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.     

吸烟校正因素间接调整法在职业流行病学队列研究中的应用

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

Mortality pattern of silicotic subjects in the Latium region, Italy

A mortality study was carried out on 595 workers who were compensated for silicosis in the Latium region, Italy, during the period 1946-84 who died between 1 January 1969 and 31 December 1984. Respiratory disorders, tuberculosis, lung cancer, bone cancer, and cirrhosis of the liver showed significantly increased risk ratios (4.1, 3.7, 1.5, 4.1, and 1.9 respectively); excesses of brain cancer and leukaemia did not reach statistical significance. Lung cancer mortality was further analysed by age, period of compensation, final degree of disability, and occupational activity. The possible confounding role of smoking was assessed by comparing the lifetime smoking habits of a sample of silicotic subjects with those of the general male population as estimated by a national health survey; the prevalence of ever smokers among silicotic subjects (70.7%) was similar to that estimated for the general population (68.5%). The present study indicates that silicosis is associated with lung cancer even though it does not clarify the respective roles of exposure to silica and silicosis.     

Mortality pattern of silicotic subjects in the Latium region, Italy.

A mortality study was carried out on 595 workers who were compensated for silicosis in the Latium region, Italy, during the period 1946-84 who died between 1 January 1969 and 31 December 1984. Respiratory disorders, tuberculosis, lung cancer, bone cancer, and cirrhosis of the liver showed significantly increased risk ratios (4.1, 3.7, 1.5, 4.1, and 1.9 respectively); excesses of brain cancer and leukaemia did not reach statistical significance. Lung cancer mortality was further analysed by age, period of compensation, final degree of disability, and occupational activity. The possible confounding role of smoking was assessed by comparing the lifetime smoking habits of a sample of silicotic subjects with those of the general male population as estimated by a national health survey; the prevalence of ever smokers among silicotic subjects (70.7%) was similar to that estimated for the general population (68.5%). The present study indicates that silicosis is associated with lung cancer even though it does not clarify the respective roles of exposure to silica and silicosis.     

Mortality of workers compensated for silicosis during the period 1959-1963 in the Veneto region of Italy

After reports appeared from other countries indicating an excess risk of lung cancer among silicotics, a cohort of workers compensated for silicosis during the period 1959-1963 in the Veneto region of Italy was constructed and followed for mortality through 1984. The results of the study showed a large mortality excess for infectious diseases (180 observed versus 9.5 expected), due to silicotuberculosis, and for diseases of the respiratory system (270 observed versus 33.5 expected) due to silicosis. An elevated standardized mortality ratio of 239 (70 observed versus 29.3 expected) from lung cancer was also detected. An increasing pattern was observed with time since first exposure, while the relationship with employment category and duration of exposure was less clear-cut. The lung cancer excess was also strongly associated with cigarette smoking, there being a dose-response relationship with daily cigarette consumption. The study confirms the results from other epidemiologic studies on silicotics which show this pathological condition to be associated with increased lung cancer mortality.     

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.     

Silicosis and smoking strongly increase lung cancer risk in silica-exposed workers

It remains controversial whether silica is a human lung carcinogen. In this study, we estimated the relative risks of lung cancer due to silica and silicosis by meta-analysis. We collected papers published from 1966-2001 which epidemiologically reported on the relationship between silica/silicosis and lung cancer. We removed papers which did not exclude the effects of asbestos and radioactive materials including radon. We selected the most recent one if some papers were based on the same cohort. Based on the selected papers, we summarized the lung cancer risks from silica, silicosis and non-silicosis with exposure to silica, by meta-analysis using a random effects model. The pooled relative risks were 1.32 (95% confidence interval (CI), 1.23-1.41) for silica, 2.37 (95% CI, 1.98-2.84) for silicosis and 0.96 (95% CI, 0.81-1.15) for non-silicosis with exposure to silica. Since some papers on silica did not exclude silicosis, the risk due to silica itself may be smaller than 1.32. It was less possible that silica exposure directly increases lung cancer risk. On the other hand, the relative risk, 2.37 for silicosis suggested that silicosis increases lung cancer risk. Meta-analysis also revealed that cigarette smoking strongly increased the lung cancer risk in silicotic patients (relative risk, 4.47; 95% CI, 3.17-6.30). Thus, the present study suggested the great importance of preventing silicosis and smoking cessation in reducing lung cancer incidence in silica-exposed workers.     

Silicosis and lung cancer: a mortality study of compensated men with silicosis in New South Wales, Australia

BACKGROUND: Lung cancer mortality has been found to be in excess in several groups with silicosis, but allowance for smoking was not always possible. We investigated the lung cancer mortality in men with silicosis in New South Wales, Australia, who were compensated, making allowance for smoking habits. METHODS: A mortality study of 1467 men with silicosis in New South Wales who were compensated was carried out comparing observed mortality with that expected from the New South Wales death rates adjusting for age and period. Their smoking habits were compared with national survey smoking rates and the expected number of lung cancer deaths adjusted for smoking. Cases were coded for occupation and industry. RESULTS: The observed mortality was higher than expected, but the only site of cancer showing a significant excess was the lung. The group with silicosis had smoked more than the national rates. After adjusting for smoking the standardized mortality ratio for lung cancer was 1.9 (95% confidence interval 1.5-2.3). Although there were differences in lung cancer mortality between industries and occupations, these differences were not statistically significant. CONCLUSIONS: The excess lung cancer death rate may not be entirely due to silica exposure because compensation may have been influenced by the presence of chronic obstructive respiratory disease and there is some evidence that the presence of this disease increases lung cancer risk independently of smoking.     

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 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.     

A case-control study of lung cancer in relation to silica exposure and silicosis in a rural area in Japan

PURPOSE: In southeast Okayama Prefecture, Japan, there have been reports of a high prevalence of silicosis among refractory brick production workers. Recently, a high mortality rate of lung cancer among the local residents has been observed. Therefore, a population based case-control study was conducted concerning the relationship between silica, silicosis, and lung cancer using multiple cancer controls. METHODS: Cases and controls were restricted to male subjects and information was obtained from death certificates from 1986 to 1993 in the area. Three categories of deceased control groups were selected: a series of deaths from liver cancer, colon cancer, and cancers of other organs, which was assumed not to be related to silica exposure. Age and smoking habits were adjusted by stratified analysis using the Mantel-Haenszel odds ratio estimates. Unconditional logistic regression analysis was also conducted to control potential confounding factors; such as age and smoking habits. RESULTS: The age-, smoking-adjusted odds ratios were 1.94 (0.94-4.43) for the colon cancer control group, 2.13 (1.19-3.85) for the other cancer control group related to silica exposure, and 2.94 (1.30-8.90) and 2.69 (1.43-5.37) related to silicosis, respectively. The direct weighted average using the estimates for colon and the other cancer controls was 2.06 (1.29-3.29) for silica exposure, and 2.77 (1.60-4.77) for silicosis. Histological or cytological types of lung cancer cases were obtained from 64.1% of the subjects (118/184). As for the histologic type of lung cancer, small cell carcinoma was higher among those who had been silica-exposed workers than the unexposed lung cancer cases and the data from the general Japanese population. On chest x-ray findings, elevated lung cancer mortality compared with cancers other than lung cancer was demonstrated among patients without large opacities. CONCLUSIONS: Silica exposure increased the lung cancer mortality in the area. A high lung cancer mortality rate in the area could be explained by silica exposure and silicosis prevalence in this area.     

Cohort mortality study of North American industrial sand workers. II. Case-referent analysis of lung cancer and silicosis deaths

BACKGROUND: A cohort mortality study of 2670 men in nine North American industrial sand plants resulted in 83 deaths from lung cancer 20 or more years after hire (standardized mortality ratio 139) and 37 deaths from silicosis (including seven from silico-tuberculosis). The lung cancer excess was unrelated to duration of employment and not found in all plants.Objectives: The primary aim was to determine whether lung cancer risk among these employees was related to quantitative estimates of crystalline silica exposure, after allowance for cigarette smoking. A secondary aim was to do the same for silicosis mortality, partly as a means of validating the estimated levels of exposure. METHODS: A nested case-referent study was undertaken with cases matched with up to two controls on plant, age and date of first employment from men who survived the case. Exposures were estimated by linking work histories to a job-exposure matrix, undertaken separately. Cigarette smoking information was obtained from medical records and other sources, blind as to case-control status. Matched statistical analyses were conducted using conditional logistic regression. FINDINGS: Odds ratios for silicosis mortality were significantly related to cumulative silica exposures and tended to a relationship with category of average crystalline silica concentration, but inconsistently with length of employment. After accounting for a strong effect of cigarette smoking, odds ratios for lung cancer were related to cumulative crystalline silica exposure and to average silica concentration, but not to length of employment. CONCLUSION: These findings support a causal relationship between lung cancer and quartz exposure after allowance for cigarette smoking, in the absence of cristobalite or other known occupational carcinogens.     

Silica,compensated silicosis,and lung cancer in Western Australian goldminers

OBJECTIVES: Silica has recently been reclassified as carcinogenic to humans based largely on the observed increase in rates of lung cancer in subjects with silicosis. Other recent reviews have arrived at different conclusions as to whether silicosis or silica itself is carcinogenic. This study aims to examine exposure-response relations between exposure to silica and subsequent silicosis and lung cancer in a cohort of goldminers. METHODS: 2,297 goldminers from Kalgoorlie in Western Australia were examined in 1961, 1974, and 1975. Data were collected on respiratory symptoms, smoking habits, and employment history. Subjects were followed up to the end of 1993. Survival analyses for lung cancer mortality and incidence of compensated silicosis were performed with age and year matched conditional logistic regression analyses. RESULTS: 89% of the cohort were traced to the end of 1993. 84% of the men had smoked at some time and 66% were current smokers. 1386 deaths occurred during the follow up period, 138 from lung cancer, and 631 subjects were compensated for silicosis. A strong effect of smoking on mortality from lung cancer, and a smaller effect on the incidence of compensated silicosis was found. There was a strong effect of duration and intensity of exposure on the incidence of silicosis. The risk of mortality from lung cancer increased after compensation for silicosis. Of all direct measures of exposure to silica, only log cumulative exposure was significantly related to incidence of lung cancer, but this effect disappeared once the onset of silicosis was taken into account. CONCLUSIONS: The incidence of silicosis was clearly related to exposure to silica and the onset of silicosis conferred a significant increase in risk for subsequent lung cancer, but there was no evidence that exposure to silica caused lung cancer in the absence of silicosis.       

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.     

Lung cancer mortality in a french cohort of hard-metal workers

A cohort mortality study was carried out among workers of a plant producing hard metals using cobalt as a binder. This study was aimed at assessing possible lung cancer risks in relation with cobalt exposure. Seven hundred nine male workers with at least 1 year of employment were included in the cohort and followed for mortality from 1956 to 1989. Job histories were provided by the administration of the plant, whereas smoking habits were collected from medical records and by interview. The causes of deaths were ascertained from hospital and general practitioner records. The observed numbers of deaths (obs) were compared with the expected based on national rates with adjustment for age, sex, and calendar time (standardized mortality ratio; SMR). The overall mortality did not differ from that expected (obs = 75, SMR = 1.05), whereas mortality due to lung cancer was in significant excess (obs = 10, SMR = 2.13). This excess was higher among workers employed in the areas with the highest exposure (obs = 6, SMR = 5.03). No trend was observed, however, with duration of employment or time since first employment. Smoking data were available for 81% of the workers and 69% of the deceased and showed that smoking alone does not account for these lung cancer excesses, yet, because of the small numbers involved, no firm conclusion should be drawn from this study.     

Radiographic silicosis and lung cancer risk among workers in Ontario

A case-control study, nested in a cohort of workers under surveillance for silicosis in 1979 or later, was undertaken to assess lung cancer risk in relation to the ILO coding scheme for the pneumoconioses. The subjects of this study are from the 41 matched quartets, consisting of one worker with silicosis and three age-matched controls, in which a lung cancer case was diagnosed. The odds ratio for lung cancer among subjects with ILO classification 1/0 or more, in comparison to subjects with category ≤ 0/1, was 3.27 (95%CI = 1.32–8.2). Adjustment of the radiographic risk for the effect of cumulative radon exposure had the effect of increasing the odds ratio for the association between ILO category ⩾1/0 and lung cancer. Although small smoking differences could account for the increased lung cancer odds ratio among workers with silicosis, the empirical evidence suggests that these smoking differences do not exist. It is concluded on the basis of two North American studies of silica exposed workers that radiographic silicosis is a marker for an increased risk of lung cancer. Am. J. Ind. Med. 34:244–251, 1998. © 1998 Wiley-Liss, Inc.     

Meta-analysis of silicosis and lung cancer

OBJECTIVES: This study examined the association between silicosis and lung cancer in a systematic review (and meta-analysis) of the epidemiologic literature, with special reference to the methodological quality of observational studies. METHODS: We searched Medline, Toxline, BIOSIS and Embase (1966-May 2004) for original articles published in any language and systematically reviewed the bibliographies of the retrieved articles. Observational studies (cohort and case-control studies) were selected if they reported a measure of association [standardized mortality ratio (SMR), relative risk or odds ratio] relating lung cancer to silicosis. RESULTS: Thirty-one studies (27 cohort studies, 4 case-control studies) met the inclusion criteria of the meta-analysis. Without any adjustment for smoking, the meta-analysis of the cohort studies indicated that the common SMR was 2.45 [95% confidence interval (95% CI) 1.63-3.66; homogeneity P<0.0001]. When the results of the cohorts for which mortality data were adjusted for smoking were pooled, the common SMR was 1.60 (95% CI 1.33-1.93; homogeneity P=0.52). In a "dose-response" analysis, the profusion of small and large opacities found in chest X-rays correlated with the risk of death from lung cancer. Overall, the case-control studies were more conservative in their conclusions. CONCLUSIONS: Because of biases inherent to observational studies, it is likely that the risk of lung cancer among silicosis patients is overestimated in the current literature. There is nevertheless evidence, from data restricted to never-smokers and from a "dose-response" analysis, that silicosis and lung cancer are associated.     

Differences in mortality by radiation monitoring status in an expanded cohort of Portsmouth Naval Shipyard workers

Studies of leukemia and lung cancer mortality at the Portsmouth Naval Shipyard (PNS) have yielded conflicting results. In an expanded cohort of PNS workers employed between 1952 and 1992 and followed through 1996, the all-cause standardized mortality ratio (SMR) was 0.95 (95% confidence interval, 0.93-0.96). Employment duration SMRs were elevated with confidence intervals excluding 1.00 for lung cancer, esophageal cancer, and all cancers combined. Leukemia mortality was as expected overall, but standardized rate ratio analyses showed a significant positive linear trend with increasing external radiation dose. The role of solvent exposures could not be evaluated. Findings differed by radiation monitoring subcohort, with excess asbestosis deaths limited to radiation workers and several smoking-related causes of death higher among nonmonitored workers. At PNS, asbestos exposure and possibly smoking could be nonrandomly distributed with respect to radiation exposure, suggesting potential for confounding in internal analyses of an occupational cohort.     

Lung cancer among industrial sand workers exposed to crystalline silica

In 1997, the International Agency for Research on Cancer determined that crystalline silica was a human carcinogen but noted inconsistencies in the epidemiology. There are few exposure-response analyses. The authors examined lung cancer mortality among 4,626 industrial sand workers, estimating exposure via a job-exposure matrix based on 4,269 industrial hygiene samples collected in 1974--1995. The average length of employment was 9 years, and estimated average exposure was 0.05 mg/m(3) (the National Institute of Occupational Safety and Health Recommended Exposure Limit). Results confirmed excess mortality from silicosis/pneumoconioses (standardized mortality ratio = 18.2, 95% confidence interval: 10.6, 29.1; 17 deaths). The lung cancer standardized mortality ratio was 1.60 (95% confidence interval: 1.31, 1.93; 109 deaths). Limited data suggested that smoking might account for 10--20% of the lung cancer excess. Exposure-response analyses by quartile of cumulative exposure (15-year lag) yielded standardized rate ratios of 1.00, 0.78, 1.51, and 1.57 (p for trend = 0.07). Nested case-control analyses after exclusion of short-term workers, who had high overall morality, yielded odds ratios by quartile of cumulative exposure (15-year lag) of 1.00, 1.35, 1.63, and 2.00 (p for trend = 0.08) and odds ratios by quartile of average exposure of 1.00, 0.92, 1.44, and 2.26 (p = 0.005). These data lend support to the labeling by the International Agency for Research on Cancer of silica as a human carcinogen. There are approximately 2 million US workers exposed to silica; 100,000 are exposed to more than 0.1 mg/m(3).