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.     

Reanalysis of mortality from lung cancer among diatomaceous earth industry workers, with consideration of potential confounding by asbestos exposure.

OBJECTIVE: To evaluate the potential for confounding from asbestos exposure, primarily chrysotile, on the relation between crystalline silica and mortality from lung cancer among diatomaceous earth (diatomite) workers. METHODS: A reanalysis of a cohort mortality study of diatomite workers was performed to take into account quantitative estimates of asbestos exposure. The reanalysis was limited to a subset of the original cohort, comprising 2266 white men for whom asbestos exposure could be reconstructed with greatest confidence. Comparisons between mortality from lung cancer (standardised mortality ratios (SMR)) were made between rates for 1942-87 for United States white men, and workers cross classified according to cumulative exposures to crystalline silica and asbestos. Comparisons of internal rates, involving Poisson regression modeling, were conducted for exposure to crystalline silica, with and without adjustment for asbestos exposure. Exposures were lagged by 15 years to take into account disease latency. RESULTS: There was an overall excess of lung cancer (SMR 1.41; 52 observed). The SMRs for four categories of increasing crystalline silica among the workers not exposed to asbestos were 1.13, 0.87, 2.14, 2.00. An SMR of 8.31 (three observed) was found for workers with the highest cumulative exposure to both dusts. Internal analysis, after adjustment for asbestos exposure, yielded rate ratios for categories of exposure to crystalline silica: 1.00 (reference), 1.37, 1.80, and 1.79. CONCLUSIONS: Asbestos exposure was not an important confounder of the association between crystalline silica and mortality from lung cancer in this cohort. Although based on a small number of deaths from lung cancer, the data suggest possible synergy between these exposures. An extended follow up of this cohort is in progress and should enable better assessments of independent and combined effects on risk of lung cancer.     

温石棉与肺癌——二十七年追踪研究

目的 探讨单纯接触温石棉的工人恶性肿瘤,尤其肺癌是否超高。方法 采用固定队列研究方法。研究队列为515例男性石棉工人,人列条件为1972年1月1日工资在册,工龄满1年,没有明显心肺疾患者。对照队列为650例不接尘男性工人,其余条件同研究队。追踪27年（1972－1998）。结果 （1）研究队列全癌死亡50例（SMR＝144）,其中肺癌22例（SMR＝652）;．对照队列全癌死亡1例（SMR＝34）,肺癌3例（SMR＝89）。两队列间全癌和肺癌差异均有显著性（P＜0．05）。（2）不接触石棉的吸烟者肺癌RR为2．6,不吸烟的石棉接触者肺癌RR为12．2,而接触石棉的吸烟者RR高达32．1。吸烟和石棉暴露协同指数为2．2。（3）研究队列发生胸膜间皮瘤2例。结论 单纯暴露于温石棉的工人肺癌显著超高。     

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.     

Lung function predicts survival in a cohort of asbestos cement workers

Purpose  To study the predictive power of respiratory screening examinations a cohort of asbestos workers was followed from active work in an asbestos cement plant until death. Methods  From a cohort with data on individual exposure since first employment 309 workers who had a preventive medical examination in 1989/1990 were observed until death or the end of 2006. The impact of asbestos exposure (fibre years) and of smoking history on lung function was examined by linear regression, on specific causes of death and total mortality by Cox regression. The prognostic value of lung function, chest X-ray, and various clinical findings regarding total mortality was also examined by Cox regression. Results  Lung function proved to be the best predictor of survival apart from current smoking. Depending on the lung function variable an impairment by the interquartile range resulted in a hazard ratio of 1.5–1.6 while for current smokers it was 2.3. An increase of 70 fibre years (interquartile range) led to a hazard ratio of only 1.1. Lung function was influenced by asbestos exposure, current (but not former) smoking, and by pathological X-ray findings. The risk for pleural mesothelioma was dominated by time since first exposure to crocydolite in the pipe factory while the risk for bronchial cancer increased with smoking and total fibre years. An unexpected finding was an increase of gastric cancer in asbestos cement workers. Conclusion  Lung function decrease predicts risk of premature death better than exposure history and regular spirometry should therefore be offered as primary screening to all former asbestos workers. In workers with a history of high cumulative exposure or rapid lung function decrease or radiological signs (diffuse pleural thickening or small irregular opacities) more sensitive techniques (high resolution computer tomography) need to be applied. All smokers with a history of asbestos exposure should be given free smoking cessation therapy to prevent premature death and lung cancer in particular.     

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.     

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.     

Vermiculite, respiratory disease, and asbestos exposure in Libby, Montana: update of a cohort mortality study

BACKGROUND: Vermiculite from the mine near Libby, Montana, is contaminated with tremolite asbestos and other amphibole fibers (winchite and richterite). Asbestos-contaminated Libby vermiculite was used in loose-fill attic insulation that remains in millions of homes in the United States, Canada, and other countries. OBJECTIVE: This report describes asbestos-related occupational respiratory disease mortality among workers who mined, milled, and processed the Libby vermiculite. METHODS: This historical cohort mortality study uses life table analysis methods to compare the age-adjusted mortality experience through 2001 of 1,672 Libby workers to that of white men in the U.S. population. RESULTS: Libby workers were significantly more likely to die from asbestosis [standardized mortality ratio (SMR) = 165.8; 95% confidence interval (CI), 103.9-251.1], lung cancer (SMR = 1.7; 95% CI, 1.4-2.1), cancer of the pleura (SMR = 23.3; 95% CI, 6.3-59.5), and mesothelioma. Mortality from asbestosis and lung cancer increased with increasing duration and cumulative exposure to airborne tremolite asbestos and other amphibole fibers. CONCLUSIONS: The observed dose-related increases in asbestosis and lung cancer mortality highlight the need for better understanding and control of exposures that may occur when homeowners or construction workers (including plumbers, cable installers, electricians, telephone repair personnel, and insulators) disturb loose-fill attic insulation made with asbestos-contaminated vermiculite from Libby, Montana.     

Asbestos and colon cancer: a weight-of-the-evidence review.

What is the evidence that exposure to asbestos causes colon cancer? This weight-of-evidence review considers epidemiologic evidence from cohort studies of asbestos-exposed workers, case-control studies of colon cancer, animal bioassays, and other corroborative evidence. The major evidence for a causal association at high exposure is a combined colorectal standardized mortality ratio (SMR) of 1.5 for asbestos cohorts where the lung cancer SMR was greater than twofold. However, misdiagnosis may spuriously elevate the SMR. The strongest evidence against a causal association between colon cancer and asbestos exposure is the lack of an exposure-response gradient in asbestos cohorts where trends for lung cancer are observed. Population-based case-control studies of colon cancer do not show any consistent risk associated with asbestos exposure. Long-term ingestion studies show no evidence of an increased incidence of colon cancer in animals by this route of exposure and do not provide biological plausibility for a causal association between asbestos exposure and colon cancer.     

Mortality of chrysotile asbestos workers at the Balangero Mine, Northern Italy.

The mortality from 1946 to 1975 of over 900 North Italian chrysotile asbestos workers first employed between 1930 and 1965 has been studied. Nine deaths were certified as attributable to asbestosis, and eleven to lung cancer. One death was attributed to mesothelioma of pleura but this diagnosis was not supported by histological examination. Comparison with the national figures for all Italy did not reveal an excess of deaths from lung cancer but during the last quinquennium of observation, the SMR for lung cancer rose to 206. Simulation experiments enabled a dust index in fibre/years to be attached to each man in the cohort. All but two of the deaths from lung cancer occurred in the higher exposure group. The relative risk of lung cancer in this group was 2.89. The eleven workers who died from lung cancer were all cigarette smokers. A further period of observation is required to monitor the mortality of the surviving workers.     

Mortality of chrysotile asbestos workers at the Balangero Mine, Northern Italy.

The mortality from 1946 to 1975 of over 900 North Italian chrysotile asbestos workers first employed between 1930 and 1965 has been studied. Nine deaths were certified as attributable to asbestosis, and eleven to lung cancer. One death was attributed to mesothelioma of pleura but this diagnosis was not supported by histological examination. Comparison with the national figures for all Italy did not reveal an excess of deaths from lung cancer but during the last quinquennium of observation, the SMR for lung cancer rose to 206. Simulation experiments enabled a dust index in fibre/years to be attached to each man in the cohort. All but two of the deaths from lung cancer occurred in the higher exposure group. The relative risk of lung cancer in this group was 2.89. The eleven workers who died from lung cancer were all cigarette smokers. A further period of observation is required to monitor the mortality of the surviving workers.     

The interaction of asbestos and smoking in lung cancer.

Both cigarette smoke and inhaled asbestos fibres can cause lung cancer, but the assessment of how these agents act in combination is a matter of great difficulty. In non-smokers, the condition is so rare that, in any cohort of asbestos workers, the standardised mortality ratio (SMR, that is the ratio of the numbers of deaths observed and expected) is quite imprecise. The SMR for smokers, with which it has to be compared, is also subject to sampling error, making the interaction even more unstable. This accounts for much of the variation that has bedevilled evaluation.The debate has been concentrated on two hypotheses: additive (asbestos and cigarette smoke act independently) and multiplicative (asbestos produces an effect proportional to the effect of smoking). The very few data available until 1977 failed to fit the former and fitted the latter only poorly. They would have fitted better a hypothesis of greater synergism, but the only one proposed was too convoluted. So the multiplicative model appeared the only alternative, and was deemed 'accepted'.The ratio of lung cancer SMRs for non-smokers and smokers was generalised into the relative asbestos effect, RAE, with all the advantages of a parametric statistic (Berry et al., 1985, British Journal of Industrial Medicine 42, 12). On the multiplicative hypothesis, RAE=1, while RAE>1 indicates less synergism. The RAEs for the three most recent of the six results then available were >1; for one, P<0.005. From the six results combined, it was concluded that 'overall non-smokers have a relative risk of lung cancer due to asbestos that is 1.8 times that of smokers'. Some admitted uncertainty about the figure 1.8 was seized upon and even the thrust of the conclusion has been very largely disregarded. So too has the RAE and all its benefits. As a result, all later reviewers have been led into error, much of it serious: in particular, they have failed to appreciate how much of the variation arises from the inevitable imprecision of all RAEs. This failure led reviewers in 1994 to discard, quite without justification, those interactions which were less than multiplicative and came from cohort studies. Although case-referent studies seemed to support the multiplicative hypothesis, the information from them is essentially unreliable. Thus it cannot weaken the conclusions from the cohort studies, that the multiplicative hypothesis is untenable and that the relative risk of lung cancer from asbestos exposure is about twice as high in non-smokers as in smokers; the best estimate of RAE is 2.04, with 95% confidence interval 1.28-3.25. This finding is not only of high statistical significance but of great social and scientific importance.     

Mortality study among workers producing ferroalloys and stainless steel in France.

A mortality study was carried out among the workers of a plant that had produced ferrochromium and stainless steel, and was still producing stainless steel, in order to determine whether exposure to chromium compounds, to nickel compounds, and to polycyclic aromatic hydrocarbons (PAH) could result in a risk of lung cancer for the exposed workers. The cohort comprised 2269 men whose vital status were recorded between 1 January 1952 and 31 December 1982. The smoking habits of 67% of the cohort members were known from medical records. The observed numbers of deaths were compared with the expected ones based on national rates with adjustment for age, sex, and calendar time. A low mortality, achieving statistical significance, was found from all causes (observed = 137, standardised mortality ratio (SMR) = 0.82) and from benign respiratory diseases (observed = one, SMR = 0.15). With regard to mortality from lung cancer, a non-significant excess appeared in the whole cohort (observed = 12, SMR = 1.40). Among the exposed workers, however, a significant lung cancer excess was found (observed = 11, SMR = 2.04) that contrasted with a low SMR (0.32) in the non-exposed group. This excess is unlikely to be explained by smoking, as the tobacco consumption of these two groups was similar. No trend was observed for mortality from lung cancer either according to time since first exposure, or according to duration of exposure. A nested case-control study clearly suggested that this excess of deaths from lung cancer was attributable to former PAH exposures in the ferrochromium production workshops rather than to exposures in the stainless steel manufacturing areas.     

Mortality study among workers producing ferroalloys and stainless steel in France

A mortality study was carried out among the workers of a plant that had produced ferrochromium and stainless steel, and was still producing stainless steel, in order to determine whether exposure to chromium compounds, to nickel compounds, and to polycyclic aromatic hydrocarbons (PAH) could result in a risk of lung cancer for the exposed workers. The cohort comprised 2269 men whose vital status were recorded between 1 January 1952 and 31 December 1982. The smoking habits of 67% of the cohort members were known from medical records. The observed numbers of deaths were compared with the expected ones based on national rates with adjustment for age, sex, and calendar time. A low mortality, achieving statistical significance, was found from all causes (observed = 137, standardised mortality ratio (SMR) = 0.82) and from benign respiratory diseases (observed = one, SMR = 0.15). With regard to mortality from lung cancer, a non-significant excess appeared in the whole cohort (observed = 12, SMR = 1.40). Among the exposed workers, however, a significant lung cancer excess was found (observed = 11, SMR = 2.04) that contrasted with a low SMR (0.32) in the non-exposed group. This excess is unlikely to be explained by smoking, as the tobacco consumption of these two groups was similar. No trend was observed for mortality from lung cancer either according to time since first exposure, or according to duration of exposure. A nested case-control study clearly suggested that this excess of deaths from lung cancer was attributable to former PAH exposures in the ferrochromium production workshops rather than to exposures in the stainless steel manufacturing areas.     

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.     

Epidemiology of occupational asbestos-related diseases in China

In 1950s and 60s, asbestosis had been a major health hazard for asbestos exposed workers. In the late 1970s, lung cancers with or without asbestosis were found among asbestos workers. All cohort studies on asbestos workers and on chrysotile miners in China showed excess deaths from lung cancer. In a large scale of cohort study on asbestos workers, a synergistic effect was found between cigarette smoking and asbestos exposure in the production of lung cancer. There have been not so many cases of malignant mesotheliomas reported, so far. In the cohort of chrysotile miners, 4 cases of pleural mesothelioma were observed. In the large scale of cohort study on asbestos workers in 9 factories using only chrysotile only one case of pleural mesothelioma was detected for 10 years' observation. In another 2 cohort studies, 2 cases of peritoneal mesotheliomas were found, one in Shanghai asbestos factory where a small amount of crocidolite had been used in 1960s, and one in Anqing asbestos factory that was located near tremolite mine. Further study is needed especially for the relationship between exposure to Chinese chrysotile and malignant mesotheliomas.     

A cohort study of art glass workers in the Empoli area

The investigation aimed at studying cause-specific mortality of art glass workers employed in 17 industrial facilities in Tuscany, Italy. A cohort of 3390 workers employed for at least 1 year was obtained from company payrolls. Follow-up was between the year each factory started operations, mostly in the mid-fifties, and the end of 1993. The cause specific expected mortality was computed relative to Tuscany rates, specified for gender, 5-year age groups and calendar year. Separate analyses were carried out for the job titles of makers, batch mixers and grinders. For males, 3180 individuals, the observed mortality for cancer causes was above the expected for the lung [standardized mortality ratio (SMR) 123, 10 observed (Obs)], larynx (SMR 166, 10 Obs), stomach (SMR 105, 30 Obs) and brain (SMR 150, 7 Obs). For non-cancer causes observed mortality was above expected for hypertensive diseases (SMR 178, 10 Obs) and diseases of the genitourinary system (SMR 169, 11 Obs). Increases for the above listed causes were shown also among makers. Mortality for larynx and lung cancer increased with time since first exposure and significantly increased SMRs were observed for 21 or more years since first exposure: this pattern was still present with smoking adjustment. The results showed consistently increased mortality for lung and larynx cancer in the overall cohort and among makers. Stomach cancer, brain cancer, hypertensive diseases and diseases of the genitourinary system were also increased in the overall cohort and among makers.     

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.     

Mortality among workers in the diatomaceous earth industry.

A cohort mortality study was conducted among workers from two plants in the diatomaceous earth mining and processing industry in California. Diatomaceous earth consists of the skeletal remains of diatoms. Exposure to amorphous (non-crystalline) and crystalline silica in the form of quartz results from open pit mining and exposure to crystalline silica (principally cristobalite) occurs in the processing of the material. Lung cancer and non-malignant respiratory diseases have been the health outcomes of greatest concern. The main study cohort included 2570 white men (533 Hispanic and 2017 non-Hispanic workers) who were employed for at least 12 months cumulative service in the industry and who had worked for at least one day during the follow up period, 1942-87. Vital status was ascertained for 91% of the cohort and death certificate information was retrieved for 591 of 628 (94%) identified deaths. The all causes combined standardised mortality ratio (SMR) was slightly increased (SMR = 1.12; 628 observed) compared with rates among US white males. The principal contributors to this excess were increased risks from lung cancer (SMR = 1.43; 59 observed) and non-malignant respiratory disease (NMRD) excluding infectious diseases and pneumonia (SMR = 2.59; 56 observed). The excess of lung cancer persisted when local county rates were used for comparison (SMR = 1.59). Internal rate comparisons by Poisson regression analysis were conducted to assess potential dose-response relations for lung cancer and NMRDs. Mortality trends were examined in relation to duration of employment in dust exposed jobs and with respect to an index of cumulative exposure to crystalline silica. The crystalline silica index was a semiquantitative measure that combined information on duration of exposure, differences in exposure intensity between jobs and calendar periods, the crystalline content of the various product mixes, and the use of respiratory protection devices. Increasing gradients of risk were detected for lung cancer and NMRD with both exposure indices. The relative risk trends for lung cancer and NMRD with crystalline silica exposure lagged 15 years were respectively: 1.00, 1.19, 1.37, and 2.74, and 1.00, 1.13, 1.58, and 2.71. Based on a review of available but limited data on cigarette smoking in the cohort and from application of indirect methods for assessing confounding variables, it seems unlikely that smoking habits could account for all of the association between exposure to dust and lung cancer. The intense and poorly controlled dust exposures encountered before the 1950s were probably the most aetiologically significant contributors to risks from lung cancer and NMRDs. The absence of an excess of lung cancer among workers hired since 1960, and the finding of no deaths attributed to pneumoconiosis as an underlying cause of death among workers hired since 1950 indicate that exposure reductions in the industry during the past 40 years have been successful in reducing excess risks to workers. Further mortality follow up of the cohort and the analysis of radiographic data will be needed to determine conclusively the long term patterns of disease risks in this industry.