Mortality of workers exposed to toluene diisocyanate in the polyurethane foam industry.

OBJECTIVE: To evaluate cancer mortality among United States workers exposed to toluene diisocyanate (TDI) in the manufacture of polyurethane foam. METHODS: This cohort mortality study included 4611 men and women employed in four polyurethane foam plants for at least three months between the late 1950s and 1987. The mortality experience of the cohort was then compared with that of the general United States population. RESULTS: Current and past industrial hygiene data indicated that air concentrations in 1984-5 were below the current United States standard of 0.04 mg/m3 but exceeded the standard before 1980. Mortality ratio (SMR) 2.78, 95% confidence interval (95% CI) 0.57-8.13) and non-Hodgkin's lymphoma (SMR 1.54, 95% CI 0.42-3.95) were increased, but not significantly. There was one male breast cancer. However, breast cancer was not increased in women (SMR 0.74). No other cancer category had an increased number of deaths compared with the general population. Only non-Hodgkin's lymphoma and Hodgkin's disease showed a possible relation with time since first employment and no cancer death category showed a strong relation with duration of employment. Mortality from non-malignant respiratory disease was not increased (SMR 0.86). CONCLUSIONS: This young cohort has few deaths and short follow up. The findings are therefore not conclusive. Further years of follow up will enable better evaluation of mortality.     

Increased risk for lung cancer and for cancer of the gastrointestinal tract among Geneva professional drivers.

A historical prospective cohort study of 6630 drivers from the Canton of Geneva was carried out to evaluate mortality and incidence of cancer in this occupation. The study population was all men (of all vocations) who held in 1949 a special licence for driving lorries, taxis, buses, or coaches and all new licence holders in the period 1949-61. Men born before 1900 and those with only an ordinary driving licence were excluded. According to the occupation registered on their licence, the 6630 drivers were distributed into three groups: (1) professional drivers (n = 1726), (2) non-professional drivers "more exposed" to exhaust gas and fumes (this group included occupations such as vehicle mechanic, policeman, road sweeper; n = 712), and (3) non-professional drivers "less exposed," composed of all other occupations (n = 4192). The cohort was followed up from 1949 to December 1986 and the trace of 197 men (3%) was lost. Compared with the general population of the Canton of Geneva, professional drivers experienced significant excess risks, taking into account 15 years of latency, for all causes of death (standardised mortality ratio (SMR) 115, 90% confidence interval (90% CI) 107-123) and for all malignant neoplasms (SMR 125, 90% CI 112-140; standardised incidence ratio (SIR) 128, 90% CI 115-142). Cause specific analysis showed significant excesses for lung cancer (SMR 150, 90% CI 123-181; SIR 161, 90% CI 129-198), oesophageal cancer (SMR 183, 90% CI 108-291), stomach cancer (SMR 179, 90% CI 117-263; SIR233, 90% CI 156-336), rectal cancer (SMR 258, 90% CIU 162-392; SIR 200, 90% CI 127-300), and cirrhosis of the liver (SMR 145, 90% CI 104-198). Risk of lung cancer increased significantly with time from first exposure. Among non-professional drivers no significant excess risk was found except for lung cancer mortality among the "less exposed" group (SMR 121, 90% CI 103-140), and for incidence of lung cancer among the "more exposed" group (SIR 161, 90% CI 111-227). The possible casual relation between exposure to engine exhaust emissions and the increased risk for lung cancer and for cancer of the gastrointestinal tract found among professional drivers is discussed.     

Increased risk for lung cancer and for cancer of the gastrointestinal tract among Geneva professional drivers.

A historical prospective cohort study of 6630 drivers from the Canton of Geneva was carried out to evaluate mortality and incidence of cancer in this occupation. The study population was all men (of all vocations) who held in 1949 a special licence for driving lorries, taxis, buses, or coaches and all new licence holders in the period 1949-61. Men born before 1900 and those with only an ordinary driving licence were excluded. According to the occupation registered on their licence, the 6630 drivers were distributed into three groups: (1) professional drivers (n = 1726), (2) non-professional drivers "more exposed" to exhaust gas and fumes (this group included occupations such as vehicle mechanic, policeman, road sweeper; n = 712), and (3) non-professional drivers "less exposed," composed of all other occupations (n = 4192). The cohort was followed up from 1949 to December 1986 and the trace of 197 men (3%) was lost. Compared with the general population of the Canton of Geneva, professional drivers experienced significant excess risks, taking into account 15 years of latency, for all causes of death (standardised mortality ratio (SMR) 115, 90% confidence interval (90% CI) 107-123) and for all malignant neoplasms (SMR 125, 90% CI 112-140; standardised incidence ratio (SIR) 128, 90% CI 115-142). Cause specific analysis showed significant excesses for lung cancer (SMR 150, 90% CI 123-181; SIR 161, 90% CI 129-198), oesophageal cancer (SMR 183, 90% CI 108-291), stomach cancer (SMR 179, 90% CI 117-263; SIR233, 90% CI 156-336), rectal cancer (SMR 258, 90% CIU 162-392; SIR 200, 90% CI 127-300), and cirrhosis of the liver (SMR 145, 90% CI 104-198). Risk of lung cancer increased significantly with time from first exposure. Among non-professional drivers no significant excess risk was found except for lung cancer mortality among the "less exposed" group (SMR 121, 90% CI 103-140), and for incidence of lung cancer among the "more exposed" group (SIR 161, 90% CI 111-227). The possible casual relation between exposure to engine exhaust emissions and the increased risk for lung cancer and for cancer of the gastrointestinal tract found among professional drivers is discussed.     

Ethylene oxide: an assessment of the epidemiological evidence on carcinogenicity.

Mortality from cancer among workers exposed to ethylene oxide (EtO) has been studied in 10 distinct cohorts that include about 29,800 workers and 2540 deaths. This paper presents a review and meta-analysis of these studies, primarily for leukaemia, non-Hodgkin's lymphoma, stomach cancer, pancreatic cancer, and cancer of the brain and nervous system. The magnitude and consistency of the standardised mortality ratios (SMRs) were evaluated for the individual and combined studies, as well as trends by intensity or frequency of exposure, by duration of exposure, and by latency (time since first exposure). Exposures to other workplace chemicals were examined as possible confounder variables. Three small studies by Hogstedt initially suggested an association between EtO and leukaemia, but in seven subsequent studies the SMRs for leukaemia have been much lower. For the combined studies the SMR = 1.06 (95% confidence interval (95% CI) 0.73-1.48). There was a slight suggestion of a trend by duration of exposure (p = 0.19) and a suggested increase with longer latency (p = 0.07), but there was no overall trend in risk of leukaemia by intensity or frequency of exposure; nor did a cumulative exposure analysis in the largest study indicate a quantitative association. There was also an indication that in two studies with increased risks the workers had been exposed to other potential carcinogens. For non-Hodgkin's lymphoma there was a suggestive risk overall (SMR = 1.35, 95% CI 0.93-1.90). Breakdowns by exposure intensity or frequency, exposure duration, or latency did not indicate an association, but a positive trend by cumulative exposure (p = 0.05) was seen in the largest study. There was a suggested increase in the overall SMR for stomach cancer (SMR = 1.28, 95% CI 0.98-1.65 (CI 0.73-2.26 when heterogeneity among the risk estimates was taken into account)), but analyses by intensity or duration of exposure or cumulative exposure did not support a causal association for stomach cancer. The overall SMRs and exposure-response analyses did not indicate a risk from EtO for pancreatic cancer (SMR = 0.98), brain and nervous system cancer (SMR = 0.89), or total cancer (SMR = 0.94). Although the current data do not provide consistent and convincing evidence that EtO causes leukaemia or non-Hodgkin's lymphoma, the issues are not resolved and await further studies of exposed populations.     

Wisconsin Farmer Cancer Mortality, 1981 to 1990: Selected Malignancies

Abstract: Cancer mortality risks for Wisconsin white male farmers were examined during the years 1981 to 1990. Four malignancies were studied: Non-Hodgkin's lymphoma, melanoma, colon cancer, and rectal cancer. Occupation coded deaths were segmented into farmer and nonfarmer groups and population counts for the groups were estimated from 1980 and 1990 Bureau of the Census data. Standardized mortality ratios (SMRs) were constructed from the ratio of observed farmer deaths and the expected number of farmer deaths. Expected deaths were generated from the underlying statewide nonfarmer rate for the malignancy multiplied into the farmer population at risk. Farmers had significantly lower mortality risks for melanoma (SMR: 0.659; 95% CI: 0.993-0.326) and colon cancer (SMR: 0.763; 95% CI: 0.928-0.599). Farmers also exhibited a nonsignificant decrement for non-Hodgkin's lymphoma (SMR 0.930; 95% CI: 1.214-0.645). For rectal cancer, farmers experienced a slightly higher but essentially the same risk as nonfarmers (SMR: 1.013; 95%CI: 1.418-0.608)—the SMR was not significant. This study corroborates a number of cancer incidence and mortality investigations demonstrating that farmers generally experience the same or lower mortality risks for these malignancies.     

Evaluation of mortality and cancer incidence among alachlor manufacturing workers.

Alachlor is the active ingredient in a family of preemergence herbicides. We assessed mortality rates from 1968 to 1993 and cancer incidence rates from 1969 to 1993 for manufacturing workers with potential alachlor exposure. For workers judged to have high alachlor exposure, mortality from all causes combined was lower than expected [23 observed, standardized mortality ratio (SMR) = 0.7, 95% CI, 0.4-1.0], cancer mortality was similar to expected (6 observed, SMR = 0.7, 95% CI, 0.3-1.6), and there were no cancer deaths among workers with 5 or more years high exposure and 15 or more years since first exposure (2.3 expected, SMR = 0, 95% CI, 0-1.6). Cancer incidence for workers with high exposure potential was similar to the state rate [18 observed, standardized incidence ratio (SIR) = 1.2, 95% CI, 0.7-2.0], especially for workers exposed for 5 or more years and with at least 15 years since first exposure (4 observed, SIR = 1.0, 95% CI, 0.3-2.7). The most common cancer for these latter workers was colorectal cancer (2 observed, SIR 3.9, 95% CI, 0.5-14.2 among workers). Despite the limitations of this study with respect to small size and exposure estimating, the findings are useful for evaluating potential alachlor-related health risks because past manufacturing exposures greatly exceeded those characteristic of agricultural operations. These findings suggest no appreciable effect of alachlor exposure on worker mortality or cancer incidence rates during the study period.     

Mortality and cancer incidence among Swedish lumberjacks exposed to phenoxy herbicides

OBJECTIVES—To determine mortality and cancer incidence relative to exposure to phenoxy herbicides.
METHODS—A cohort of Swedish lumberjacks of which 261 were exposed to phenoxy herbicides, and 250 were unexposed, was followed up for mortality from 1954 to 1994, and for cancer incidence from 1958 to 1992. The number of days of exposure to phenoxy herbicides was determined from pay slips. With the county population as a reference, standardised mortality ratios and cancer incidence ratios (SMR and SIR) were calculated.
RESULTS—Mortality and cancer incidence were low with two exceptions; a small but highly exposed group of foremen showed an increased cancer incidence (SIR 274, 95% confidence interval (95% CI) 100 to 596), and over all mortality (SMR 141, 95% CI 68 to 260). Of three cases of non-Hodgkin's lymphoma, two were found among the most exposed workers.
CONCLUSIONS—The results provide some support to claims of previous studies that exposure to phenoxy herbicides might be related to non-Hodgkin's lymphoma and to an increased overall cancer risk.


Keywords: phenoxy herbicides; lumberjacks; cancer     

Mortality among workers exposed to polychlorinated biphenyls (PCBs) in an electrical capacitor manufacturing plant in Indiana: an update

An Indiana capacitor-manufacturing cohort (n=3,569) was exposed to polychlorinated biphenyls (PCBs) from 1957 to 1977. The original study of mortality through 1984 found excess melanoma and brain cancer; other studies of PCB-exposed individuals have found excess non-Hodgkin lymphoma and rectal, liver, biliary tract, and gallbladder cancer. Mortality was updated through 1998. Analyses have included standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) using rates for Indiana and the United States, standardized rate ratios (SRRs), and Poisson regression rate ratios (RRs). Estimated cumulative exposure calculations used a new job-exposure matrix. Mortality overall was reduced (547 deaths; SMR, 0.81; 95% CI, 0.7-0.9). Non-Hodgkin lymphoma mortality was elevated (9 deaths; SMR, 1.23; 95% CI, 0.6-2.3). Melanoma remained in excess (9 deaths; SMR, 2.43; 95% CI, 1.1-4.6), especially in the lowest tertile of estimated cumulative exposure (5 deaths; SMR, 3.72; 95% CI, 1.2-8.7). Seven of the 12 brain cancer deaths (SMR, 1.91; 95% CI, 1.0-3.3) occurred after the original study. Brain cancer mortality increased with exposure (in the highest tertile, 5 deaths; SMR, 2.71; 95% CI, 0.9-6.3); the SRR dose-response trend was significant (p=0.016). Among those working >or= 90 days, both melanoma (8 deaths; SMR, 2.66; 95% CI, 1.1-5.2) and brain cancer (11 deaths; SMR, 2.12; 95% CI, 1.1-3.8) were elevated, especially for women: melanoma, 3 deaths (SMR, 5.99; 95% CI, 1.2-17.5); brain cancer, 3 deaths (SMR, 2.87; 95% CI, 0.6-8.4). These findings of excess melanoma and brain cancer mortality confirm results of the original study. Melanoma mortality was not associated with estimated cumulative exposure. Brain cancer mortality did not demonstrate a clear dose-response relationship with estimated cumulative exposure.     

Mortality from cancer and other causes of death among synthetic rubber workers

OBJECTIVES: This study evaluated the mortality experience of workers from the styrene-butadiene rubber industry. Concerns about a possible association of 1,3-butadiene and styrene with lymphohaematopoietic, gastrointestinal, and lung cancers prompted the investigation. METHODS: A retrospective follow up study was conducted of 15,649 men employed for at least one year at any of eight North American styrene-butadiene rubber plants. Analyses used standardised mortality ratios (SMRs) to compare styrene-butadiene rubber workers' cause specific mortalities (1943-91) with those of the United States and Ontario general populations. RESULTS: On average, there were 25 years of follow up per subject. The standardised mortality ratio (SMR) was 87 (95% confidence interval (95% CI) 85 to 90) for all causes of death combined and was 93 (95% CI 87 to 99) for all cancers. There was an excess of leukaemia (SMR 131, 95% CI 97 to 174), restricted to hourly workers (SMR 143, 95% CI 104 to 191). For causes of death other than leukaemia, SMRs were close to or below the null value of 100. Results by work area (process group) were unremarkable for non-Hodgkin's lymphoma, multiple myeloma, and stomach cancer. Maintenance workers had a slight increase in deaths from lung cancer, and certain subgroups of workers had more than expected deaths from cancer of the large intestine and the larynx. CONCLUSION: This study found an excess of leukaemia that is likely to be due to exposure to butadiene or to butadiene plus other chemicals. Deaths from non-Hodgkin's lymphoma, multiple myeloma, and stomach cancer did not seem to be related to occupational exposure. The excess deaths from lung cancer among maintenance workers may be due in part to confounding by smoking, which was not controlled for, and in part to an unidentified occupational exposure other than butadiene or styrene. Increases in cancer of the large intestine and larynx were based on small numbers, did not seem to be due to exposure to butadiene or styrene, and may be chance observations.

 

     

Mortality and cancer morbidity among cement workers.

OBJECTIVE--To explore associations between exposure to cement dust and cause specific mortality and tumour morbidity, especially gastrointestinal tumours. DESIGN--A retrospective cohort study. SUBJECTS AND SETTING--2400 men, employed for at least 12 months in two Swedish cement factories. MAIN OUTCOME MEASURES--Cause specific morality from death certificates (1952-86). Cancer morbidity from tumour registry information (1958-86). Standardised mortality rates (SMRs; national reference rates) and standardised morbidity incidence rates (SIRs; regional reference rates) were calculated. RESULTS--An increased risk of colorectal cancer was found > or = 15 years since the start of employment (SIR 1.6, 95% confidence interval (95% CI) 1.1-2.3), mainly due to an increased risk for tumours in the right part of the colon (SIR 2.7, 95% CI 1.4-4.8), but not in the left part (SIR 1.0, 95% CI 0.3-2.5). There was a numerical increase of rectal cancer (SIR 1.5, 95% CI 0.8-2.5). Exposure (duration of blue collar employment)-response relations were found for right sided colon cancer. After > or = 25 years of cement work, the risk was fourfold (SIR 4.3, 95% CI 1.7-8.9). There was no excess of stomach cancer or respiratory cancer. Neither total mortality nor cause specific mortality were significantly increased. CONCLUSIONS--Diverging risk patterns for tumours with different localisations within the large bowel were found in the morbidity study. Long term exposure to cement dust was a risk factor for right sided colon cancer. The mortality study did not show this risk.     

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 and cancer incidence among Lithuanian cement producing workers

Aims: To investigate mortality and cancer incidence of cement producing workers.

Methods: A total of 2498 cement workers who have been employed at Portland cement producing departments for at least one year from 1956 to 2000 were followed up from 1 January 1978 to 31 December 2000. The cohort contributed 43 490 person-years to the study. Standardised incidence ratios (SIR) and standardised mortality ratios (SMR) were calculated as ratios between observed and expected numbers of cancers and deaths. The expected numbers were based on sex specific incidence and mortality rates for the total Lithuanian population.

Results: Significantly increased SMRs were found for all malignant neoplasms (SMR 1.3, 95% CI 1.0 to 1.5) and for lung cancer (SMR 1.4, 95% CI 1.0 to 1.9) among male cement workers. SIR for all cancer sites was 1.2 (95% CI 1.0 to 1.4). Excess risk was found for cancer of the lung (SIR 1.5, 95% CI 1.1 to 2.1). The SIR for urinary bladder cancer was also increased (SIR 1.8, 95% CI 0.9 to 3.5). The overall cancer incidence was not increased among females (SIR 0.8, 95% CI 0.6 to 1.1). With increasing cumulated exposure to cement dust, there were indications of an increasing risk of lung and stomach cancers among males.

Conclusions: This study supported the hypothesis that exposure to cement dust may increase the lung and bladder cancer risk. A dose related risk was found for stomach cancer, but no support was found for an increased risk of colorectal cancer.

     

Mortality and exposure response among 14,458 electrical capacitor manufacturing workers exposed to polychlorinated biphenyls (PCBs)

BACKGROUND: We expanded an existing cohort of workers (n = 2,588) considered highly exposed to polychlorinated biphenyls (PCBs) at two capacitor manufacturing plants to include all workers with at least 90 days of potential PCB exposure during 1939-1977 (n = 14,458). Causes of death of a priori interest included liver and rectal cancers, previously reported for the original cohort, and non-Hodgkin lymphoma (NHL), melanoma, and breast, brain, intestine, stomach, and prostate cancers, based on other studies. METHODS: We ascertained vital status of the workers through 1998, and cumulative PCB exposure was estimated using a new job exposure matrix. Analyses employed standardized mortality ratios (SMRs; U.S., state, and county referents) and Poisson regression modeling. RESULTS: Mortality from NHL, melanoma, and rectal, breast, and brain cancers were neither in excess nor associated with cumulative exposure. Mortality was not elevated for liver cancer [21 deaths; SMR 0.89; 95% confidence interval (CI), 0.55-1.36], but increased with cumulative exposure (trend p-value = 0.071). Among men, stomach cancer mortality was elevated (24 deaths; SMR 1.53; 95% CI, 0.98-2.28) and increased with cumulative exposure (trend p-value = 0.039). Among women, intestinal cancer mortality was elevated (67 deaths; SMR 1.31; 95% CI, 1.02-1.66), especially in higher cumulative exposure categories, but without a clear trend. Prostate cancer mortality, which was not elevated (34 deaths; SMR 1.04; 95% CI, 0.72-1.45), increased with cumulative exposure (trend p-value = 0.0001). CONCLUSIONS: This study corroborates previous studies showing increased liver cancer mortality, but we cannot clearly associate rectal, stomach, and intestinal cancers with PCB exposure. This is the first PCB cohort showing a strong exposure-response relationship for prostate cancer mortality.     

Mortality in a cohort of tannery workers.

OBJECTIVES: To evaluate the mortality of a group of tannery workers. METHODS: The cohort consisted of 1244 workers (870 men and 374 women) employed at a chrome tannery between 1955 and 1988. A total of 36414 person-years of follow up was calculated (369 people had died). National and regional mortalities were used to estimate the expected numbers. RESULTS: All cause mortality was similar to that of the general population. The most remarkable excess was for bladder cancer (observed 10, standardised mortality ratio (SMR) 242, 95% confidence interval (95% CI) 116 to 446). An excess of colorectal cancer (observed 17, SMR 180, 95% CI 105 to 288) was also found, based on an increased risk of both colon (SMR 166) and rectal cancer (SMR 206). No recognisable patterns emerged from the analyses by years since first employment, calendar year of hire, or lagging exposures. CONCLUSIONS: The increased mortality from bladder cancer is likely due to exposure to benzidine based leather dyes. If the apparent excess of colorectal cancer is real, its causes are as yet unknown.     

Cause specific mortality and cancer incidence among employees exposed to 2,3,7,8-TCDD after a 1953 reactor accident.

OBJECTIVE: To evaluate the long term health consequences of past occupational exposure to 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). METHODS: Cancer incidence and cause specific mortality were examined up to and including 1992 in a group of 243 men with external comparisons and internal dose-response analyses. Model based estimates of TCDD dose (expressed in micrograms/kg body weight) were developed for all cohort members with an approach that incorporated detailed accounts of each employee's work activities, analyses of TCDD in blood lipid of 138 employees, and internally derived estimates of elimination rates of TCDD. RESULTS: The estimated dose of TCDD for 135 men was > or = 0.1 microgram/kg body weight and for 69 men > or = 1 microgram/kg body weight. Increased cancer risk ratios were found with higher doses of TCDD and longer interval since first exposure for all sites combined and digestive and respiratory cancers in particular. Within the high dose group (> or = 1 microgram/kg body weight), total cancer mortality was increased > or = 20 years after first exposure (13 cases, standardised mortality ratio (SMR) 1.97, 95% confidence interval (95% CI) 1.05-3.36) as was respiratory cancer (six cases, SMR 3.06; 95% CI 1.12-6.66). Among current cigarette smokers, 12 cancer deaths occurred in the high dose group (SMR 3.42, 95% CI 1.77-5.97) compared with seven deaths at lower doses of TCDD (SMR 1.29, 95% CI 0.52-2.66). Regression analyses based on the Cox's proportional hazards model provided further evidence of a relation between cumulative dose of TCDD and occurrence of both overall and digestive cancer. No evidence of an effect of TCDD on overall mortality or deaths due to circulatory disease was found and no cases of non-Hodgkin's lymphoma or soft tissue sarcoma have been found to date. CONCLUSIONS: Our findings are consistent with a carcinogenic effect induced by TCDD at doses > or = 1 microgram/kg body weight. With such a small cohort, the risk estimates are not very stable and could be affected by selection and confounding.     

Cancer risk for chemical workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Aims: To describe the long term mortality experience of a cohort of 2187 male chemical production workers previously exposed to substantial levels of dioxin.

Methods: Vital status for a previously identified cohort was determined for an additional 10 years, to 1995. Dioxin exposures took place before 1983 and were sufficient to result in chloracne in 245 individuals. Mortality rates were compared with national figures and with a large pool of co-workers in unrelated production jobs.

Results: All cancers combined (standardised mortality ratio (SMR) = 1.0, 95% CI 0.8 to 1.1) and lung cancer (SMR = 0.8, 95% CI 0.6 to 1.1) were at or below expected levels. Rates for soft tissue sarcoma (SMR = 2.4, 95% CI 0.3 to 8.6) and non-Hodgkin's lymphoma (SMR = 1.4, 95% CI 0.6 to 2.7) were greater than expected overall, but below expectation in the update period. No trend of increasing risk with increasing exposure was observed for these cancers. Workers who developed chloracne had very low all-cancer rates (SMR = 0.5, 95% CI 0.3 to 1.0), and lung cancer rates (SMR = 0.3, 95% CI 0.0 to 1.1).

Conclusions: We found no coherent evidence of increased cancer risk from dioxin exposure in this cohort. Our study highlights the wide range of cancer rates and the lack of consistency across dioxin studies.

     

Mortality patterns among workers exposed to acrylamide: 1994 follow up

OBJECTIVE: To update the mortality experience of a cohort of 8508 workers with potential exposure to acrylamide at three plants in the United States from 1984-94. METHODS: Analyses of standardised mortality ratios (SMR) with national and local rates and relative risk (RR) regression modelling were performed to assess site specific cancer risks by demographic and work history factors, and exposure indicators for acrylamide and muriatic acid. RESULTS: For the 1925-94 study period, excess and deficit overall mortality risks were found for cancer sites of interest: brain and other central nervous system (CNS) (SMR 0.65, 95% confidence interval (95% CI) 0.36 to 1.09), thyroid gland (SMR 2.11, 95% CI 0.44 to 6.17), testis and other male genital organs (SMR 0.28, 95% CI 0.01 to 1.59), and cancer of the respiratory system (SMR 1.10, 95% CI 0.99 to 1.22); however, none was significant or associated with exposure to acrylamide. A previously reported excess mortality risk of cancer of the respiratory system at one plant remained increased among workers with potential exposure to muriatic acid (RR 1.50, 95% CI 0.86 to 2.59), but was only slightly increased among workers exposed or unexposed to acrylamide. In an exploratory exposure-response analysis of rectal, oesophageal, pancreatic, and kidney cancer, we found increased SMRs for some categories of exposure to acrylamide, but little evidence of an exposure-response relation. A significant 2.26-fold risk (95% CI 1.03 to 4.29) was found for pancreatic cancer among workers with cumulative exposure to acrylamide > 0.30 mg/m3.years; however, no consistent exposure-response relations were detected with the exposure measures considered when RR regression models were adjusted for time since first exposure to acrylamide. CONCLUSION: The contribution of 1115 additional deaths and nearly 60,000 person-years over the 11 year follow up period corroborate the original cohort study findings of little evidence for a causal relation between exposure to acrylamide and mortality from any cancer sites, including those of initial interest. This is the most definitive study of the human carcinogenic potential of exposure to acrylamide conducted to date.

 

     

Mortality and cancer incidence in a cohort of meatworkers

Methods: In a retrospective cohort study, a list of members of a meatworkers union in Australia was matched with the national death and cancer registries. Standardised mortality ratios (SMR) and standardised incidence ratios (SIR) were calculated using Australian population rates. Exposure to animal viruses, animal blood, animal faeces, and plastic pyrolysis products was assigned according to job title. A nested case control analysis examined the risk of mortality and cancer incidence by each exposure.

Results: There were approximately 20 000 subjects available for analysis. Male workers had increased risk of mortality from all causes (SMR 116, 95% CI 105 to 128) and from injury (SMR 131, 95% CI 108 to 157). Risk of incident lung cancer in males was non-significantly increased (SIR 164, 95% CI 97 to 259) and males had a raised risk of head and neck cancer (SIR 188, 95% CI 103 to 315). There were no significant associations with specific exposures.

Conclusions: Compared to the general Australian population, meatworkers have increased risk of death from all causes, death from injury, and incident lung and head and neck cancer. Analysis by occupational exposures did not disclose any strong evidence of specific occupational risk factors, although this analysis was limited by small numbers of some outcomes and exposure assessment which was based on job titles only.

     

Mortality and cancer incidence in a copper-zinc cohort

Previous studies of copper-zinc workers have primarily observed significant increases in lung and other respiratory cancers. This study concurrently examined cancer incidence and cause-specific mortality for a cohort of workers at a copper-zinc producer in Ontario, Canada, from 1964 to 2005. Significant elevations in lung cancer incidence were observed for males in the overall cohort (standardized incidence ratio [SIR] = 124, 95% confidence interval [CI] = 102-150) and for surface mine (SIR = 272, 95% CI = 124-517), concentrator (SIR = 191, 95% CI = 102-327), and central maintenance (SIR = 214, 95% CI = 125-343) employees. Significant elevations of non-Hodgkin's lymphoma incidence were observed for male underground mine employees (SIR = 232, 95% CI = 111-426). Occupational etiology cannot be ascertained with the current exploratory study design. Future studies could (1) incorporate exposure assessment for subgroups within the existing cohort and (2) determine the efficacy of wellness programs in partnership with the local health unit.     

Mortality and cancer incidence in Swedish battery workers exposed to cadmium and nickel

OBJECTIVE: To follow up cancer incidence and mortality in a group of Swedish battery workers exposed to nickel hydroxide and cadmium oxide. METHODS: 869 workers, employed at least one year between the years 1940 and 1980 were followed up until 1992. Vital status and causes of death were obtained from the Swedish cause of death registry. Cancer morbidity was retrieved from the Swedish cancer registry. Regional reference rates were used to compute the expected numbers of deaths and cancers. RESULTS: Up to 31 December, 1992, a total of 315 deaths (292 in men and 23 in women) had occurred in the cohort. For men, the overall standardised mortality ratio (SMR) was 106 (95% confidence interval (95% CI) 93.7 to 118) and for women 83.8 (95% CI 53.1 to 126). The SMRs for total cancer mortality were 125 (95% CI 98.2 to 157) for men and 69.5 (95% CI 25.5 to 151) for women. The SMR for lung cancer in men was 176 (95% CI 101 to 287). No lung cancers were found among female workers. Up to 31 December, 1991, a total of 118 cancers had occurred in the cohort. A significantly increased standardised incidence ratio (SIR) was found for cancer of the nose and nasal sinuses in men, three cases v 0.36 expected, yielding an SIR of 832 (95% CI 172 to 2430). Applying a 10 year latency period in cohort members exposed to > or = 1000 micrograms cadmium/m3, the SIR was 1107 (95% CI 134 to 4000). Similarly, for cohort members exposed to 2000 micrograms nickel/m3, the SIR was 1080 (95% CI 131 to 3900). CONCLUSION: There was an increased overall risk for lung cancer, but no exposure-response relation between cumulative exposure to cadmium or nickel and risk of lung cancer. There was a highly significant increased risk of cancer of the nose and nasal sinuses, which may be caused by exposure to nickel or cadmium or a combination of both exposures.