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Elizabeth Delzell

Publications and source records attributed to Elizabeth Delzell.

At least 19 recordsLinked to original sources
PubMed2006

A follow-up study of women in the synthetic rubber industry: study methods.

BACKGROUND: Concerns about the possible toxic effects of workplace exposures in the synthetic rubber industry have centered on 1,3-butadiene (BD), styrene and dimethyldithiocarbamate (DMDTC). Our previous mortality studies of over 17,000 male synthetic rubber workers found an excess of leukemia that may be due to BD or BD plus other chemicals. Experimental studies have shown that BD produces mammary tumors in female mice and rats and ovarian tumors in female mice. AIM: This paper presents the methods of a follow-up study that evaluates the mortality experience of women employed in the North American synthetic rubber industry. METHODS: Women employed for at least 1 day at any of eight North American styrene-butadiene rubber plants were followed up from 1943 to 2002. Identifying and work history information were obtained from personnel records. Estimated quantitative exposure to BD, styrene and DMDTC, developed for our previous study of men, were used in this study. External analyses use the standardized mortality ratios (SMRs) to compare the cohort's cause-specific mortality rates to the rates of the female general population of the states or the province where the plants are located. Internal analyses use the Poisson regression and Cox proportional hazards models to examine specific cancer mortality rates in relation to BD, styrene and DMDTC exposure, by comparing an exposed cohort subgroup with the rate of unexposed cohort members.

Animals↗
PubMed2006

1,3-Butadiene and leukemia among synthetic rubber industry workers: exposure-response relationships.

Previous research updated the mortality experience of North American synthetic rubber industry workers during the period 1944-1998, determined if leukemia and other cancers were associated with several employment factors and carried out Poisson regression analysis to examine exposure-response associations between estimated exposure to 1,3-butadiene (BD) or other chemicals and cancer. The present study used Cox regression procedures to examine further the exposure-response relationship between several unlagged and lagged, continuous, time-dependent BD exposure indices (BD parts per million (ppm)-years, the total number of exposures to BD concentrations >100 ppm ("peaks") and average intensity of BD) and leukemia, lymphoid neoplasms and myeloid neoplasms. All three BD exposure indices were associated positively with leukemia. Using continuous, untransformed BD ppm-years the regression coefficient (beta) from an analysis that controlled only for age was 2.9 x 10(-4) (p<0.01); the regression coefficient adjusted for all covariates (age, year of birth, race, plant, years since hire and dimethyldithiocarbamate) was similar in magnitude (beta=3.0 x 10(-4), p=0.04). Lagging exposure had minimal impact on the results for leukemia for any of the three BD exposure indices. In models that controlled only for age, lymphoid neoplasms were associated with BD ppm-years and myeloid neoplasms, with BD peaks, but neither trend was statistically significant after adjusting for multiple covariates. The present results support the presence of a causal relationship between high cumulative exposure and high intensity of exposure to BD and leukemia.

Butadienes↗
PubMed2006

Validation of 1,3-butadiene exposure estimates for workers at a synthetic rubber plant.

PURPOSE: This investigation assessed the validity of estimates of exposure to 1,3-butadiene (BD) developed for a plant included in a study of mortality among synthetic rubber industry workers. The estimates were developed without using historical measurement data and have not been validated previously. METHODS: Personal BD measurements came from an exposure-monitoring program initiated in 1977. For each job, we computed the year-specific difference between the BD estimate and the mean of BD measurements. We also computed rank correlation coefficients and calculated the mean, across all measurements, of the difference between the estimate and the measurement. RESULTS: The mean BD concentration was 5.2 ppm for 4978 measurements and 4.7 ppm for the corresponding estimates. The mean difference between estimates and measurements was -0.50 ppm (standard deviation, 26.5 ppm) overall and ranged from -227.9 to +27.0 ppm among all 306 job/year combinations. Estimates were correlated with measurements for all 306 combinations (rank correlation coefficient, r=0.45, p<0.0001), for 82 combinations pertaining to jobs that were well-defined by a specific set of tasks and typically found in styrene-BD rubber (SBR) plants (r=0.81, p<0.0001), for 70 combinations pertaining to jobs that were well-defined but not typical (r=0.29, p=0.01) and for 92 combinations pertaining to poorly-defined jobs typically found in SBR plants (r=0.56, <0.0001). Estimates were not correlated with measurements for poorly defined jobs not typically found in SBR plants (r=0.01, p=0.93). For well-defined typical SBR jobs with measurement means that were over 7.0 ppm, estimates were consistently lower than measurements. CONCLUSIONS: Possible reasons for differences between estimates and measurements included faulty assumptions used in developing BD estimates, unstable or nonrepresentive measurements and errors in linking measurement data to the job-exposure matrix. Exposure misclassification may have been more severe for subjects from the validation study plant than for subjects from other plants in the mortality study. BD estimates for typical SBR jobs, which comprise most operations at all but one of the plants in the mortality study, appeared to be useful for ranking workers by cumulative exposure. Uncertainty analyses would enhance the utility of the BD exposure estimates for quantitative risk assessment.

Butadienes↗
PubMed2006

Cancer risk assessment for 1,3-butadiene: dose-response modeling from an epidemiological perspective.

The dose-response assessment of the association between 1,3-butadiene (BD) and leukemia mortality among workers in the North American synthetic rubber industry is explored. Analyses are based on the most recent University of Alabama at Birmingham epidemiological study and exposure estimation. The U.S. EPA Science Advisory Board recommendations of using the most recent data and giving consideration to peak exposures to BD have been followed. If cumulative BD ppm-years is to be used as the predictor of the leukemia rate ratio, then the performance of that predictor is statistically significantly improved if the slope in the predictor is estimated with age and the cumulative number of BD peaks (where a BD peak is any exposure, regardless of duration, to a BD concentration above 100 ppm) added as categorical covariates. After age and the cumulative number of BD peaks are incorporated as categorical covariates in the Poisson regression model, the estimated concentration (EC(001)) corresponding to an excess risk of 0.001 as a result of continuous environmental exposure is 11.2 ppm; however, the estimated slope for BD cumulative ppm-years in the linear rate ratio for leukemia used to derive this EC(001) is not statistically significantly different from zero. Sensitivity analyses using alternative models indicate either essentially no risk or estimated EC(001) values of 9 and 77 ppm. Analyses suggesting the absence of a statistically significant low-dose risk versus cumulative BD ppm-years are presented. Sensitivity analyses of other malignant neoplasms of lymphatic and hematopoietic tissue (specifically, lymphoid and myeloid neoplasms) resulted in conclusions about the dose-response modeling methodology that were supportive of the methodology used for leukemia.

Aging↗
PubMed2006

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.

Aged↗
PubMed2005

Methodologic issues in follow-up studies of cancer incidence among occupational groups in the United States.

PURPOSE: Incidence studies of occupational factors and cancer in the United States are problematic because the use of population-based registries to identify cases requires development of historical data on subjects' residences and often severely restricts the time period of follow up. This article describes procedures for addressing these challenges. METHODS: We used data from studies of cancer incidence and mortality among microelectronics industry employees to assess various methods for developing residential histories and the relative informativeness of the two studies. RESULTS: We developed residential histories for 98% of 99,229 mortality study subjects. Analyses making alternative assumptions about residential histories yielded standardized incidence ratios varying by at most 6%. Use of postemployment residential histories increased person-years by up to 62% and increased the observed number of cancers by up to 28%. The proportion of mortality study person-years included in the cancer incidence study ranged from 40% to 77% among work activity subcohorts. The number of observed cancer cases in the incidence study was 60% higher than the number of observed cancer deaths in the mortality study. CONCLUSIONS: Assumptions about residential history had little impact on validity. Use of information sources with national coverage to develop residential histories increased the incidence study's precision. Despite geographic and temporal restrictions, incidence studies provide more data than mortality studies on cancers with good survival. However, the potential for selection bias in incidence studies may vary considerably among subcohorts, indicating the need for cautious interpretation of such research.

Adult↗
PubMed2005

Chemical exposures in the synthetic rubber industry and lymphohematopoietic cancer mortality.

OBJECTIVE: This study evaluated the association between exposure to several chemicals and mortality from lymphohematopoietic cancer (LHC) among 16,579 synthetic rubber industry workers who were followed up from 1943 to 1998. METHODS: Poisson regression analyses examined LHC rates in relation to butadiene, styrene, and DMDTC exposure. Models provided maximum likelihood estimates of the relative rate for the contrast between categories of one agent, adjusting for other agents and for additional potential confounders. RESULTS: Cumulative exposure to 1,3-butadiene was associated positively with all leukemia (relative rates of 1.0, 1.4, 1.2, 2.9, and 3.7, respectively, for exposures of 0, >0 to <33.7, 33.7 to <184.7, 184.7 to <425.0, and 425.0+ ppm-years), chronic myelogenous leukemia and to a lesser extent with chronic lymphocytic leukemia. Adjusting for styrene and DMDTC attenuated these associations. After controlling for butadiene, neither styrene nor DMDTC displayed a consistent exposure-response trend with all leukemia, chronic myelogenous leukemia, or chronic lymphocytic leukemia. CONCLUSIONS: This study found a positive association between butadiene and leukemia that was not explained by exposure to other agents examined.

Adult↗
PubMed2005

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.

Computer Storage Devices↗
PubMed2005

Styrene and ischemic heart disease mortality among synthetic rubber industry workers.

OBJECTIVE: We examined the relation between styrene and ischemic heart disease (IHD) mortality among 16,579 men in the synthetic rubber industry. METHODS: Associations were measured using stratified and multivariable analysis. RESULTS: Compared with workers with no exposure to styrene, men in the highest quintile of average intensity of exposure (5.50+ parts per million [ppm]) and in the highest quintile of cumulative exposure (60.67+ ppm-years) had IHD rate ratios of 1.14 (95% confidence interval [CI]=0.96-1.35) and 1.07 (95% CI=0.90-1.27), respectively. Acute IHD was not associated with average intensity of exposure within the most recent 2 years or with other indices of exposure. Chronic IHD rates were elevated in subjects with the highest exposure; these associations were weak and imprecise, and evidence of a positive exposure-response relation was limited. CONCLUSION: This study does not indicate that exposure to styrene causes fatal IHD.

Adult↗
PubMed2005

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.

Adult↗
PubMed2005

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.

Adult↗
PubMed2004

Historical estimation of exposure to 1,3-butadiene, styrene, and dimethyldithiocarbamate among synthetic rubber workers.

Quantitative estimates of exposure to 1,3-butadiene (BD), styrene (STY), and dimethyldithiocarbamate (DMDTC) were developed for a follow-up study of workers at six North American synthetic rubber plants. Procedures entailed identifying tasks and jobs involving exposure, identifying factors influencing historical changes in exposure potential, and using mathematical models to calculate job- and time-period-specific exposures. Exposure metrics included 8-hour time-weighted average (TWA) intensity, the annual number of peak exposures (BD: >100 ppm, STY: >50 ppm) and TWA intensity below and above the peak threshold. The 5th and 95th percentiles of the approximate probability distribution of each exposure estimate served as its 90% uncertainty interval. Job- and year-specific estimates were linked with subjects' work histories to obtain cumulative exposure indices. Exposure estimates varied among tasks, jobs, plants, and time periods. BD TWAs were approximately 10 ppm during the 1940s-1960s and declined during the 1970s and 1980s. STY TWAs were always <2 ppm. DMDTC exposure began in the 1950s, was high through the 1960s, and later declined. BD peak exposure accounted for a large proportion of cumulative BD exposure, whereas almost none of the STY exposure was experienced at levels >50 ppm. Exposure indices were correlated. Exposures were higher than previously estimated. Multiple correlations among DMDTC, BD, and STY exposure estimates make it difficult to estimate agent-specific effects. Limitations of the methodology include the potential inaccuracy of the estimates, the lack of adequate industrial hygiene data to validate the estimates, the additional inaccuracy of linkage with poorly specified job groups, and the potential for differential exposure misclassification because the jobs and work areas where excess leukemia mortality occurred were well-known at the time of this study. Nevertheless, the new exposure estimates were highly correlated with the old, yielding equivalent exposure ranking of workers and were comparable to limited industrial hygiene data published by NIOSH.

Butadienes↗
PubMed2003

Occupational exposure to glycol ethers and human congenital malformations.

OBJECTIVES: This commentary reviews toxicological information and critically evaluates epidemiological information on the relationship between glycol ethers and congenital malformations. METHODS: The authors identified and assessed toxicological and epidemiological research on glycol ethers used in occupational settings and congenital malformations. Sensitivity analyses evaluated the possible role of methodological problems in explaining the findings of the epidemiological studies. RESULTS: Exposure to certain glycol ethers, including ethylene glycol monomethyl ether and ethylene glycol mono-ethyl ether, throughout the period of major organogenesis, has induced malformations of many organ systems in some of the animal models studied. Other glycol ethers, including ethylene glycol butyl and propyl ethers and most propylene glycol ethers, have not induced fetal malformations in the animal models studied. Four epidemiological studies have assessed the relationship between occupational exposure to glycol ethers and congenital malformations in humans. One study was uninformative because of small numbers, two found a positive association between glycol ethers and malformations of a number of different organs, and one found no association with neural-tube defects. Sensitivity analyses indicated that the results of the latter three investigations could be due to methodological problems. The positive studies, further, lack biological plausibility, in that the glycol ethers to which the subjects were exposed have not been, for the most part, teratogenic in the animal models that have been studied. CONCLUSIONS: The current evidence is insufficient for one to determine whether occupational exposure to glycol ethers causes human congenital malformations. We suggest that future studies quantify the effect of methodological problems on study results, using methods such as validation studies and sensitivity analysis.

Abnormalities, Drug-Induced↗
PubMed2003

Mortality among triazine herbicide manufacturing workers.

Atrazine produces mammary gland cancer in one strain of rats and has been classified as an endocrine modulator. Epidemiologic studies have reported associations between agricultural use of atrazine and several forms of cancer. This study evaluated mortality patterns among workers at a plant that made atrazine and other triazine herbicides. The study covered the time period 1970-1997 and included 2213 people employed for at least 6 mo in operations related to the manufacture or formulation of atrazine and other triazine herbicides at a plant in Louisiana (LA). Vital status was determined for all but six subjects. Standardized mortality ratios (SMRs) with 95% confidence intervals (CIs) compared employees' mortality rates with those of the LA industrial corridor general population. Subjects had a total of 32,473 person-years of observation and a median of 15.8 yr since hire. There were 84 observed/118 expected deaths from all causes combined (SMR = 72, CI = 57-89) and 22/21 total cancer deaths (SMR = 106, CI = 66-160). Subjects had 4/1.1 deaths from non-Hodgkin's lymphoma (SMR = 372, CI = 101-952); this increase was not concentrated in the subgroup with long duration of employment and many years since hire. There were 6/4.8 (SMR = 124, CI = 46-271) digestive cancer and 7/6.3 (SMR = 112, CI = 45-230) lung cancer deaths. Data on other forms of cancer were sparse. This study was limited by its small size, by the relatively young age and short follow-up of its subjects, and by the lack of exposure data. It did not provide evidence that employment in triazine herbicide manufacturing and formulating operations was associated causally with overall or cause-specific mortality.

Adult↗
PubMed2003

Mortality among hourly motor vehicle manufacturing workers.

We evaluated mortality among 198,245 motor vehicle industry workers during the period of 1973 to 1995. Workers' mortality rates were lower than expected overall (40,131 observed/43,859 expected deaths, standardized mortality ratio [SMR] = 92, CI = 91-92) and for all major cause of death categories except cancer (SMR = 100, CI = 98-102). Mortality rates were higher than expected for lung cancer overall (SMR = 110, CI = 107-113) and among employees in transmission/gear manufacturing (SMR = 121, CI = 112-130), casting operations (SMR = 122, CI = 110-135), engine manufacturing (SMR = 111, CI = 101-123), and vehicle assembly (SMR = 111, CI = 105-117); for stomach cancer in engine manufacturing (SMR = 147, CI = 110-192); and for prostate cancer in casting operations (SMR = 128, CI = 102-158). Excesses of lung cancer in transmission, vehicle assembly, and casting operations and of stomach cancer in engine manufacturing have been observed in other investigations. Further information on employees' occupational exposures and personal attributes is required to clarify the interpretation of these results.

Accidents, Occupational↗
PubMed2002

Mortality among workers at a talc mining and milling facility.

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

Dust↗
PubMed2002

Assessment of historical exposures to talc at a mining and milling facility.

The purpose of this study was to develop an estimate of exposure to respirable dust for all job categories and all years in a retrospective follow-up study of worker mortality in a talc mining and milling facility. All jobs were assigned to work areas that were considered to have similar exposure profiles. Uniform exposure time periods during which non-random, deterministic variables were thought to be constant were identified and an experienced rater assigned categorical exposure scores to each work area/time period. These scores and measured baseline respirable dust concentrations were used to calculate the estimated job area/year concentrations for each work area/time period. Estimates were compared to available historical measurements. The estimated exposures ranged from 1.7 to 0.1 mg/m(3) and displayed a decreasing trend over time. When compared with measured exposures, the estimated exposures had a correlation coefficient of 0.55 with an average difference of 0.01 mg/m(3) and a range of 0.60 to -0.48 mg/m(3). The estimates were considered to be acceptable for determining relative ranking of subjects according to cumulative exposure.

Follow-Up Studies↗