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Epidemiologic Study to Determine Possible Adverse Effects to Rocketdyne/Atomics International Workers from Exposure to Selected Chemicals

<-- LA Rocketdyne Nuclear Meltdown

Download: UCLA Addendum Report (PDF)

To the Public Health Institute
(Formerly the California Public Health Foundation)
Berkeley, California

Subcontract No. 324A-8701-S0163
Epidemiologic Study to Determine Possible Adverse Effects
to Rocketdyne/Atomics International Workers
from Exposure to Selected Chemicals

January 1999


Principal Investigator Hal Morgenstern, Ph.D.
Professor of Epidemiology
UCLA School of Public Health

Co-Principal Investigator John Froines, Ph.D.
Professor of Toxicology
UCLA School of Public Health

Co-Investigator & Study Coordinator Beate Ritz, M.D., Ph.D.
Assistant Professor of Epidemiology
UCLA School of Public Health

Co-Investigator Bambi Young, Ph.D., M.P.H.
Assistant Researcher
UCLA School of Public Health


Background and Objective. In the early 1990s, a worker health study was initiated in response to strong concerns voiced by area residents about the use of radioactive and toxic chemical substances at the Santa Susana Field Laboratory (SSFL) of Rocketdyne/Atomics International (AI), a division of Boeing North American (formerly Rockwell International). The effects of radiation exposures on cancer mortality were described in our previous report (dated May 1997 and released on September 11, 1997). In this addendum report, we describe the results of selected chemical effects on cancer mortality.

We determined that between 1955 and 1993, especially before 1980, many workers in the areas of rocket-engine testing were probably exposed to monomethyl hydrazine and other hydrazine compounds (referred to collectively as hydrazine throughout this report), kerosene fuels, trichloroethylene (TCE), asbestos, and other chemicals. Some radiation-monitored workers at the SSFL were exposed to asbestos, beryllium, and various solvents. Because we did not have enough information or resources to measure most of these chemical exposures, we restricted our attention to two chemicals--hydrazine and asbestos--for which proxy measures of exposure could be developed from available information. To examine the hypothesized effects of these exposures on cancer mortality, we conducted a retrospective cohort study in two separate groups employed at the SSFL. We examined whether workers presumptively exposed to hydrazine during rocket-engine testing experienced an increased rate of dying from lung cancer and other types of cancer that have been previously linked with toxic chemicals. In addition, we examined the possible effect of presumptive exposure to asbestos on lung-cancer mortality.

Methods. The hydrazine analyses included 6,107 men who were employed before 1980 at the SSFL, who worked at least two years at any Rockwell facility, and who were never monitored for radiation exposure at Rocketdyne/AI. The asbestos analyses included 4,563 men and women who were monitored for external radiation (the externally monitored cohort in our previous report). We used job-title and job-code information abstracted from personnel records to categorize the probability of exposure to hydrazine and asbestos. Workers were assigned to four categories of probable hydrazine exposure (high, medium, low, and unexposed), using two separate criteria for defining the three exposed categories--a minimum of 6 or 24 months in selected jobs. A similar method was used to measure asbestos exposure, but categorization was based on the 6-month criterion only.

All effects in this report were estimated by applying conditional logistic regression analysis to cancer deaths and their risk sets of survivors (as in the previous report). Hydrazine effects were estimated for several outcomes: death from lung cancer, all hemato- and lymphopoietic cancers, bladder and kidney cancers, upper-aerodigestive-tract cancers (oral cavity, pharynx, larynx, and esophagus), pancreatic cancer, and emphysema. Asbestos effects were estimated for lung-cancer mortality. Estimated effects were expressed as rate ratios (and 95% confidence intervals [CI]), comparing each exposed category with the unexposed group, and were adjusted for three potential confounders: age, pay type (a proxy for socioeconomic status), and time since hire or transfer to SSFL. Since the asbestos effect was estimated in the cohort monitored for radiation, we also adjusted this effect for cumulative doses of external and internal radiation. In addition, we examined the associations between smoking status and both exposure variables in subsets of subjects for whom smoking information was available. Chemical exposures were treated as time-dependent covariates and were lagged by zero, 10, and 15 years in the prediction models.

Results. The estimated rate ratio for lung-cancer mortality, comparing high versus no hydrazine exposure, ranged from 1.68 (95% CI = 1.12, 2.52) to 2.10 (95% CI = 1.36, 3.25), depending on the minimum criterion for defining exposure (6 or 24 months) and the lag for measuring exposure (0-15 years). No excess rates were observed for subjects in the medium- or low-exposure groups. The analysis of high exposure to hydrazine by decade suggested that this observed effect was limited primarily to exposure received during the 1960s. Similar results were obtained for hemato- and lymphopoietic-cancer mortality and for bladder- and kidney-cancer mortality, comparing high versus no hydrazine exposure, but these estimates are rather imprecise (all 95% CIs are wide and include one). No association was observed between hydrazine exposure and mortality from other smoking-related diseases or between hydrazine exposure and smoking in a subset of subjects. In addition, we found no association between asbestos exposure and lung-cancer mortality among radiation-monitored workers.

Discussion. We observed positive associations between our proxy measure of hydrazine exposure and the rates of dying from cancers of the lung, blood and lymph system, and bladder and kidney. The mortality rates for these cancers were approximately twice as great among workers classified in the high-exposure group as they were among workers classified in the unexposed group. Nevertheless, consistent effects were not observed for medium-exposure levels, except for cancer of the blood and lymph system. Although the lung-cancer results are consistent with those of animal studies, there are four methodologic problems that limit causal inference. First, effect estimation was relatively imprecise for most cancer outcomes, due to the small numbers of cancer deaths in the exposed categories. Thus, most of the 95% confidence intervals (around estimated rate ratios) were wide and included the null value (one) for all outcomes except lung cancer. Second, exposure classifications were based entirely on job titles not quantitative doses. Thus, there was certainly exposure misclassification, which could have biased the results. Since, we have no reason to believe, however, that this misclassification was differential with respect to cancer outcome, we would expect the bias to be toward the null value. Such misclassification, therefore, might explain the negative findings for asbestos and lung cancer, but it implies that our hydrazine effects might be underestimated. Third, our effect estimates might be confounded by risk factors that were not included in the analyses, such as smoking and occupational exposures to other chemicals. We do not believe that confounding by smoking was appreciable because we observed little association between smoking status and hydrazine exposure in a subset of workers and because an effect of hydrazine was not observed for all smoking-related diseases. Nevertheless, we cannot rule out confounding by other chemical carcinogens, such as TCE, to which many subjects were likely exposed, including workers in the same jobs that were classified as probably involving exposure to hydrazine. Fourth, all outcome variables in this study were based on mortality, not cancer incidence. Thus, the findings reported here might not be an accurate reflection of risk-factor effects, especially for nonfatal cancers.

In conclusion, the results of this study suggest that occupational exposure to hydrazine and/or other chemicals associated with the same rocket-engine-testing jobs increased the risk of dying from lung cancer, and possibly other cancers, in this population of aerospace workers; however, causal inference is limited and our results need to be replicated in other populations. We recommend that the follow-up of our study cohorts be continued for the detection of both cancer mortality and incidence.

Download: UCLA Addendum Report (PDF)

<-- LA Rocketdyne Nuclear Meltdown

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