Colleen Beall

Mortality among semiconductor and storage device-manufacturing workers.

Problem: We evaluated mortality during 1965 to 1999 among 126,836 workers at two semiconductor facilities and one storage device facility. Method: We compared employees’ cause-specific mortality rates with general population rates and examined mortality patterns by facility, duration of employment, time since first employment, and work activity. Results: Employees had lower-than-expected mortality overall (6579 observed deaths, standardized mortality ratio [SMR] = 65; 95% confidence interval [CI] = 64–67), for all cancers combined (2159 observed, SMR = 78, 95% CI = 75–81) and for other major diseases. Central nervous system cancer was associated with process equipment maintenance at one of the semiconductor facilities (10 observed, SMR = 247, 95% CI = 118–454). Prostate cancer was associated with facilities/laboratories at the storage device facility (18 observed, SMR = 198, (5% CI = 117–313). Conclusions: Further evaluation of workplace exposures or independent investigations of similar occupational groups may clarify the interpretation of associations observed in this study

Brain tumors among electronics industry workers.

We evaluated the relation between work experience in the United States operations of an electronics company and brain tumor mortality, focusing on video display terminal (VDT) development jobs. Subjects were 149 brain tumor cases and 591 matched controls selected from a company registry of all employees dying between 1975 and 1989. Company databases and interviews with company personnel constituted the basis for work histories, including information on whether subjects had held VDT development jobs. Subjects who worked at plants with hardware or VDT development operations had slightly but imprecisely elevated odds ratios (OR). The study found no meaningful association between VDT development work and brain tumor mortality. Other results included an elevated OR for 10 or more years of employment in engineering/technical jobs [OR = 1.7; 95% confidence interval (CI) = 1.0–3.0] or in programming jobs (OR = 2.8; 95% CI = 1.1–7.0). The OR for glioma for all subjects who had accrued 5 years of programming work 10 years before the cases death was 3.9 (95% CI = 1.2–12.4). These associations were limited in large part to one of four division groups. Also, only male programmers experienced an elevated OR. These patterns indicate that the associations may be due to chance, although unidentified causal exposures present in a subset of engineering/technical and programming jobs cannot be ruled out.

Exposure Reconstruction for the TCDD-Exposed NIOSH Cohort Using a Concentration- and Age-Dependent Model of Elimination

Recent studies demonstrating a concentration dependence of elimination of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suggest that previous estimates of exposure for occupationally exposed cohorts may have underestimated actual exposure, resulting in a potential overestimate of the carcinogenic potency of TCDD in humans based on the mortality data for these cohorts. Using a database on U.S. chemical manufacturing workers potentially exposed to TCDD compiled by the National Institute for Occupational Safety and Health (NIOSH), we evaluated the impact of using a concentration- and age-dependent elimination model (CADM) (Aylward et al., 2005) on estimates of serum lipid area under the curve (AUC) for the NIOSH cohort. These data were used previously by Steenland et al. (2001) in combination with a first-order elimination model with an 8.7-year half-life to estimate cumulative serum lipid concentration (equivalent to AUC) for these workers for use in cancer dose-response assessment. Serum lipid TCDD measurements taken in 1988 for a subset of the cohort were combined with the NIOSH job exposure matrix and work histories to estimate dose rates per unit of exposure score. We evaluated the effect of choices in regression model (regression on untransformed vs. ln-transformed data and inclusion of a nonzero regression intercept) as well as the impact of choices of elimination models and parameters on estimated AUCs for the cohort. Central estimates for dose rate parameters derived from the serum-sampled subcohort were applied with the elimination models to time-specific exposure scores for the entire cohort to generate AUC estimates for all cohort members. Use of the CADM resulted in improved model fits to the serum sampling data compared to the first-order models. Dose rates varied by a factor of 50 among different combinations of elimination model, parameter sets, and regression models. Use of a CADM results in increases of up to five-fold in AUC estimates for the more highly exposed members of the cohort compared to estimates obtained using the first-order model with 8.7-year half-life. This degree of variation in the AUC estimates for this cohort would affect substantially the cancer potency estimates derived from the mortality data from this cohort. Such variability and uncertainty in the reconstructed serum lipid AUC estimates for this cohort, depending on elimination model, parameter set, and regression model, have not been described previously and are critical components in evaluating the dose-response data from the occupationally exposed populations.

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 ≥15 years since hiring and ≥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.

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.

TCDD exposure-response analysis and risk assessment

We examined the relation between cancer mortality and time-dependent cumulative exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) estimated from a concentration- and age-dependent kinetic model of elimination, and we estimated incremental cancer risks at age 75. Data from the National Institute for Occupational Safety and Health study of 3,538 workers with occupational exposure to TCDD were analyzed using standardized mortality ratios and Cox regression procedures. Analyses adjusted for potential confounding by age, year of birth, and race and considered exposure lag periods of 0, 10, or 15 years. Other potential confounders including smoking and other occupational exposures were evaluated indirectly. To explore the influence of extreme values of cumulative TCDD ppt-years, we restricted the analysis to observations with exposure below the 95th percentile or used logarithmic (ln) transformed exposure values. We applied penalized smoothing splines to examine variation in the exposure-response relation across the exposure range. TCDD was not statistically significantly associated with cancer mortality using the full data set, regardless of the lag period. When we restricted the analysis to observations with exposure below the 95th percentile, TCDD was associated positively with cancer mortality, particularly when a 15-year lag was applied (untransformed exposure data: regression coefficient , standard error (s.e.) = 1.4 x 10(-6), p < 0.05; ln-transformed exposure data: , s.e. = 2.9 x 10(-2), p < 0.05). The estimated incremental lifetime risk of mortality at age 75 from all cancers was about 6 to more than 10 times lower than previous estimates derived from this cohort using exposure models that did not consider the age and concentration dependence of TCDD elimination.

Exposure assessment for retrospective follow-up studies of semiconductor- and storage device-manufacturing workers.

Objective: This exposure assessment was conducted in the first large study of mortality and cancer incidence in semiconductor and storage device manufacturing. Methods: Unique combinations of division, department and job codes and names (DDJ) from work history records were assigned to work groups and exposure categories. Agent exposure matrices assessed differences in potential exposures between groups. Changes in exposure over time were tracked by dividing the production history into manufacturing eras. Results: Nineteen work groups were developed to capture 310,351 unique DDJs from 1965–1999. Agent exposure matrices contrasted exposure potential to solvents, metals, and work in cleanrooms between groups, and three manufacturing eras were identified for each site. Conclusions: The work groups, manufacturing eras and agent matrices have been used to classify workers in the study of cancer incidence and mortality.

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.

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.

Cancer mortality among women employed in motor vehicle manufacturing

This article summarizes published data on employment and cancer patterns in the motor vehicle manufacturing (MVM) industry and presents results from a new study of female MVM workers. Historically, female MVM employees worked primarily in aerospace; electric and electronic equipment manufacturing; and paint, plastic, and trim operations. Women are now moving into vehicle assembly and metal parts production. Investigations of cancer have focused on men and reported excesses of lung cancer in foundry operations, of gastrointestinal cancer in metal processing operations involving exposure to machining fluids, and of colorectal cancer in wood pattern making. Numbers of women were insufficient for a meaningful evaluation of their cancer patterns. A recent study found that white women employed at a MVM company, compared to the female general US population, had small excesses of lung cancer (standardized mortality ratio (SMR) = 1.26; 95% confidence interval (CI) = 0.96-1.63) and of colorectal cancer (SMR = 1.27, 95% CI = 0.87-1.78) and a deficit of breast cancer (SMR = 0.68, 95% CI = 0.48-0.92). The lung cancer increase was concentrated among women in assembly jobs (SMR = 1.58, 95% CI = 1.07-2.26); the colorectal cancer increase, among women in nonproduction jobs (SMR = 1.78, 95% CI = 0.97-2.98); and the breast cancer deficit, among women in production-related jobs (SMR = 0.60, 95% CI = 0.37-0.91). Further investigation is needed to determine if these patterns are due to the occupational environment and to clarify causes of cancer among women in the MVM industry.