Pancreatic cancer in workers at a transformer manufacturing plant.
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Biomedical subjects
Publications and source records attributed to O Wong.
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A large number of epidemiologic studies of workers in the petroleum industry have been conducted to investigate the carcinogenic and other health effects of exposure to petroleum products during manufacture and distribution. Of particular interest is the relationship between exposure to benzene or benzene-containing liquids in the petroleum industry and leukemia risk. However, few studies have investigated cell-type-specific leukemia risk. In the present investigation, all cohort studies of petroleum workers in the United States and the United Kingdom were combined into a single database for cell-type-specific leukemia analysis. The majority of these workers were petroleum refinery employees, but production, pipeline, and distribution workers in the petroleum industry were also included. The combined cohort consisted of 208,741 petroleum workers. Between 1937 and 1989, these workers contributed a total of 4,665,361 person-years of observation. More than 56 thousand deaths were reported among these workers during the 53 years of observation. Cell-type-specific leukemia risks were calculated using a meta-analysis procedure appropriate for combining occupational cohort studies. These risks were expressed in terms of cell-type-specific leukemia standardized mortality ratios (meta-SMRs). The meta-SMR for acute myelogenous leukemia was 0.96. The lack of an increase of acute myelogenous leukemia was attributed to the low levels of benzene exposure in the petroleum industry, particularly in comparison to benzene exposure levels in some previous studies of workers in other industries, who had been found to experience increased risk of acute myelogenous leukemia. Similarly, no increase in chronic myelogenous, acute lymphocytic, or chronic lymphocytic leukemias was found in petroleum workers (meta-SMRs of 0.89, 1.16, and 0.84, respectively). Meta-analyses restricted to refinery studies or to studies with at least 15 years of follow-up yielded similar results. The findings of the present investigation are consistent with those from several recent case-control studies.
OBJECTIVE: To determine the risk of developing acute myeloid leukaemia (AML) and multiple myeloma in a cohort of workers exposed to benzene. The results were used to show the importance of taking specificity of disease into consideration in causation analysis. METHODS: Data were derived from a cohort of workers employed at two Goodyear plants in Ohio in the manufacture of Pliofilm. Based on data in the Pliofilm study, several papers that examined the relation between exposure to benzene and leukaemia (all cell types combined) have been published. In the current analyses based on updated data in the study, standardised mortality ratios (SMRs) and 95% confidence intervals (95% CIs) were calculated for AML and multiple myeloma by cumulative exposure to benzene. The results based on AML were compared with those for leukaemia (all cell types combined) published previously. RESULTS: An exposure response relation was shown between cumulative exposure to benzene and AML. No increased risk of AML was detected for cumulative exposure to benzene below 200 ppm-years (SMR 0.91). Above 200 ppm-years, risk of AML rose drastically; reaching a significant SMR of 98.37 for > 400 ppm-years. For multiple myeloma, no relation with exposure to benzene was detected. CONCLUSION: Analysis specific to AML shows the importance of taking specificity of disease into consideration in causation analysis. This investigation shows that previous analyses based on all leukaemia cell types combined have incorrectly set the estimated threshold too low, and have underestimated risk above the threshold. Current regulatory policies that rely on previous analyses based on all leukaemia cell types combined should be re-examined.
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OBJECTIVES: The purpose of the study was to investigate potential reproductive effects of sodium borates on occupationally exposed male employees at a large mining and production facility in the Mojave Desert of California. METHODS: The standardised birth ratio (SBR) was used to assess fertility of the male employees. Live births were the measured end point, and the rate of female to male offspring was also assessed. Data were collected through a questionnaire after a series of on site introductory and explanatory meetings with the employees. Initial non-responders were followed up by telephone. Medical insurance records were assessed for those who declined to participate. RESULTS: The questionnaire was a good method of ascertainment for live births. There was no evidence of selection bias in the results. There was a highly significant excess of offspring fathered by the male employees. There was no evidence of a relation between exposure and this excess of offspring, nor were there any temporal differences during the period of observation (> 30 years). Also, there was an excess of the percentage of female offspring fathered by these male employees. This excess of female offspring was not significant. There was no evidence of an exposure relation to sodium borates with this excess of female offspring nor were there any temporal differences. CONCLUSION: Under the conditions studied, there were no adverse reproductive effects of high borate doses as reported from oral ingestion studies in animals.
Mortality data have been updated for a further 12 years for a cohort of workers in the reinforced plastics and composites industry with exposures to styrene monomer and other chemicals. The cohort consisted of 15,826 male and female employees who were exposed to styrene for at least six months between 1948 and 1977 at 30 participating manufacturing plants in the United States. A total of 1628 deaths were reported during the extended observation period, 1948-89. Mortality from several causes showed significant increases--namely, all causes, all cancers, oesophageal cancer, lung cancer, cancer of the cervix uteri, cancer of other female genital organs, hypertensive heart disease, certain non-malignant respiratory diseases, motor vehicle accidents, and homicides. When, however, mortality data were examined in terms of duration of employment, durations of styrene exposure, and cumulative styrene exposure no upward trend was detected in any of these causes of death. Most of the increases in mortality were among workers who were employed for only six months to a year or who had very low cumulative exposure (< 10 ppm-years). Therefore, the increased mortality was not likely to be related to exposure to styrene. Several explanations for the increased mortality are offered, including low socioeconomic class, smoking, and lifestyle factors characteristic of short term workers. There was no increased mortality from lymphatic and haematopoietic cancers overall or from any specific haematological malignancies. In particular, no increase in mortality from non-Hodgkin's lymphoma, Hodgkin's disease, multiple myeloma, or leukaemia was found. Furthermore, detailed exposure-response analyses did not show any relation between exposure to styrene and any of these haematological malignancies. The lack of an exposure-response relation further supports the conclusion that workers in the reinforced plastics industry in this study did not experience any increased risk of lymphatic and haematopoietic cancers as a result of their exposure to styrene.
Exposure to man-made mineral (or vitreous) fiber (MMMF or MMVF) is a potential health concern in both occupational and environmental settings. Previous epidemiologic studies have reported a small increase of lung cancer among workers exposed to MMVF. Most of these studies were cohort studies and lacked information on fiber concentration, occupational coexposures, and cigarette smoking. Some of the coexposures were known human lung carcinogens and could have accounted for the small lung cancer excess. In a recently completed epidemiologic case-control study of lung cancer in MMVF workers exposed to slag wool fibers, we analyzed lung cancer risk in relation to cumulative fiber exposure (concentration and duration) and smoking history and controlled for other coexposures such as asbestos contamination. No increased lung cancer risk with exposure to slag wool fibers was found. As expected, however, we detected a strong confounding effect of smoking. The findings from this epidemiologic study were consistent with the results of recently completed toxicologic studies, which found that slag wool fibers of dimension classically associated with tumor induction ("Stanton" fibers) do not stay in the lung in sufficient quantity or time to induce tumors in animals. In this paper we emphasize the importance of confounding effects due to coexposures and provide guidelines to estimate the magnitude of potential confounding effects of coexposures such as smoking.
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This epidemiological study was of 18,728 employees at 14 United States facilities producing sterilised medical supplies and spices, who were potentially exposed to ethylene oxide (EO) for at least 90 days. The mortality of the cohort was studied to the end of 1988. A total of 1353 deaths was identified. The cohort had a significantly lower mortality than the general population from all causes, all cancers, and non-malignant diseases. In the entire cohort, mortality was not significantly increased from any of the cancer sites examined. In particular, no significant increase in mortality was found in the cancer sites of interest based on previous studies--namely, stomach, leukaemia (including major specific cell types), pancreas, and brain. The lack of an increased mortality for these cancer sites was further strengthened by the lack of a dose-response relation with duration of employment and latency. Among the men, a statistically significant increase in mortality from non-Hodgkin's lymphoma was found. There was no indication for a dose-response relation for non-Hodgkin's lymphoma and no specific job categories seemed to be responsible for the increase. Among the women, a deficit of non-Hodgkin's lymphoma was found, which was not consistent with the finding in the men. Therefore, the increase among the men did not seem to be related to exposure to EO.
Personal exposures were estimated for a large cohort of workers in the U.S. domestic system for distributing gasoline by trucks and marine vessels. This assessment included development of a rationale and methodology for extrapolating vapor exposures prior to the availability of measurement data, analysis of existing measurement data to estimate task and job exposures during 1975-1985, and extrapolation of truck and marine job exposures before 1975. A worker's vapor exposure was extrapolated from three sets of factors: the tasks in his or her job associated with vapor sources, the characteristics of vapor sources (equipment and other facilities) at the work site, and the composition of petroleum products producing vapors. Historical data were collected on the tasks in job definitions, on work-site facilities, and on product composition. These data were used in a model to estimate the overall time-weighted-average vapor exposure for jobs based on estimates of task exposures and their duration. Task exposures were highest during tank filling in trucks and marine vessels. Measured average annual, full-shift exposures during 1975-1985 ranged from 9 to 14 ppm of total hydrocarbon vapor for truck drivers and 2 to 35 ppm for marine workers on inland waterways. Extrapolated past average exposures in truck operations were highest for truck drivers before 1965 (range 140-220 ppm). Other jobs in truck operations resulted in much lower exposures. Because there were few changes in marine operations before 1979, exposures were assumed to be the same as those measured during 1975-1985. Well-defined exposure gradients were found across jobs within time periods, which were suitable for epidemiologic analyses.
In this study, the cohort consisted of 18,135 distribution employees with potential exposure to gasoline for at least one year at land-based terminals (n = 9,026) or on marine vessels (n = 9,109) between 1946 and 1985. The primary objective of the study was to determine the relationship, if any, between exposure to gasoline and mortality from kidney cancer or leukemia. In addition, other causes of death of secondary interest included multiple myeloma and heart diseases. The mortality of the cohort was observed through June 30, 1989. The results of this study indicated that there was no increased mortality from either kidney cancer or leukemia among marketing and marine distribution employees who were exposed to gasoline in the petroleum industry when compared to the general population. Among the land-based terminal employees, the kidney cancer standardized mortality ratio (SMR) was 65.4 (12 deaths) and leukemia SMR was 89.1 (27 deaths). For the marine cohort, the SMRs were 83.7 for kidney cancer (12 deaths) and 70.0 for leukemia (16 deaths), respectively. More importantly, based on internal comparisons, there was no association between mortality from kidney cancer or leukemia and various indices of gasoline exposure. In particular, neither duration of employment, duration of exposure, age at first exposure, year of first of exposure, job category, cumulative exposure, frequency of peak exposures, nor average intensity of exposure had any effect on kidney cancer or leukemia mortality. For acute myeloid leukemia, a nonsignificant mortality increase was found in land-based terminal employees (SMR = 150.5, 13 deaths), but no trend was detected when the data were analyzed by various gasoline exposure indices. This nonsignificant excess was limited to land-based terminal employees hired before 1948. On the other hand, a deficit of mortality from acute myeloid leukemia was observed among marine employees (SMR = 74.2, 5 deaths). For the two cohorts combined, SMR for acute myeloid leukemia was 117.1 based on 18 deaths. We did not find any relationship in our study between gasoline exposure and mortality from multiple myeloma or heart diseases. In general, we did not find any significantly increased mortality, either overall or from specific causes, associated with gasoline exposure in this study of marketing and marine distribution employees.
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We conducted an epidemiologic study of skin cancer incidence rates for four counties in Montana. The two counties considered to be exposed to arsenic were Deer Lodge, containing the former Anaconda copper smelter, and Silver Bow, containing an open pit copper mine. Residents in these counties had potential exposure to arsenic and other heavy metals. Gallatin and Park counties served as controls. All histologically proven skin cancer cases during the period January 1980 through June 1986 were collected from pathology services and dermatologists in these four counties. In addition, all skin cancer cases from four dermatologists practicing in urban referral areas outside the counties were reviewed. Results were analyzed by individual as well as by two different definitions of anatomically distinct lesions: the National Cancer Institute (NCI) definition and the study definition. There were 1616 individuals with skin cancer in the four counties during the period under consideration, yielding 2252 (NCI definition) and 2451 (study definition) cases. The clinical features of the skin cancers in the exposed counties were not similar to those described for arsenic-related skin cancer. The age-adjusted annual skin cancer rates were higher for the two control counties as compared to either the county with the former smelter, Deer Lodge, or the county with the mine, Silver Bow. Our results cannot be explained by differences in ascertainment, latitude, or altitude. They can be partially explained by differences in both outdoor employment and medical practice. The overall skin cancer incidence rates for the exposed counties were well within the range of skin cancer rates observed for other locations in the United States.
An update of a cohort study of 14,074 employees at the Richmond and El Segundo refineries of Chevron USA in California was conducted to further examine mortality patterns. The update added six years of follow up (1981-6) and 941 deaths. As in the previous study, mortality from all causes (standard mortality ratio (SMR) = 73) was significantly lower among men compared with the general United States population. Significant deficits were also found for all cancers combined (SMR = 81), several site specific cancers, and most non-malignant causes of death. Mortality from suicide was increased relative to the United States as a whole. Based on a comparison with California rates, however, men had fewer deaths from suicide than expected. Standard mortality ratios were raised for several other causes of death, but only leukaemia and lymphoreticulosarcoma exhibited a pattern suggestive of an occupational relation. The increase appeared to be confined to those hired before 1949, and in the case of lymphoreticulosarcoma, to Richmond workers.