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.     

A mortality study of workers at seven beryllium processing plants.

The International Agency for Research on Cancer (IARC) has found that the evidence for the carcinogenicity of beryllium is sufficient based on animal data but "limited" based on human data. This analysis reports on a retrospective cohort mortality study among 9,225 male workers employed at seven beryllium processing facilities for at least 2 days between January 1, 1940, and December 31, 1969. Vital status was ascertained through December 31, 1988. The standardized mortality ratio (SMR) for lung cancer in the total cohort was 1.26 (95% confidence interval [CI] = 1.12-1.42); significant SMRs for lung cancer were observed for two of the oldest plants located in Lorain, Ohio (SMR = 1.69; 95% CI = 1.28-2.19) and Reading, Pennsylvania (SMR = 1.24; 95% CI = 1.03-1.48). For the overall cohort, significantly elevated SMRs were found for "all deaths" (SMR = 1.05; 95% CI = 1.01-1.08), "ischemic heart disease" (SMR = 1.08; 95% CI = 1.01-1.14), "pneumoconiosis and other respiratory diseases" (SMR = 1.48; 95% CI = 1.21-1.80), and "chronic and unspecified nephritis, renal failure, and other renal sclerosis" (SMR = 1.49; 95% CI = 1.00-2.12). Lung cancer SMRs did not increase with longer duration of employment, but did increase with longer latency (time since first exposure). Lung cancer was particularly elevated (SMR = 3.33; 95% CI = 1.66-5.95) among workers at the Lorain plant with a history of (primarily) acute beryllium disease, which is associated with very high beryllium exposure. The lung cancer excess was not restricted to plants operating in the 1940s, when beryllium exposures were known to be extraordinarily high. Elevated lung cancer SMRs were also observed for four of the five plants operating in the 1950s for workers hired during that decade. Neither smoking nor geographic location fully explains the increased lung cancer risk. Occupational exposure to beryllium compounds is the most plausible explanation for the increased risk of lung cancer observed in this study. Continued mortality follow-up of this cohort will provide a more definitive assessment of lung cancer risk at the newer plants and among cohort members hired in the 1950s or later at the older plants. Further clarification of the potential for specific beryllium compounds to induce lung cancer in humans, and the possible contribution of other exposures in specific processes at these plants, would require a nested case-control study. We are currently assessing whether available industrial hygiene data would support such an analysis.     

Exposures to silica mixed dust and cohort mortality study in tin mines: exposure-response analysis and risk assessment of lung cancer

BACKGROUND: Mineral dusts that contain crystalline silica have been associated directly or indirectly with the development of pneumoconiosis or silicosis, non-malignant respiratory diseases, lung cancer, and other diseases. The health impacts on workers with silica mixed dust exposure in tin mines and dose-response relationships between cumulative dust exposure and the mortality from lung cancer are investigated. METHODS: A cohort of 7,837 workers registered in the employment records in 4 Chinese tin mines between 1972 and 1974 was identified for this study and the mortality follow-up was traced through 1994. Of the cohort, the cause of death was ascertained for 1,061 (97%) of the 1,094 deceased workers. Standardized mortality ratios (SMRs) were calculated for all workers, non-exposed workers, and dust-exposed workers with different exposure levels, silicotics, and non-silicotics based on Chinese national rates. RESULTS: The mortality from all causes in four tin mines was nearly the same as the national mortality. Malignant neoplasm, cerebrovascular disease, and cardiovascular disease accounted for 68.6% of all deaths. Mortality excess from lung cancer, liver cancer, all malignant diseases, and non-malignant respiratory diseases was observed among dust-exposed workers; a 50-fold excess of pneumoconiosis was observed. There was an upward trend for SMRs of lung cancer was noted from no exposure to low, medium, and high exposure levels (SMRs=1.29, 2.65, 2.66, 3.33). The shape of the exposure-response curve for risk of lung cancer at high exposure levels was inconsistent in these four mines. CONCLUSIONS: The findings indicated a positive dose-response relation between exposure to cumulative dust and the mortality of lung cancer. High arsenic content in dust particles, together with crystalline silica, may play an important role in causing increased mortality from lung cancer.     

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.     

Mortality of workers at a plant manufacturing nickel alloys, 1958-2000

BACKGROUND: Excess risks of respiratory cancer have been demonstrated in some groups of nickel-exposed workers. It is clear, however, that not all forms of nickel exposure are implicated in these excess risks. Aim To determine whether occupational exposures received in the manufacture of nickel alloys lead to increased risks of cancer, in particular nasal cancer and lung cancer. METHODS: The mortality experienced by a cohort of 1999 workers employed at a plant manufacturing nickel alloys has been investigated. Study subjects were all those male workforce employees first employed in the period 1953-1992 who had at least 5 years employment with the company. Observed numbers of cause-specific deaths were compared with expectations based on national mortality rates. Standardized mortality ratios (SMRs) were calculated by period from commencing employment and by operating area of first job. In addition, rate ratios derived from Poisson regression and based on an internal standard were calculated by levels of duration of employment. RESULTS: SMRs were significantly below 100 for all causes (observed 557, expected 704.3, SMR 79), all neoplasms (observed 169, expected 209.4, SMR 81) non-malignant diseases of the respiratory system (observed 50, expected 73.0, SMR 69) and diseases of the circulatory system (observed 261, expected 335.5, SMR 78). Significantly elevated SMRs were not shown for any cause of death and mortality was below expectation for stomach cancer (observed 8, expected 16.0, SMR 50), lung cancer (observed 64, expected 73.6, SMR 87) and bladder cancer (observed 3, expected 8.0, SMR 38). There were no deaths from nasal cancer (expected 0.33). More detailed findings were unexceptional. CONCLUSIONS: The analyses did not suggest the presence of an occupational cancer hazard in the mortality experience of the cohort.     

The Drake Health Registry Study: cause-specific mortality experience of workers potentially exposed to beta-naphthylamine

OBJECTIVE: To examine the cause-specific mortality experience of an occupational cohort with probable past exposure to beta-naphythylamine (BNA). METHODS: Subjects were 374 male and 26 female workers employed at a Pennsylvania chemical plant that produced or used beta-naphthylamine (BNA) between 1940 and 1981. Vital status through 1998 was determined for 97.5% of the cohort and cause of death for 100% of 79 deaths. Limited industrial hygiene data and reports from former employees were used to categorize workers as high, medium, or low risk for BNA exposure. Statistical analyses included US and local county-based standardized mortality ratios (SMRs). RESULTS: We observed statistically significantly elevated county rate-based SMRs for all causes combined (SMR = 1.98, 95% confidence interval (CI) = 1.56-2.49), all malignant neoplasms combined (28 deaths, SMR = 3.08, 95% CI = 2.05-4.46), respiratory system cancer (12 deaths, SMR = 3.91, 95% CI = 2.02-6.83), and bladder cancer (four deaths, SMR = 16.83, 95% CI = 4.59-43.1). Three bladder cancer cases were classified as high risk (SMR = 26.79, 95% CI = 5.53-78.29). Mortality risks were also elevated for most other malignant and non-malignant cause of death categories examined. CONCLUSIONS: Bladder cancer risk remains highly elevated among Drake/Kilsdonk workers and appears to be causally related to past BNA exposure. While lifestyle and behavioral risk factors may explain some of the mortality excesses for non-urological cancers, the possibility remains that BNA exposure may have also played a role in these and other observed cancer excesses.     

Mortality among Ontario members of the International Union of Bricklayers and Allied Craftworkers

BACKGROUND: Dust exposed workers may be at increased risk of pneumoconiosis, stomach cancer, lung cancer, and obstructive lung disease. Bricklayers may experience high exposures to silica and inorganic dusts. The aim of this study was to examine the mortality pattern of bricklayers to identify occupational associations with mortality. METHODS: A cohort of 10,953 workers was assembled from records of the International Union of Bricklayers and Allied Craftworkers (IUBAC). Mortality was ascertained by linkage to the Canadian Mortality Registry at Statistics Canada. Standardized Mortality Ratios (SMRs) were computed using Ontario general population mortality rates as the reference. RESULTS: Twenty or more years from first membership, SMRs for lung (158; 130-190) and stomach (235; 140-370) cancers were significantly elevated. There were four deaths from pneumoconiosis, but non-malignant respiratory mortality SMRs were not increased. CONCLUSIONS: Bricklayers and Allied Craftworkers are at risk from diseases associated with heavy exposure to inorganic dust: lung cancer, stomach cancer, and pneumoconiosis. Dust control as well as education and training of these workers to protect themselves against inhalation hazards is necessary.     

Mortality among chemical plant workers exposed to acrylonitrile and other substances.

OBJECTIVES: To examine the association between exposure to acrylonitrile (AN) and cancer mortality by performing an independent and extended historical cohort study of workers from a chemical plant in Lima, Ohio included in a recent NCI-NIOSH study. METHODS: Subjects were 992 white males who were employed for three or more months between 1960 and 1996. We identified 110 deaths and cause of death for 108. Worker exposures were estimated quantitatively for AN and qualitatively for nitrogen products. Statistical analyses included U.S. and local county-based SMRs and internal relative risk regression of internal cohort rates. RESULTS: No statistically significant excess mortality risks were observed among the total cohort for the cancer sites implicated in previous studies: stomach, lung, breast, prostate, brain, and hematopoietic system. We observed a statistically significant bladder cancer excess based on four deaths (SMR=7.01, 95% CI=1.91-17.96) among workers not exposed to AN. Among 518 AN-exposed workers, we observed a not statistically significant excess of lung cancer based on external (SMR=1.32, 95% CI=.60-2.51) and internal (RR=1.98, 95% CI=.60-6.90) comparisons. Although the trends were not statistically significant, exposure-response analyses of internal cohort rates showed monotonically increasing lung cancer rate ratios with increasing AN exposure, with RRs exceeding 2.0 in the highest exposure categories. CONCLUSIONS: With the possible exception of lung cancer, this study provides little evidence that exposure to AN at levels experienced by Lima plant workers is associated with an increased risk of death from any cause including the implicated cancer sites.     

Cancer mortality among workers in the German rubber industry: 1981-91.

OBJECTIVES: To determine the cancer specific mortality of active and retired workers of the German rubber industry with emphasis on cancer sites which have been associated with the rubber industry in previous studies. METHODS: A cohort of 11,663 German men was followed up for mortality from 1 January 1981 to 31 December 1991. Cohort members were active (n = 7536) or retired (n = 4127) at the beginning of the study, and had been employed for at least one year in one of five study plants producing types or general rubber goods. Vital status was ascertained for 99.7% of the cohort members, and cause of death found for 96.8% of the 2719 decedents. Age and calendar year adjusted standardised mortality ratios (SMR) and 95% confidence intervals (95% CI) were calculated overall from national reference rates and stratified by year of hire and by years since hire. RESULTS: Mortalities from all causes (SMR 108; 95% CI 104-112) and all cancers (SMR 111; 95% CI 103-119) were significantly increased in the study cohort. Significant excesses in the mortalities from lung cancer (SMR 130; 95% CI 115-147) and pleural cancer (SMR 401; 95% CI 234-642) were identified. SMRs higher than 100 were found for cancers of the pharynx (SMR 144; 95% CI 76-246), oesophagus (SMR 120; 95% CI 74-183), stomach (SMR 110; 95% CI 86-139), rectum (SMR 123; 95% CI 86-170), larynx (SMR 129; 95% CI 69-221), prostate (SMR 108; 95% CI 84-136), and bladder (SMR 124; 95% CI 86-172), as well as for leukaemia (SMR 148; 95% CI 99-213). Mortalities from liver cancer, brain cancer, and lymphoma were lower than expected. CONCLUSIONS: Mortalities from cancer of several sites previously associated with the rubber industry were also increased among workers of the German rubber industry. Results of the stratified analyses are consistent with a role of occupational exposure in the aetiology of some of these cancers.     

Mortality of workers at a nickel carbonyl refinery, 1958-2000

Background: Excess risks of respiratory cancer have been shown in some groups of nickel exposed workers. It is clear, however, that not all forms of nickel exposure are implicated in these excess risks.

Aim: To determine whether occupational exposures received in a modern nickel carbonyl refinery lead to increased risks of cancer, in particular nasal cancer and lung cancer.

Methods: The mortality experienced by a cohort of 812 workers employed at a nickel refinery was investigated. Study subjects were all male workforce employees first employed in the period 1953–92 who had at least five years' employment with the company. Observed numbers of cause specific deaths were compared with expectations based on national mortality rates; SMRs were also calculated by period from commencing employment, year of commencing employment, and type of work.

Results: Overall, standardised mortality ratios (SMRs) were close to 100 for all causes (Obs 191, SMR 96, 95% CI 83 to 111), all neoplasms (Obs 63, SMR 104, 95% CI 80 to 133), non-malignant diseases of the respiratory system (Obs 18, SMR 97, 95% CI 57 to 153), and diseases of the circulatory system (Obs 85, SMR 94, 95% CI 75 to 116). There were no significantly increased SMRs for any site of cancer. There was a non-significant excess for lung cancer (Obs 28, Exp 20.17, SMR 139, 95% CI 92 to 201), and in subgroup analyses a significantly increased SMR of 231 (Obs 9) was found for those 142 workers with at least five years' employment in the feed handling and nickel extraction departments. In the total cohort there was a single death from nasal cancer (Exp 0.10).

Conclusions: The non-significant excess of lung cancer deaths may well be a chance finding, but in light of previous studies some role for nickel exposures cannot be excluded.

     

A cohort mortality study among titanium dioxide manufacturing workers in the United States.

Although titanium dioxide (TiO2) is generally regarded as a nontoxic mild pulmonary irritant, some laboratory studies have reported lung adenomas in rats exposed to high levels of TiO2. Limited data on health effects among humans exist. A retrospective cohort mortality study was conducted among 4241 TiO2 workers who were employed for at least 6 months, on or after January 1, 1960, at four TiO2 plants in the United States. Exposure categories, defined by plant, job title, and calendar years in the job, were created to examine mortality patterns in those jobs where the potential for TiO2 exposure is greatest. Standardized mortality ratios (SMRs) and their 95% confidence intervals (CI) were calculated to compare the mortality pattern of the workers with the general background population. Relative risks were estimated and trend tests were conducted to examine risk of disease among different exposure level groups in internal analyses. Workers experienced a significantly low overall mortality (SMR = 0.8; 95% CI = 0.8-0.9). No significantly increased SMRs were found for any specific cause of death. Deaths from lung cancer were as expected, and SMRs for this cancer did not increase with increasing TiO2 levels. Workers in jobs with greatest TiO2 exposure had significantly fewer than expected total deaths (SMR = 0.7; 95% CI = 0.6-0.9). Internal analyses revealed no significant trends or exposure-risk associations for total cancers, lung cancer, or other causes of death. Results from our study indicate that the exposures at these United States plants are not associated with increases in the risk of death from cancer or other diseases. Moreover, workers with likely higher levels of TiO2 exposure had similar mortality patterns to those with less exposure, as internal analyses among workers revealed no increase in mortality by level of TiO2 exposure.     

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.     

A cohort mortality study of U.K. carbon black workers, 1951-1996

BACKGROUND: Carbon black, a powdered form of elemental carbon is used in the manufacture of rubber products, paints, plastics, and inks. In 1974, the Health and Safety Executive initiated a cohort mortality study on possible carcinogenic effects on carbon black workers. METHODS: The mortality of a cohort of 1,147 male manual workers from five U.K. factories manufacturing carbon black was investigated for the period 1951-1996. All subjects were employed in the carbon black industry for 12 months or more, and all were first employed before 1975. Limited work histories were used to calculate estimates of individual cumulative exposure to carbon black, using a job-exposure matrix derived by the study team. RESULTS: Based on serial rates for the general population of England and Wales, significantly elevated mortality was observed in the main study cohort for all causes (Obs 372, Exp 328.7, SMR 113, P < 0.05) and for lung cancer (Obs 61, Exp 35.3, SMR 173, P < 0.001). There were highly elevated lung cancer SMRs at two of the factories, and unexceptional SMRs at the remaining three factories. There was no indication of lung cancer SMRs increasing with period from first employment. Poisson regression analyses failed to find significant trends of lung cancer risks increasing either with cumulative exposure to carbon black (4 levels) or with duration of employment at the participating factories (4 levels). CONCLUSIONS: Confident interpretation of the elevated SMRs found for lung cancer in two of the factory subcohorts is not possible but the study has been unable to link cumulative exposure to carbon black with elevated risks of lung cancer.     

矽肺对肺癌及总死亡影响的回顾性队列研究

目的 利用香港矽肺患者队列的资料进行分析,探讨矽尘、矽肺与肺癌的关系.方法 选择1981年1月1日至1998年12月31日期间在香港尘肺诊所登记的2789例男性矽肺病例为研究对象,取用同时期一般男性人群作为对照.用人年的方法估计各死因的标化死亡比(SMR),用Axelson's法间接调整吸烟的混杂影响.矽尘与肺癌的剂量-效应关系采用多因素p-spline平滑法模型来拟合最佳风险模型.结果 该组研究队列人数为2789,共观察24 992.6人年,失访率仅为2.9%.该队列主要工种为建筑工人(5 1.09%)和地下沉箱操作工人(37.54%).队列总死亡人数为853人,平均死亡年龄为(63.8±10.27)岁,整个队列中86例死于肺癌.全死因及全癌的SMR均明显上升,首位死因是呼吸道疾病,肺癌的5MR明显增加(SMR:1.69,95%CI:1.35～2.09).去除年龄、时期和吸烟的混杂因素的影响,矽肺对肺癌的相对危险度下降到1.12(95%CI:0.89～1.38).间接调整吸烟的混杂影响后建筑工人及地下沉箱工人肺癌的相对危险度分别为1.09(95%CI:0.82～1.42)和1.56(0.98～2.36).多因素p-spline平滑法风险模型分析显示,肺癌与累积呼吸性矽尘总量或平均矽尘浓度的关系无剂量-效应关系.结论 队列研究未发现接触矽尘或矽肺能增加肺癌死亡的危险,平滑法模型拟合的风险模型并不支持矽尘与肺癌死亡之间存在剂量-效应关系.     

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 study of employees with potential exposure to epichlorohydrin: a 10 year update.

OBJECTIVES: A 10 year extension of follow up (up to 1993) of 863 employees who had potential exposure to epichlorohydrin at two chemical plants between May 1948 and December 1965 was conducted to further evaluate the previously reported potential association between exposure to epichlorohydrin and heart disease. METHODS: The mortality observed was compared with that expected from the death rates from the local male population where these chemical plants are located. Workers were assigned to one of five exposure categories based on their job with the highest level of potential exposure. Vital status was ascertained to the end of 1993. RESULTS: Among diseases of particular interest, there were no excess deaths from heart disease (standardised mortality ratio (SMR) 63.3), lung cancer (SMR 63.8), or non-malignant respiratory disease (SMR 37.7) for employees with 20 or more years after first exposure. Based on the level of potential exposure to epichlorohydrin, mortality for heart disease was slightly higher (SMR 75.7, 95% confidence interval (95% CI) 51.8-106.7) in the moderate to heavy exposure group than in the none to light exposure group (SMR 59.5, 95% CI 37.7-89.3); this difference is well within the range of random variation. The SMR for heart disease was 90.4 among employees who had both probable exposure to allyl chloride and moderate to heavy exposure to epichlorohydrin, although it was 88.1 among employees who had moderate to heavy potential exposure to epichlorohydrin but no exposure to allyl chloride. CONCLUSIONS: This study does not support an association between exposure to epichlorohydrin and heart disease or lung cancer. There were no additional deaths from leukaemia in this update; the raised SMR for leukaemia noted in the previous study has substantially decreased from 500.0 to 161.3 (95% CI 33.2-471.0) and is not significant. The overall mortality and cancer mortality of employees potentially exposed to epichlorohydrin continued to be lower than that of the local population.     

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.     

Lung cancer in mild steel welders

To investigate lung cancer risk, the authors conducted a historical cohort mortality study of 4,459 mild steel welders who had been employed at three midwestern plants which manufactured heavy equipment. Follow-up began in the mid-1950s and extended through 1988. All welders had at least 2 years welding experience (average duration, 8.5 years). This cohort had no occupational exposure to asbestos or stainless steel fumes (containing nickel and chromium), two potential confounders in previous welders studies. A comparison population of 4,286 nonwelders, all with at least 2 years employment at the same plants, was also studied. Nonwelders had never been welders and were allowed to have no more than 90 days employment as a painter, foundryman, or machinist. Sampling data collected from 1974-1987 indicated that welders were exposed to 6-7 mg/m3 of total particulate and 3-4 mg/m3 of iron oxide, while nonwelders had negligible exposures to welding fumes. When compared with the United States population, both welders and nonwelders had elevated rates for lung cancer (standardized mortality ratios (SMRs): welders, SMR = 1.07; nonwelders, SMR = 1.17), but neither SMR was significantly elevated. Limited smoking data based on a 1985 survey indicated that both welders and nonwelders smoked more than the United States population, possibly accounting for part of their elevated lung cancer rates. There was no trend of increased risk for welders with increased duration of exposure. The only other cause of death significantly elevated was emphysema among welders. Nonmalignant respiratory disease was not elevated for welders (SMR = 0.96). When welders were compared with nonwelders directly for lung cancer, the rate ratio was 0.90.     

Does low-level lead exposure increase risk of death? A mortality study of newspaper printers.

This exploratory study examined the mortality experience of a cohort of newspaper printers in order to investigate the effects of low-level exposure to lead. In this industry, historic lead exposure levels have been below the current US permissible exposure level (PEL) of 50 micrograms/m3. The study population was 1261 typesetters, employed in 1961 and followed until the end of 1984; this was a cohort of convenience, assembled as a comparison for a different study. Standardized mortality ratios (SMRs) were calculated using New York City comparison rates. The all-cause SMR was 0.74, and was significantly different from 1.00. Other statistically significant deficits were deaths from arteriosclerotic heart disease (SMR = 0.63) and non-malignant diseases of the respiratory system (SMR = 0.57) and digestive system (SMR = 0.65). These can be attributed to the comparison bias known as the healthy worker effect. The SMR for cerebrovascular disease (CVD) was 1.35, on the edge of statistical significance (95% confidence interval (CI): 0.98-1.82). When the cohort was stratified by years of union membership, a surrogate for length of exposure, only one cause of death was significantly elevated. For those printers employed for 30 years or more, the CVD SMR was 1.68 (95% CI: 1.18-2.31; p = 0.002). No significant excesses were seen for any other cause of death in any exposure stratum. Several studies of workers with much higher levels of lead exposure have reported elevated CVD risk. These findings suggest the possibility that lead exposure at levels below the current US PEL may also be associated with CVD mortality.     

Mortality among aircraft manufacturing workers

OBJECTIVES: To evaluate the risk of cancer and other diseases among workers engaged in aircraft manufacturing and potentially exposed to compounds containing chromate, trichloroethylene (TCE), perchloroethylene (PCE), and mixed solvents. METHODS: A retrospective cohort mortality study was conducted of workers employed for at least 1 year at a large aircraft manufacturing facility in California on or after 1 January 1960. The mortality experience of these workers was determined by examination of national, state, and company records to the end of 1996. Standardised mortality ratios (SMRs) were evaluated comparing the observed numbers of deaths among workers with those expected in the general population adjusting for age, sex, race, and calendar year. The SMRs for 40 cause of death categories were computed for the total cohort and for subgroups defined by sex, race, position in the factory, work duration, year of first employment, latency, and broad occupational groups. Factory job titles were classified as to likely use of chemicals, and internal Poisson regression analyses were used to compute mortality risk ratios for categories of years of exposure to chromate, TCE, PCE, and mixed solvents, with unexposed factory workers serving as referents. RESULTS: The study cohort comprised 77,965 workers who accrued nearly 1.9 million person-years of follow up (mean 24.2 years). Mortality follow up, estimated as 99% complete, showed that 20,236 workers had died by 31 December 1996, with cause of death obtained for 98%. Workers experienced low overall mortality (all causes of death SMR 0.83) and low cancer mortality (SMR 0.90). No significant increases in risk were found for any of the 40 specific cause of death categories, whereas for several causes the numbers of deaths were significantly below expectation. Analyses by occupational group and specific job titles showed no remarkable mortality patterns. Factory workers estimated to have been routinely exposed to chromate were not at increased risk of total cancer (SMR 0.93) or of lung cancer (SMR 1.02). Workers routinely exposed to TCE, PCE, or a mixture of solvents also were not at increased risk of total cancer (SMRs 0.86, 1.07, and 0.89, respectively), and the numbers of deaths for specific cancer sites were close to expected values. Slight to moderately increased rates of non-Hodgkin''s lymphoma were found among workers exposed to TCE or PCE, but none was significant. A significant increase in testicular cancer was found among those with exposure to mixed solvents, but the excess was based on only six deaths and could not be linked to any particular solvent or job activity. Internal cohort analyses showed no significant trends of increased risk for any cancer with increasing years of exposure to chromate or solvents. CONCLUSIONS: The results from this large scale cohort study of workers followed up for over 3 decades provide no clear evidence that occupational exposures at the aircraft manufacturing factory resulted in increases in the risk of death from cancer or other diseases. Our findings support previous studies of aircraft workers in which cancer risks were generally at or below expected levels.