Mortality and lead exposure: a retrospective cohort study of Swedish smelter workers.

The study is based on the work histories and mortality data for 3832 male workers first employed before 1967 at a copper smelter in northern Sweden and followed up from 1950 to 1981. From the 3832 workers a lead cohort consisting of 437 workers employed for at least three years at sites with considerable lead exposure during 1950-74 was selected. These workers had regularly had blood lead measurements performed since 1950. Based on the cumulative blood lead dose 1950-74 and peak blood lead values, the cohort was subdivided into high mean, low mean, high peak, and low peak groups. Standardised mortality ratios (SMR) were calculated for the six groups using general and local reference populations. The original cohort of 3832 workers showed considerable excess of deaths for total mortality, malignant neoplasms especially lung and stomach cancer, ischaemic heart diseases, and cerebrovascular diseases when compared with the general population. In the lead cohort where the workers had been subjected to a considerable lead exposure only the raised SMR for lung cancer was sustained (SMR = 162; not significant). No significant differences were found between high lead and low lead exposed smelter workers.     

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

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

Mortality and cancer incidence among secondary lead smelter workers.

OBJECTIVES--To examine the mortality pattern and the cancer incidence in a cohort of long term smelter workers exposed to lead. METHODS--The cohort consists of 664 male lead battery workers, employed for at least three months in 1942-87. From 1969 the values of all blood lead samples repeatedly obtained from these workers every two to three months, have been collected in a database. The expected mortality and morbidity 1969-89 was estimated from the county rates, specified for cause, sex, five-year age groups, and calendar year. Individual exposure matrices have been calculated and used for dose-response analyses. RESULTS--The total cohort showed an increased overall mortality (standardised mortality ratio (SMR) 1.44; 95% confidence interval (95% CI) 1.16-1.79), an increased mortality from ischaemic heart diseases (SMR 1.72; 95% CI 1.20-2.42) and all malignant neoplasms (SMR 1.65; 95% CI 1.09-2.44). These risk estimates were unaffected or slightly decreased when applying a latency period of 15 years, and no dose-response pattern was shown. The non-significantly raised cancer incidence in the gastrointestinal tract (11 malignancies) in the total cohort, increased to a barely significant level in the quartile with the highest cumulative lead exposure (standardised incidence ratio (SIR) 2.34, 95% CI 1.07-4.45). No clear dose response pattern was evident when further subdividing the data into those first employed up to 1969 v those first employed after 1969 when the blood lead monitoring programme started. The risk estimate for malignancies in the gastrointestinal tract was not related to latency time. The cancer incidence was not increased at other sites. CONCLUSIONS--A slightly increased incidence of gastrointestinal cancers was found in workers exposed to lead and employed before 1970. The lead cohort also showed an increased mortality from ischaemic heart diseases. These risk estimates did not show a dose-response pattern and were not associated with latency time. The results must also be interpreted with caution because of limited numbers, and lack of dietary and smoking data.     

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.     

A dose-response analysis and quantitative assessment of lung cancer risk and occupational cadmium exposure.

We performed a quantitative assessment of the risk of lung cancer from exposure to cadmium based on a retrospective cohort mortality study of cadmium-exposed workers. The study population consisted of white male workers who were employed for at least 6 months at a cadmium smelter between January 1, 1940, and December 31, 1969, and who were first employed at the facility on or after January 1, 1926. The study findings were analyzed using a modified life-table analysis to estimate standardized mortality ratios (SMRs), and various functional forms (i.e., exponential, power, additive relative rate, and linear) of Poisson and Cox proportional hazards models to examine the dose-response relationship. Estimates of working lifetime risk (45 years) were developed using an approach that corrects for competing causes of death. An excess in mortality from lung cancer was observed for the entire cohort (SMR = 149, 95% confidence interval (CI) = 95, 222). Mortality from lung cancer was greatest among non-Hispanic workers (SMR = 211, 95% CI = 131, 323), among workers in the highest cadmium exposure group (SMR = 272, 95% CI = 123, 513), and among workers with 20 or more years since the first exposure (SMR = 161, 95% CI = 100, 248). A statistically significant dose-response relationship was evident in nearly all of the regression models evaluated. Based on our analyses, the lifetime excess lung cancer risk at the current Occupational Safety and Health Administration standard for cadmium fumes of 100 micrograms/m3 is approximately 50 to 111 lung cancer deaths per 1000 workers exposed to cadmium for 45 years.     

Cumulative arsenic exposure and lung cancer in smelter workers: a dose-response study

The cause-specific mortality was followed through 1981 in a cohort of 3,916 male Swedish smelter workers employed for at least 3 months from 1928 through 1967. Arsenic levels in the air of all workplaces within the smelter were estimated for three different time periods. Using this exposure matrix and detailed information of the work history, cumulative arsenic exposure could be computed for each worker. Standardized mortality ratios (SMRs) were calculated for several dose categories using age-specific mortality rates from the county where the smelter was situated. A positive dose-response relationship was found between cumulative arsenic exposure and lung cancer mortality with an overall SMR of 372 (304-450, 95% confidence interval). The lung cancer mortality was related to the estimated average intensity of exposure to arsenic but not to the duration. No positive dose-response relationship was found between arsenic and ischemic heart disease or cerebrovascular disease. There was also no evident dose-response relationship between estimated exposure to sulfur dioxide and lung cancer.     

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.     

Lung cancer risk among refractory brick workers exposed to crystalline silica: a retrospective cohort study.

We conducted a retrospective cohort study among 1,022 refractory brick workers exposed to crystalline silica. Mortality from lung cancer (SMR = 1.77) and respiratory diseases (SMR = 3.15) was elevated in workers first employed less than or equal to 1957 who are likely to have shared the highest exposure to crystalline silica. Workers with at least 19 years of cumulative employment in the plant experienced particularly increased risks for lung cancer (SMR = 2.01) and respiratory diseases (SMR = 3.89). Relative mortality from these specific causes increased with years since first employment (that is, first exposure) and decreased with age at first employment. Indirect adjustment for smoking habits and the lack of excess mortality from cardiovascular diseases and emphysema indicated little effect of smoking on the increased risks for lung cancer and respiratory diseases.     

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.     

A mortality study of cobalt production workers: An extension of the follow-up

The follow-up of a cohort of workers employed in an electrochemical plant producing cobalt and sodium, previously studied from 1950–1980, has been extended from 1981–1988. The standardized mortality ratio (SMR) for all causes of death was 0.85 (95% confidence interval [CI] + 0.76–0.95, 309 observed) for the whole cohort, and 0.95 (95% CI + 0.83–1.08, 247 observed) for the subcohort of workers born in France. With regard to lung cancer mortality among cobalt production workers, which is the main objective of the study, the SMRs were, respectively, 0.85 (95% CI + 0.18–2.50, 3 observed) and 1.16 (95% CI + 0.24–3.40, 3 observed). Neither did any excess of mortality from diseases of the circulatory and of the respiratory systems appear among cobalt production workers. Maintenance workers, however, exhibited high SMRs for lung cancer, reaching statistical significance for duration of exposure and time since first exposure ≥ 30 years. This study does not support the hypothesis of a relationship between lung cancer and cobaltexposure. © 1993 Wiley-Liss. Inc.     

上海某冶炼厂铅接触工人肿瘤死亡的回顾性队列研究

目的 了解职业铅接触工人肿瘤死亡情况,探讨职业铅接触与肿瘤的关系。方法 1985年1月1日前在本厂工人1年以上,且1985年1月1日仍存活的男性工人共6971名组成全队列,其中3344名在铅接触车间工作的工人组成的亚队列为接触队列。随访从1985年1月1日至1997年12月31日。以上海市人口的肿瘤死亡率作为标准对照,计算标化死亡比（SMR）;以本厂非接触人群作内对照计算相对危险度（RR）;估计累计接触剂量进行剂量－反应关系分析。结果 全队列6971人共观察87576人年,接触队列3344人共观察41505人年。全队列中,肺癌的SMR（95％CI）为128．0（101．1－159．7）。1965年后入厂的工人肺癌的SMR为463．7（P＜0．01）。有铅接触工作史且工龄超过20年的工人鼻咽癌的SMR＝408．0（P＜0．01）,肺癌的SMR＝156．6（P＜0．01）。肿瘤总计、恶性肿瘤总计、食管癌、胃癌、肝和胆道癌、肺癌和膀胱癌的RR（95％CI）分别为3．25（2．43－3．89）、3．28（2．54－4．32）、3．57（1．08－10．47）、2．93（1．15－4．87）、4．58（2．03－9．97）、8．58（4．82－15．11）、6．66（2．83－13．01）。将累计接触剂量分为高、中、低3个组,中、高组工人恶性肿瘤RR分别为1．62（P＜0．05）和1．70（P＜0．05）,且有随累计接触剂量增加危险性升高的趋势。中、高组工人的肺癌RR分别为2．55（P＜0．05）,和2．31（P＜0．05）。结论 工人肿瘤死亡危险性升高可能与铅接触有关,但还需要在控制其他职业有害因素接触和非职业性有害因素接触的情况下作进一步的研究。     

Mortality among workers at a talc mining and milling facility

BACKGROUND: This study evaluated mortality among workers at a talc mining and milling facility. METHODS: Subjects were white men actively employed between 1948 and 1989 and known to have been alive in or after 1950. Analyses assessed cancer mortality during the period 1950-89 (809 subjects) and non-cancer mortality during 1960-89 (782 subjects). RESULTS: Comparisons with regional general population death rates for 1960-89 indicated that the workers had more than expected deaths from all causes combined [209 observed/160 expected, standardized mortality ratio (SMR) = 131, 95% confidence interval (CI) = 114-150], due mainly to increased mortality from lung cancer (31/13, SMR = 232, CI = 157-329) and non-malignant respiratory disease (NMRD) (28/13, SMR = 221, CI = 147-320). The lung cancer excess was concentrated in miners (18/4.6, SMR = 394, CI = 233-622); millers had only a small increase (7/5.5, SMR = 128, CI = 51-263). An excess of NMRD occurred both in miners (10/4.2, SMR = 241, CI = 116-444) and in millers (11/4.8, SMR = 227, CI = 113-407). The median estimated exposure to respirable dust was 511 mg/m(3)-days for all exposed employees, 739 mg/m(3)-days for mine workers and 683 mg/m(3)-days for mill workers. Employees with high, compared with low, estimated exposure to dust had a rate ratio of 0.5 (CI = 0.2-1.3) for lung cancer and of 11.8 (CI = 3.1-44.9) for pulmonary fibrosis. CONCLUSIONS: Exposure to talc ore dust may not have been responsible for the lung cancer excess among these workers but probably contributed to the elevated rate of NMRD, particularly pulmonary fibrosis.     

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 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.     

A mortality study among workers in a French aluminium reduction plant

Objective: A mortality study on the association between lung cancer and occupational exposure to polycyclic aromatic hydrocarbons (PAHs) was carried out in a French aluminium reduction plant. This study updated a previous mortality study. Method: The historical cohort included every male worker who had been employed in the plant for at least 1 year between 1950 and 1994. Workers were followed-up for mortality from 1968 to 1994. Causes of death were obtained from death certificates. Standardised mortality ratios (SMRs) and 95% confidence intervals (CI) were computed using regional mortality rates as external reference to compare observed and expected numbers of deaths, adjusted for gender, age and calendar time. Results: The cohort comprised 2,133 men, of whom 335 died during the follow-up period. The observed mortality was lower than expected for all causes of death (SMR=0.81, CI 0.72–0.90) and for lung cancer (observed=19, SMR=0.63, CI 0.38–0.98). No lung cancer excess was observed in workshops where PAH exposure was likely to have occurred, and no trend was observed according to duration of exposure and time since first exposure. This low lung cancer mortality could be partly explained by a marked healthy worker effect and a possible negative confounding by smoking. An excess was observed for bladder cancer (observed=7, SMR=1.77, CI 0.71–3.64) in the whole cohort, that was higher among workers employed in workshops where PAH exposure was likely to have occurred (observed=6, SMR=2.15, CI 0.79–4.68). In addition, an SMR higher than unity was observed for “psychoses and neuro-degenerative diseases” (observed=6, SMR=2.39, CI 0.88–5.21), that could not be related to occupational aluminium exposure. Conclusion: No lung cancer risk was detected. Non-significant excesses were observed for bladder cancer and for psychoses and neuro-degenerative diseases. Received: 11 June 1999 / Accepted: 22 January 2000     

Cancer mortality in a cohort of male German iron foundry workers

BACKGROUND: Observations of an increased incidence of cancers of the upper aero-digestive tract (pharynx, esophagus, larynx, lung) among workers of local German foundries gave rise to concern about a potentially elevated occupational risk of those cancer sites. The purpose of the study was to examine whether occupational exposure in iron foundries increases the risk of cancer. METHODS: A historical cohort study of 17,708 male German production workers in 37 iron foundries who were first employed in 1950-1985 with a minimum employment period of 1 year was initiated. Employment and occupational histories were collected. Mortality was compared with that of the German general population during 1950-1993 using a new method for computing the SMR when not all causes of death are available (called SMR*). RESULTS: Mortality from all causes was elevated to SMR = 115.4 (95% confidence interval (CI) = 111.9-119.1), as was for total cancer (SMR* = 123.8, CI = 102.1-152.6), especially cancers of the lung (SMR* = 163.9, CI = 123.9-223.0) and liver (SMR* = 322.5, CI = 149.5-844.8), and diseases of the respiratory system (SMR* = 147.6, CI = 100.4-221.5). Non-significant elevations of mortality were also found for cancers of the mouth and pharynx (SMR* = 153.5, CI = 82.3-359.8) and larynx (SMR* = 173.1, CI = 85.5-550.5). Mortality from various causes of death was higher among workers with shorter exposure periods than among long-term employees. The elevated mortality persisted for years and decades after termination of employment. CONCLUSIONS: The results provide further evidence for an increased risk of lung cancer and possibly other cancers of the upper aero-digestive tract among foundry workers. Special attention should be paid to the strongly increased mortality from liver cancer and the mortality pattern among employees having terminated work.     

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.     

铁矿工人队列死因研究

目的 探索危害铁矿作业工人健康的主要疾患及职业有害因素对工人寿命的影响.方法 用流行病学队列研究方法,对武钢大冶铁矿7 469名职工从1972年开始随访30余年,以全国城市居民年龄别死亡率为参照,用标化死亡比（SMR）作为统计指标,并计算95%可信区间.结果 自1972年至2003年底,共计199 108.0人年,死亡1 752人,累积死亡率为23.5%.影响铁矿工人寿命的主要疾病按累积死亡率从高到低排序分别是：肿瘤（7.8%）、脑血管疾病（3.9%）、心血管系疾病（3.4%）和呼吸系疾病（2.9%）,恶性肿瘤以肺癌和肝癌最多,分别占总死亡数的10%和7.4%.全死因SMR为1.06,高于全国平均水平.死亡率明显升高的疾病有鼻咽癌、肝癌、肺癌、尘肺和意外事故,SMR分别为1.84、1.51、1.83、14.94和1.25.队列中接尘工人与非接尘工人比较,接尘工人全死因、胃癌、肺癌、呼吸系统疾病、心血管疾病和意外事故的累积死亡率明显升高（相对危险度分别为1.35、1.83、1.61、2.27、1.34和1.69）.结论 以粉尘为主的职业有害因素明显影响铁矿工人健康和寿命.     

A "lugged" analysis of lung cancer risks in UK carbon black production workers, 1951-2004

BACKGROUND: Previously published analyses of excess lung cancer risks in UK carbon black production workers attracted no confident interpretation. METHODS: The mortality of a cohort of 1,147 male manual workers from five UK factories manufacturing carbon black was investigated for the period 1951-2004. All subjects were first employed in the period 1947-74 and were employed for 12 months or more. Limited work histories were available to calculate estimates of individual cumulative exposure to carbon black. RESULTS: Based on serial rates for the general population of England and Wales, significantly elevated mortality was observed for lung cancer (Obs 67, SMR 146, P < 0.01) but not for all other causes combined (Obs 426, SMR 106). There was highly elevated lung cancer mortality at two of the plants (SMR 230, Obs 35) but no excess mortality at the other three plants combined (SMR 104, Obs 32). Analyses by period since leaving employment indicated elevated lung cancer risks were limited to those workers with some employment in the most recent 15 years. SMR analyses found an overall positive significant trend between lung cancer risks and cumulative carbon black exposure received in the most recent 15 years. Poisson regression analyses provided different results depending on which variables were adjusted for. CONCLUSIONS: The findings suggest that carbon black, or chemicals associated with the production of carbon black, had an effect on later stages of lung cancer carcinogenesis at two of the plants but that no such effect was found at the other plants.