer SMR showed a curvilinear trend along time since first exposure, the peak being detected at 35 years. Finally, SMRs from our cohort were compared to a previously described cohort including workers from the same plant compensated for asbestosis by INAIL.     

An update of a mortality study of talc miners and millers in Italy

BACKGROUND: While talc containing asbestiform fibers is considered a human carcinogen, only limited animal and human data are available on non-asbestiform talc. To provide further evaluation on the issue, we updated the analysis of an Italian cohort of talc miners and millers in Val Chisone; talc found here is free from asbestiform fibers. METHODS: The cohort was comprised of 1,795 men who had worked for at least 1 year in the mine and/or in the factory between 1946 and 1995. Vital status and death certificates were obtained from registration offices in the municipality of death or of birth. Employment, termination of employment, and detailed job history were obtained from personnel records at the plant. RESULTS: No excess was found for total cancer mortality, nor mortality for lung cancer. No case of mesothelioma was reported. There was a significant excess mortality from non-neoplastic respiratory diseases (SMR 228.2, 95% CI 190.2-271.5). Mortality excess for non-neoplastic respiratory diseases was mainly due to silicosis. CONCLUSIONS: This study provides additional support for an association between talc in mining and milling and non-neoplastic respiratory diseases, while showing no significant excess risk for lung cancer and mesothelioma. The results also provide additional information of interest to evaluate the potential association between silica and lung cancer.