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E Delzell

Publications and source records attributed to E Delzell.

At least 19 recordsLinked to original sources
PubMed2006

Cancer incidence among semiconductor and electronic storage device workers.

AIMS: To evaluate cancer incidence among workers at two facilities in the USA that made semiconductors and electronic storage devices. METHODS: 89 054 men and women employed by International Business Machines (IBM) were included in the study. We compared employees' incidence rates with general population rates and examined incidence patterns by facility, duration of employment, time since first employment, manufacturing era, potential for exposure to workplace environments other than offices and work activity. RESULTS: For employees at the semiconductor manufacturing facility, the standardised incidence ratio (SIR) for all cancers combined was 81 (1541 observed cases, 95% confidence interval (CI) 77 to 85) and for those at the storage device manufacturing facility the SIR was 87 (1319 observed cases, 95% CI 82 to 92). The subgroups of employees with > or =15 years since hiring and > or =5 years worked had 6-16% fewer total incidents than expected. SIRs were increased for several cancers in certain employee subgroups, but analyses of incidence patterns by potential exposure and by years spent and time since starting in specific work activities did not clearly indicate that the excesses were due to occupational exposure. CONCLUSIONS: This study did not provide strong or consistent evidence of causal associations with employment factors. Data on employees with long potential induction time and many years worked were limited. Further follow-up will allow a more informative analysis of cancer incidence that might be plausibly related to workplace exposures in the cohort.

Adult↗
PubMed2005

An updated study of mortality among North American synthetic rubber industry workers.

AIM: This study evaluated the mortality experience of workers from the styrene-butadiene industry. METHODS: The authors added seven years of follow up to a previous investigation of mortality among 17 924 men employed in the North American synthetic rubber industry. Analyses used the standardised mortality ratios (SMRs) to compare styrene-butadiene rubber workers' cause specific mortality (1943-98) with those of the United States and the Ontario general populations. RESULTS: Overall, the observed/expected numbers of deaths were 6237/7242 for all causes (SMR = 86, 95% CI 84 to 88) and 1608/1741 for all cancers combined (SMR = 92, 95% CI 88 to 97), 71/61 for leukaemia, 53/53 for non-Hodgkin's lymphoma, and 26/27 for multiple myeloma. The 16% leukaemia increase was concentrated in hourly paid subjects with 20-29 years since hire and 10 or more years of employment in the industry (19/7.4, SMR = 258, 95% CI 156 to 403) and in subjects employed in polymerisation (18/8.8, SMR = 204, 95% CI 121 to 322), maintenance labour (15/7.4, SMR = 326, 95% CI 178 to 456), and laboratory operations (14/4.3, SMR = 326, 95% CI 178-546). CONCLUSION: The study found that some subgroups of synthetic rubber workers had an excess of mortality from leukaemia that was not limited to a particular form of leukaemia. Uncertainty remains about the specific agent(s) that might be responsible for the observed excesses and about the role of unidentified confounding factors. The study did not find any clear relation between employment in the industry and other forms of lymphohaematopoietic cancer. Some subgroups of subjects had more than expected deaths from colorectal and prostate cancers. These increases did not appear to be related to occupational exposure in the industry.

Aged↗
PubMed2004

Mortality and cancer incidence among alachlor manufacturing workers 1968-99.

BACKGROUND: Alachlor is the active ingredient in pre-emergent herbicide formulations that have been used widely on corn, soybeans, and other crops. It has been found to cause nasal, stomach, and thyroid tumours in rodent feeding studies at levels that are much higher than likely human exposures. AIMS: To evaluate mortality rates from 1968 to 1999 and cancer incidence rates from 1969 to 1999 for alachlor manufacturing workers at a plant in Muscatine, Iowa. METHODS: Worker mortality and cancer incidence rates were compared to corresponding rates for the Iowa state general population. Analyses addressed potential intensity and duration of exposure. RESULTS: For workers with any period of high alachlor exposure, mortality from all causes combined was lower than expected (42 observed deaths, SMR 64, 95% CI 46 to 86) and cancer mortality was slightly lower than expected (13 observed deaths, SMR 79, 95% CI 42 to 136). Cancer incidence for workers with potential high exposure was similar to that for Iowa residents, both overall (29 observed cases, SIR 123, 95% CI 82 to 177) and for workers exposed for five or more years and with at least 15 years since first exposure (eight observed cases, SIR 113, 95% CI 49 to 224). There were no cases of nasal, stomach, or thyroid cancer. CONCLUSIONS: There were no cancers of the types found in toxicology studies and no discernible relation between cancer incidence for any site and years of alachlor exposure or time since first exposure. Despite the small size of this population, the findings are important because these workers had chronic exposure potential during extended manufacturing campaigns, while use in agriculture is typically limited to a few days or weeks each year.

Acetamides↗
PubMed2004

A cross-sectional study of triallate exposure and neurological health among workers at a pesticide manufacturing and formulating facility.

AIMS: To evaluate the relation between an indicator of cumulative exposure to triallate and selected measures of neurological function, including nerve conduction, the prevalence of certain neurological deficits as determined by a medical examination, and vibration perception threshold testing in workers at a pesticide manufacturing plant. METHODS: Subjects were 50 workers with high estimated triallate exposure ("high triallate" group) and 50 workers with no or low triallate exposure ("no/low triallate" group). Industrial hygienists used existing work histories and personal knowledge of plant operations to develop a triallate score. In-person interviews elicited information on past medical history and on occupational and non-occupational exposures. A neurologist carried out nerve conduction tests of the sural and the peroneal nerves, a standardised neurological examination, and vibration sensation testing. RESULTS: Differences between the high and the no/low triallate groups were minimal for all but one of the six nerve conduction tests, for the prevalence of neurological abnormalities, and for vibration sensation perception. The high triallate group had lower mean sural nerve peak amplitude than the no/low triallate group (11.7 v 15.2 microV, p = 0.03). This difference was reduced when adjusted for other potential risk factors (12.5 v 14.5 microV, p = 0.25) and was not associated with cumulative triallate score. We also noted several associations between factors other than triallate and nerve conduction measures. CONCLUSION: The results were consistent with the absence of an association between triallate and measures of neurological function.

Adult↗
PubMed2001

Leukemia and exposure to 1,3-butadiene, styrene and dimethyldithiocarbamate among workers in the synthetic rubber industry.

This study evaluated relations between exposure to 1,3-butadiene (BD), styrene (STY) and dimethyldithiocarbamate (DMDTC) and mortality from leukemia among synthetic rubber industry workers. Subjects were 13130 men employed for at least 1 year during 1943-1991 at any of six plants that manufactured synthetic rubber. Death certificates and medical records identified workers with leukemia. Cumulative exposure estimates were based on plant- and time period-specific process and task characteristics, linked to subjects' work histories. Poisson regression estimated relative rates (RRs) for workers exposed to each agent compared to unexposed workers. Leukemia (N=59) was positively associated with BD ppm-years (RRs of 1.0, 1.2, 2.0 and 3.8, for exposures of 0, >0-<86.3, 86.3-<362.2 and 362.2+ ppm-years; only the RR for the highest exposure category was statistically significant), STY ppm-years (RRs of 1.0, 1.2, 2.3 and 3.2, for exposures of 0, >0-<20.6, 20.6-<60.4 and 60.4+ ppm-years; only the RR for the highest exposure category was statistically significant) and DMDTC mg-years/cm (RRs of 1.0, 2.3, 4.9 and 2.9, for 0, >0-<566.6, 566.6-<1395.1 and 1395.1+ mg-years/cm; the RR for each non-zero exposure category was statistically significant) after adjusting for age and years since hire. After further adjusting each agent-specific set of RRs for the other two agents, a positive but imprecise relation remained for BD and DMDTC but not for STY. The association with BD was stronger for ppm-years due to exposure intensities >100 ppm than for ppm-years due to lower concentrations. BD and DMDTC, but not STY, were positively associated with leukemia in multivariable analyses. The independent effect of each agent was difficult to evaluate because of correlations with other agents and imprecision.

Butadienes↗
PubMed2001

Mortality among employees at a petrochemical research facility.

BACKGROUND: This retrospective follow-up study evaluated mortality during 1970-1996 among 6,956 employees at a petrochemical research facility in Illinois. METHODS: Standardized mortality ratios (SMRs) compared employees' mortality rates with those of the Illinois general population. Poisson regression procedures estimated rate ratios for various subject subgroups compared to other facility employees. RESULTS: Subjects had 267 observed/524 expected deaths (SMR = 51) from all causes combined and a large deficit of deaths from all cancers (76/136, SMR = 56) and from most other major diseases. Other results included fewer than expected brain cancers (1/4.0, SMR = 25) and a slight increase in colorectal cancer (20/14, SMR = 139) that was concentrated in white male scientists employed for one of the three main companies at the facility (SMR = 295, RR = 2.6). CONCLUSIONS: The deficit of brain cancer deaths contrasts with an excess incidence seen in a companion study. Subjects' generally favorable mortality experience probably reflects socioeconomic advantages of employees relative to the Illinois general population.

Adult↗
PubMed2001

Cancer incidence among employees at a petrochemical research facility.

This investigation evaluated cancer incidence among workers at a petrochemical research facility in Illinois. A cluster of brain cancer and other intracranial tumors had occurred at the facility before the study began. The subjects were 5641 people who had worked at the facility from 1970 through 1996 and who had lived in Illinois at any time between 1986 and 1997. Data on cancer cases came primarily from the Illinois State Cancer Registry. Analyses compared the 1986-to-1997 cancer incidence rates of employees with Illinois general population rates. Subjects had 18% fewer than expected total cancers (125 observed/153 expected cases; standardized incidence ratio [SIR], 82; 95% confidence interval [CI], 68 to 98), which was primarily attributed to a large deficit of lung cancer (10/26; SIR, 39; CI, 19 to 72). Brain cancer was increased in the overall study group (6/2.7; SIR, 222; CI, 81 to 484). This excess was restricted to white men who were scientists or technicians for one of the three companies at the facility (6/0.8; SIR, 750; CI, 275 to 1633); all cases in this group had worked in the "500 building complex" (6/0.6; SIR, 968; CI, 355 to 2106). Subjects also had an increased incidence of thyroid cancer (7/2.6; SIR, 265; CI, 106 to 546) that was not concentrated in particular occupational or building groups. The brain cancer incidence patterns indicated that an unidentified occupational exposure might have been responsible for the excess. Chance, socioeconomic factors leading to better case detection in facility employees than in the general population, and confounding by potential nonoccupational risk factors are plausible explanations of the observed increase in thyroid cancer.

Adult↗
PubMed2001

Cancer and benign tumor incidence among employees in a polymers research complex.

The detection of several intracranial tumors among employees in one building complex (C500) at a petrochemical research facility prompted investigation of a possible workplace cause. This retrospective follow-up study included 1847 subjects, of whom 1735 had worked in C500. Medical records, death certificates, and Illinois State Cancer Registry data confirmed self-reported cancers and tumors. Analyses compared the subjects' cancer and benign intracranial tumor incidence rates with national general population rates. C500 employees had 15% fewer than expected total cancers (92 observed/108 expected; standardized incidence ratio [SIR], 85; 95% confidence interval [95% CI], 69 to 104). An excess of brain cancer (6/2.0; SIR, 302; 95% CI, 111 to 657) was concentrated among white men who had 10 or more years since hire and 5 or more years of C500 employment (4/0.7; SIR, 602; 95% CI, 165 to 1552) and who had worked in a particular building of C500 (5/0.7; SIR, 735; 95% CI, 239 to 1716). An excess of benign intracranial tumors (6/1.6; SIR, 385; 95% CI, 142 to 839) was not restricted to a single type of tumor and was not concentrated in any particular building. Occupational exposure may have caused the increased rate of brain cancer but is a less likely explanation for the elevated rate of benign intracranial tumors.

Adult↗
PubMed2001

Case-control study of intracranial tumors among employees at a petrochemical research facility.

This case-control study evaluated the relation between potential exposure to chemical and physical agents and the occurrence of intracranial tumors among employees at a petrochemical research facility. Cases were employees with glioma (n = 6) or benign intracranial tumors (n = 6). Controls (n = 119) were individually matched to cases on gender and birth year, and they were alive and did not have an intracranial tumor at the case's diagnosis date. Exposure information came from interviews with subjects or surrogates and from corporate records on agents used in research projects. Analyses computed matched odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for self-reported exposure to 15 agents and project-based estimates of exposure to 29 agents. For gliomas, the OR was elevated for self-reported exposure to ionizing radiation (OR, 15.7; CI, 1.4 to 179.4), n-hexane (OR, infinity; CI, 1.4 to infinity), organometallics (OR, 9.4; CI, 1.5 to 59.7), and amines other than nitrosamines (OR, 6.0; CI, 1.0 to 35.7). The OR also was elevated for project-based potential use of ionizing radiation (OR, 9.6; CI, 1.7 to 55.2) and for potential use of n-hexane lasting at least 4 years (OR, 16.2; CI, 1.1 to 227.6). For benign intracranial tumors, the OR was elevated only for self-reported exposure to ionizing radiation (OR, 5.4; CI, 1.7 to 43.1) and other amines (OR, 5.2; CI, 0.9 to 29.5). Occupational exposure may have contributed to the glioma excess, but the specific causal agents remain unknown. The study indicated that benign intracranial tumors were unlikely to be work-related.

Adult↗
PubMed2000

Motor vehicle manufacturing and prostate cancer.

BACKGROUND: The purpose of this investigation was to evaluate the relation between employment in motor vehicle manufacturing (MVM) and fatal prostate cancer. METHODS: The study included 322 prostate cancer deaths occurring in 1973 through 1987 and 1,285 controls, selected from a cohort of 126,100 male MVM workers. RESULTS: Men employed in casting operations had an odds ratio of 1.5 (95% CI = 1. 1-2.0). The association was consistent across casting facilities and was attributable primarily to work in core and mold making (OR = 1.5, 95% CI = 1.1-2.2) and metal melting and pouring jobs (OR = 1.9, 95% CI = 1.0-3.6). Other results included ORs of 1.9 (95% CI = 1.0-3.7) for warehousing and distribution operations and 2.1 (95% CI = 1.2-3. 7) for electric and electronic equipment manufacturing. The latter two associations exhibited little internal consistency. CONCLUSIONS: The relationships seen in this study were weak and may have been due to chance. Core and mold making and metal melting and pouring foundry operations entail potential exposure to metal dusts and fumes, to polycyclic aromatic hydrocarbons (PAHs), and to other chemicals. However, associations between these exposures and prostate cancer have not been reported consistently, nor have other studies of foundry workers consistently noted an excess of prostate cancer.

Adult↗
PubMed2000

Relationship between nonphenacetin combined analgesics and nephropathy: a review. Ad Hoc Committee of the International Study Group on Analgesics and Nephropathy.

BACKGROUND: The debate on the association between nonphenacetin-containing combined analgesics and renal disease has lasted for several years. METHOD: A peer review committee of scientists, selected jointly by the regulatory authorities of Germany, Switzerland, and Austria and the pharmaceutical industry was asked to critically review data on the relationship between nonphenacetin combined analgesics and nephropathy. RESULTS: The committee regarded epidemiologic evidence on nonphenacetin combined analgesics as inconclusive because of sparse information and substantial methodological problems. The committee also noted that a diagnosis of analgesic-associated nephropathy (AAN) in clinical practice usually depends on information about exposure before or in the early stages of the disease and is seldom accompanied by specific histologic evidence. The morphologic finding of papillary calcification can arise from other conditions and is not specific for AAN. For these reasons, the identification criteria for AAN should be reappraised with scientific methods to validate the diagnostic procedure. In the limited amount of experimental pharmacological data in humans and animals, the committee found no convincing evidence to confirm or refute the hypothesis that nonphenacetin combined analgesics are more nephrotoxic than single formulations. For caffeine taken with combined analgesics, the currently available information is not sufficient to postulate a harmful toxicological effect. CONCLUSION: The committee's two main conclusions were that sufficient evidence is absent to associate nonphenacetin combined analgesics with nephropathy and that new studies should be done to provide appropriate data for resolving the question.

Acetaminophen↗
PubMed2000

An updated mortality study of workers at a dye and resin manufacturing plant.

This investigation evaluated the mortality experience of workers at a dye and resin manufacturing plant in New Jersey. The retrospective follow-up study included 3266 workers employed for at least 6 months at the plant. Plant production areas were South Dyes, where anthraquinone dyes and intermediates were produced; North Dyes, where azo dyes and intermediates were produced; and plastics and additives, where various resins and additives for plastics were made. Analyses used standardized mortality ratio (SMRs) to compare the cohort's cause-specific mortality rates during 1952 to 1995 with the rates of the New Jersey population. There were fewer than expected deaths from all causes combined (728 observed vs 810 expected) and similar numbers of observed and expected cancer deaths (225 vs 232). Statistically significant work area-specific cancer excesses were limited to white men and included an excess of lung cancer in Maintenance workers (40 observed vs 26 expected; SMR, 153; 95% confidence interval [CI], 109 to 208) and in South Dyes workers (32 observed vs 19 expected; SMR, 168; CI, 115 to 237) and an excess of stomach cancer (5 observed vs 1.3 expected; SMR, 386; CI, 125 to 901), bladder cancer (4 observed vs 0.8 expected; SMR, 515; CI, 140 to 1318) and central nervous system cancer (5 observed vs 1 expected; SMR, 517; CI, 168 to 1206) in North Dyes workers. None of these increases was concentrated in work area subgroups with long duration of employment and long potential induction time. It was concluded that the excess of bladder cancer probably was due to exposure to carcinogenic arylamines at another facility, where some employees had worked before coming to the study plant. The other cancer increases may be attributable to chance, to uncontrolled confounding by smoking, or to an unidentified occupational exposure.

Cause of Death↗
PubMed1999

Case-series investigation of intracranial neoplasms at a petrochemical research facility.

BACKGROUND: From 1970 through 1997, 17 intracranial neoplasms were identified among 6,800 employees of a petrochemical research facility. This investigation describes the case-series. METHODS: The intracranial neoplasms were identified by self reports and record linkages, and were confirmed by medical records and a pathology review. Standardized incidence ratios (SIRs) compare observed and expected numbers of cases according to certain work characteristics. RESULTS: Overall, there were 17 observed and 10.5 expected intracranial neoplasms, including 11/4.7 benign intracranial tumors and 6/5.9 brain cancers. All brain cancers occurred among male research scientists or technicians. Four had worked at some time on the same floor of one building (SIR=12.6, 95% CI=3.4-32.1), and several had worked on a research project with at least one other brain cancer case. The benign intracranial neoplasm cases did not have common building assignments or work activities. CONCLUSIONS: The occurrence pattern of brain cancers, but not that of benign tumors, suggests a possible occupational etiology.

Adenoma↗
PubMed1998

A review of epidemiologic studies of nonnarcotic analgesics and chronic renal disease.

The relationship of long-term and heavy exposure of nonnarcotic analgesics to the risk of chronic renal disease (CRD) has been the object of intensive clinical, pharmacologic, toxicologic, and epidemiologic research for 4 decades. The clinical evidence of an increased risk has been suggestive but inconclusive. The experimental evidence in animal models has been inconsistent, and in any case it cannot be generalized to humans. The epidemiologic evidence has been unsatisfactory for the most part: most of the early studies had severe methodologic limitations; moreover, they related mainly to phenacetin-containing drugs and did not have useful information on other analgesics. Since 1980, 9 analytical epidemiologic studies have attempted to confirm that a causal relationship exists between phenacetin or other analgesics and CRD. In the aggregate, despite methodologic flaws, this work suggests that excessive use of phenacetin-containing analgesics probably causes renal papillary necrosis and interstitial nephritis. In contrast, there is no convincing epidemiologic evidence that nonphenacetin-containing analgesics (including acetaminophen, aspirin, and mixtures of these two compounds) or that nonsteroidal antiinflammatory drugs cause CRD. Moreover, the nature of dose-response relationships, the types of renal disease possibly caused by analgesics, and the cofactors that might be related both to analgesic use and to the development of CRD in humans are still uncertain, and the pathologic mechanisms of analgesic-induced CRD in humans remain unclear. It may take many years before all the outstanding issues are settled. Until they are, as a matter of good clinical judgment it would be prudent to consider all analgesics as potentially nephrotoxic and, as much as possible, to avoid excessive, protracted use.

Adult↗
PubMed1998

Using the National Death Index to obtain underlying cause of death codes.

This study evaluated the comparability of underlying cause of death codes obtained from NDI Plus, a new feature of the National Death Index (NDI), with codes assigned by two study nosologists or by a National Center for Health Statistics (NCHS) nosologist. Two study nosologists and an NCHS nosologist independently reviewed the death certificates of 493 decedents and assigned each an International Classification of Diseases code for the underlying cause of death. Using the NCHS codes as the reference standard, we determined discrepancy rates for NDI Plus codes; for each study nosologist's original codes; and for "final study codes," derived by comparing the two sets of study nosologists' codes and resolving discrepancies by using the NCHS code. For all causes of death combined, the discrepancy rate was 4% for NDI Plus codes, 4% for the final study codes and 6%-7% for the study nosologists' original codes. The discrepancy rate for selecting the appropriate cancer site was 1% for NDI Plus codes and 3% for the final study codes. For noncancer conditions, the discrepancy rate was 5% for NDI Plus codes and 4% for the final study codes. NDI Plus underlying cause of death codes are comparable to codes developed using standard but more cumbersome procedures. The use of NDI Plus codes may enhance the validity of comparisons of an occupational cohort's mortality rates with national or state rates.

Cause of Death↗