Characterization of size-specific particulate matter emission rates for a simulated medical laser procedure--a pilot study.

Prior investigation on medical laser interaction with tissue has suggested device operational parameter settings influence laser generated air contaminant emission, but this has not been systematically explored. A laboratory-based simulated medical laser procedure was designed and pilot tested to determine the effect of laser operational parameters on the size-specific mass emission rate of laser generated particulate matter. Porcine tissue was lased in an emission chamber using two medical laser systems (CO2, λ = 10,600 nm; Ho:YAG, λ = 2100 nm) in a fractional factorial study design by varying three operational parameters (beam diameter, pulse repetition frequency, and power) between two levels (high and low) and the resultant plume was measured using two real-time size-selective particle counters. Particle count concentrations were converted to mass emission rates before an analysis of variance was used to determine the influence of operational parameter settings on size-specific mass emission rate. Particle shape and diameter were described for a limited number of samples by collecting particles on polycarbonate filters, and photographed using a scanning electron microscope (SEM) to examine method of particle formation. An increase in power and decrease in beam diameter led to an increase in mass emission for the Ho:YAG laser at all size ranges. For the CO2 laser, emission rates were dependent on particle size and were not statistically significant for particle ranges between 5 and 10 µm. When any parameter level was increased, emission rate of the smallest particle size range also increased. Beam diameter was the most influential variable for both lasers, and the operational parameters tested explained the most variability at the smallest particle size range. Particle shape was variable and some particles observed by SEM were likely created from mechanical methods. This study provides a foundation for future investigations to better estimate size-specific mass emission rates and particle characteristics for additional laser operational parameters in order to estimate occupational exposure, and to inform control strategies.

A novel method for reducing the number of agents to be studied in an occupational epidemiologic study.

A novel screening tool method to select chemicals for exposure reconstruction was developed and validated using data generated for a hypothetical work force consisting of 10 job classes (ranging from 10,000 to 55,000 person-years). To achieve the required efficiency in the reconstruction of exposures, this method treats each product (defined as a part or process) as an "exposure." Exposure to 10 products was assigned to each job class at random using a computer program. The expected rate of a given disease was assumed to be constant throughout the job classes (tested at five levels), and the observed numbers of cases in the job classes were generated based on neutral deviations from background with error rates of ± 1% to 16%. One job class was assigned to be the "excess-class" and the number of cases in that class was increased by a factor of Q, which was set at levels that ranged from 1.25 to 5. All of the experimental conditions were replicated 10,000 times in a Monte Carlo scheme for scenarios in which each job class had been designated as the excess-class. Following each run, significant excesses (if any) were determined using a modified version of Daniel's method, and the percentages of false positive and false negative identifications were tabulated. We found that the sensitivity of the method is largely dependent on the relative risk (Q) associated with the exposure. Specifically, the results indicate that as the relative risk increases, the percentage of false negative identifications of the excesses is reduced to nearly 0% and the percentage of false positive identifications is approximately 13%. When applied to real data, should an association be detected between any product and a health outcome, this preliminary analysis will yield a reduced "product" set that can then be investigated in detail and the agents involved considered further for quantitative reconstruction. The proposed method is highly efficient and has the potential to benefit future complex exposure reconstruction studies, particularly when there is no predetermined exposure associated with an observed increase in a cause-specific health end point.

Long-term health experience of jet engine manufacturing workers: III. Incidence of malignant central nervous system neoplasms.

OBJECTIVE: To explore a perceived unusual occurrence of glioblastoma at one jet engine manufacturing facility located in North Haven (NH), Connecticut (CT). METHODS: Subjects were 212,513 workers ever employed in 1 of 8 manufacturing facilities from 1952 to 2001 and at risk from 1976 to 2004. We identified 722 cases of CNS neoplasms mainly by tracing through 19 state cancer registries. We computed standardized incidence ratios (SIRs) based on CT state and national rates and modeled internal relative risks (RRs). RESULTS: We found overall deficits in cases for glioblastoma (275 cases, SIR = 0.77, CI = 0.68-0.87) and most other histology categories examined. NH workers had a not statistically significant overall 8% excess in glioblastoma (43 cases, SIR = 1.08, CI = 0.78-1.46). Salaried NH workers had a statistically significant twofold risk of glioblastoma compared with hourly workers (17 cases, RR = 2.04, CI = 1.15-3.57). Other subgroups of NH workers revealed elevated but not statistically significant glioblastoma risks but little evidence of an association with duration of employment or time since first employment. CONCLUSIONS: Incidence rates for glioblastoma and other malignant CNS neoplasm histologies were not elevated in the total cohort. The glioblastoma excesses observed among NH workers may reflect external occupational factors, non-occupational factors or workplace factors unique to NH unmeasured in the current study.

Methodological issues in a retrospective cancer incidence study.

The authors traced incidence of central nervous system cancer in a large occupational cohort of jet engine manufacturing workers from 1976 to 2004 in the 24 US states that comprised 95% of the cohort deaths. The cohort of approximately 224,000 employees was matched with cancer registry data; all central nervous system cancer matches were requested with their diagnostic data. This paper highlights the obstacles encountered while conducting this retrospective cancer incidence study. The authors spent approximately 700 hours completing applications and obtaining the cohort matches. Approximately 70% of the cases were identified in the state in which the facility of interest is located. In addition to the large amount of time involved, identified issues include complicated approval processes, high costs, temporal differences among the registries, and registry agency difficulty in performing the matching. Several states do not allow individual-level data to be used for research purposes. Researchers can gain important cancer incidence information by matching retrospective cohorts to multiple state cancer registries. However, they should carefully weigh the time and costs required and plan accordingly. Despite some serious obstacles, many of which are potentially resolvable, cancer incidence studies of retrospective cohorts using multiple cancer registries are feasible.

Mortality patterns among workers exposed to arsenic, cadmium, and other substances in a copper smelter.

OBJECTIVE: To evaluate the long-term mortality experience of workers exposed to arsenic, cadmium, and other substances at a copper mine and smelter in Copperhill, Tennessee studied earlier as part of an industry-wide study. METHODS: Subjects were 2,422 male workers employed three or more years in the smelter or mill between 1/1/46 until the plant strike and scale-down of operations in April 1996. Vital status was determined through 2000 for 99.4% of subjects and cause of death for 91.3% of 878 deaths. Historical exposures were estimated for lead, SO(2), arsenic, cadmium, dust, and cobalt. We computed standardized mortality ratios (SMRs) based on U.S. and local county rates and modeled internal relative risks (RRs). RESULTS: We observed overall deficits in deaths based on national and local county comparisons from all causes, all cancers and most of the cause of death categories examined. We found limited evidence of increasing mortality risks from cerebrovascular disease with increasing duration and cumulative arsenic exposure, but no evidence of an exposure-response relationship for cadmium exposure and bronchitis. CONCLUSIONS: Our limited evidence of an association between inhaled arsenic exposure and CVD is an exploratory finding not observed in other epidemiology studies of more highly exposed occupational populations. Possible alternative explanations include chance alone and uncontrolled confounding or effect modification by co-exposures or other factors correlated with arsenic exposure and unique to the Copperhill facility.

Chemical process based reconstruction of exposures for an epidemiological study. I. Theoretical and methodological issues.

In the occupational hygiene component of occupational epidemiological studies the goal is to assign group average exposure levels that can be used to compute individual cumulative exposures. This task requires the availability of sufficient amounts of proper individual exposure level data. Typically, the required data are either sparse, completely lacking or happenstance data collected for purposes not suitable for the aims of the study. In the epidemiological study of mortality patterns among industrial workers exposed to chloroprene and other substances, we developed and used a process analysis and modeling based exposure reconstruction to augment, extrapolate, or interpolate the available exposure data. The models developed utilize equations based on the engineering principles and chemistry associated with the processes as determined from the process documentation and task performance habits as determined from interviews of knowledgeable personnel. The resulting equations are tractable and provide a general basis for calculating exposure levels for vapors. The validation of the results with available exposure measurements suggests that comprehensive process analysis and modeling may be used to reconstruct exposures or to evaluate exposure potential with scientifically defensible methods. Furthermore, even in the absence of validating data, the methodology developed has potentially very useful applications in predicting exposure levels to newly synthesized substances. Properly interpreted, the limitations of modeling can be minimized to obtain scientifically reasonable results.

Classification of worker exposures.

The classification of jobs or workers by exposure is an important undertaking in any occupational epidemiological study. Hitherto, the exposure classification designs have been strongly motivated by a desire to generate a sufficient number of exposure classes for the determination of a potential exposure-response relationship. Thus, the partitioning of exposures has been more or less arbitrary. The misclassification problems created by the selection of an arbitrary number of exposure assignment classes have not been addressed. In any quantitative exposure classification scheme, specific job titles may be indistinguishable in existing employment records; therefore, between worker variability must be addressed when characterizing worker exposures. Also, industrial hygiene exposure measurements frequently used to characterize worker exposures are often treated as valid representations of exposures; but they are neither random nor systematic evaluations of worker exposures. As a result they do not represent sampling from the proper exposure stratification of workers. These observations suggest that the selection of exposure groups should be based on a more rigorous examination of the data and its limitations. Considering the probability of any given worker being placed into the proper class as the probability of finding the mean exposure for that worker within the class boundary, the general equations to quantify the misclassification rates for any classification design as well as the exposure class limits and their width for any acceptable misclassification rate are developed. If between worker variability could not be calculated from the available exposure measurements, then it might be estimated from the proper data compiled from the literature. By considering an acceptable level of exposure misclassification, it is possible to calculate the allowable number of exposure classes and the proper partitioning ratio for these classes. Thus, the trade-off between misclassification and number of exposure classes might be a satisfactory solution to this difficulty encountered in occupational epidemiology.

Chemical process-based reconstruction of exposures for an epidemiological study. Part II. Estimated exposures to chloroprene and vinyl chloride.

In a four-facility occupational epidemiology study of chloroprene monomer and polymer production workers, the chloroprene (CD) and vinyl chloride monomer (VCM) exposures were modeled for plant specific job title classes. In two facilities an acetylene-based process was used and in the other two plants only a butadiene-based process was used in the monomer synthesis. In the Acetylene process VCM was an undesirable by-product to be removed. In the newer butadiene-based process, VCM was not involved and the exposures to CD were considerably lower than they were in the earlier years. One of the limiting factors was the operator rotation within a number of job titles. This rotation and inability to differentiate between job titles subsumed in job classifications recorded in the work histories required an exposure classification scheme based on an order of magnitude separation of exposure classes. In the four facilities with considerable variation in the mix of the production methods, the CD exposures were remarkably similar in both calculated and measured values. The reductions in exposures were much more dependent upon the improvement of the production methods, rather than deliberate exposure control for occupational hygiene considerations. This is reasonable since the exposures were generally lower than the coeval exposure limits and/or guidelines. The estimated exposures were less than 100 ppm in the pre-1960 era and less than 10 ppm in the 1960-1980 era, less than 1 ppm 1980-1990 era and less than 0.5 ppm thereafter. The exposures were categorized in four classes for VCM and six classes for CD. The characteristic class exposure values were used to cumulate individual exposures over time with a quantification of the potential range for exposures that are reasonably certain to ascribe correct ranking to job classes.

Mortality patterns among industrial workers exposed to chloroprene and other substances. I. General mortality patterns.

We conducted an historical cohort study to investigate the mortality experience of industrial workers potentially exposed to chloroprene (CD) and other substances, including vinyl chloride (VC), with emphasis on cancer mortality, including respiratory system (RSC) and liver. In 1999, the International Agency for Research on Cancer (IARC) classified CD as a possible carcinogen (Group 2B); VC was classified in 1987 as a known human carcinogen (Group 1). Subjects were 12,430 workers ever employed at one of two U.S. industrial sites (Louisville, KY (n=5507) and Pontchartrain, LA (n=1357)) or two European sites (Maydown, Northern Ireland (n=4849) and Grenoble, France (n=717)), with earliest CD production dates ranging from 1942 (L) to 1969 (P). Two sites (L and M) synthesized CD with the acetylene process that produced VC exposures. We determined vital status through 2000 for 95% of subjects and cause of death for 95% of the deaths. Historical exposures for individual workers were estimated quantitatively for CD and VC. Workers ever exposed to CD ranged from 92.3% (M) to 100% (G); to VC from 5.5% (M) to 22.7% (L). We computed standardized mortality ratios (SMRs) (using national and regional standard populations) in relation to selected demographic, work history and exposure factors. We used worker pay type (white or blue collar) as a rough surrogate for lifetime smoking history. For the combined cohort, SMRs (95% CIs) for all causes combined, all cancers combined, RSC and liver cancer were, respectively, 0.72 (0.69-0.74), 0.73 (0.68-0.78), 0.75 (0.67-0.84) and 0.72 (0.43-1.13). Site-specific (L, M, P and G, respectively) SMRs were: for all cancers combined: 0.75 (0.69-0.80), 0.68 (0.56-0.80), 0.68 (0.47-0.95) and 0.59 (0.36-0.91); for RSC: 0.75 (0.66-0.85), 0.79 (0.58-1.05), 0.62 (0.32-1.09) and 0.85 (0.41-1.56); for liver cancer: 0.90 (0.53-1.44) (17 deaths), 0.24 (0.01-1.34) (1 death), 0.0 (0-2.39) (no deaths) and 0.56 (0.01-3.12) (1 death). Among all workers ever exposed to CD, SMRs were: for all cancers combined: 0.71 (0.66-0.76); for RSC: 0.75 (0.67-0.84); for liver cancer: 0.71 (0.42-1.14). We also observed no increased mortality risks among cohort subgroups defined by race, gender, worker pay type, worker service type (short/long term), time period, year of hire, age at hire, duration of employment, the time since first employment, and CD or VC exposure status (never/ever exposed). In summary, our study has many strengths and is the most definitive study of the human carcinogenic potential of exposure to CD conducted to date. We conclude that persons exposed to chloroprene or vinyl chloride at the levels encountered in the four study sites did not have elevated risks of mortality from any of the causes of death examined, including all cancers combined and lung and liver cancer, the cancer sites of a priori interest. This conclusion is corroborated by our detailed analyses of mortality in relation to qualitative and quantitative exposures to CD and VC at each of the four study sites, reported in our companion paper (Marsh et al., submitted for publication).

Mortality patterns among industrial workers exposed to chloroprene and other substances. II. Mortality in relation to exposure.

As part of an historical cohort study to investigate the mortality experience of industrial workers exposed to chloroprene (CD) and other substances, including vinyl chloride monomer (VC), we analyzed mortality from all cancers combined, respiratory system (RSC) and liver cancer in relation to CD and VC exposures. Subjects were 12,430 workers ever employed at one of two U.S. sites (Louisville, KY (n=5507) and Pontchartrain, LA (n=1357)) or two European sites (Maydown, Northern Ireland (n=4849) and Grenoble, France (n=717)). Historical exposures for individual workers were estimated quantitatively for CD and VC. For sites L, M, P and G, respectively, average intensity of CD exposures (median value of exposed workers in ppm) were 5.23, 0.16, 0.028 and 0.149 and median cumulative exposures (ppm years) were 18.35, 0.084, 0.133 and 1.01. For sites L and M, respectively, average intensity of VC exposures (median value of exposed workers in ppm) was 1.54 and 0.03 and median cumulative exposures (ppm years) were 1.54 and 0.094. We performed relative risk (RR) regression modeling to investigate the dependence of the internal cohort rates for all cancers combined, RSC and liver cancer on combinations of the categorical CD or VC exposure measures with adjustment for potential confounding factors. We categorized exposure measures into approximate quartiles based on the distribution of deaths from all cancers combined. We also considered 5- and 15-year lagged exposure measures and adjusted some RR models for worker pay type (white/blue collar) as a rough surrogate for lifetime smoking history. All modeling was site-specific to account for exposure heterogeneity. We also computed exposure category-specific standardized mortality ratios (SMRs) to assess absolute mortality rates. With the exception of a one statistically significant association with duration of exposure to CD and all cancers combined in plant M, we observed no evidence of a positive association with all cancers, RSC or liver cancer and exposure to CD and/or VC using both the unlagged and lagged exposure measures: duration, average intensity or cumulative exposure to CD or VC; time since first CD or VC exposure; and duration of CD exposure or time since first CD exposure in presence or absence of VC exposure. We observed elevated and statistically significantly elevated RRs for some analysis subgroups, but these were due to inordinately low death rates in the baseline categories. With the possible exception of all cancer mortality in plant G, our additional adjustment of RRs for pay type revealed no evidence of positive confounding by smoking. We conclude that exposures to CD or VC at the levels encountered in the four study sites do not elevate mortality risks from all cancers, RSC or liver cancer. This conclusion is corroborated by our analysis of general mortality patterns among the CD cohort reported in our companion paper [G. Marsh, A. Youk, J. Buchanich, M. Cunningham, N. Esmen, T. Hall, M. Phillips, Mortality patterns among industrial workers exposed to chloroprene and other substances. I. General mortality patterns, Chem.-Biol. Interact., submitted for publication].

Chemical process based reconstruction of exposures for an epidemiological study. III. Analysis of industrial hygiene samples.

As part of an historical cohort study to investigate the mortality experience of industrial workers exposed to chloroprene (beta-CD) and other substances, all available industrial hygiene exposure monitoring data were collected and summarized. From discussions with on-site industrial hygiene personnel, it was apparent that these data were not collected for epidemiological purposes and, therefore, their use in characterization of exposures was problematic as the data mostly pertained to samples collected to investigate the performance of specific tasks. These data were, however, informative for validating the exposure modeling process used to estimate historical exposures. The data summarized below clearly indicate that exposures to beta-CD were lowered across the time period of this study. Typically, the exposures recorded were less than the occupational exposure limits of the periods in which the exposures were recorded. Additionally, exposure measurements recorded in the recent past do not represent the exposure actually experienced by the worker as a strict personal protective equipment use program has been in place for the facilities studied since the mid-1980s.

Mortality Among Hardmetal Production Workers: Occupational Exposures.

OBJECTIVE: To generate quantitative exposure estimates for use in retrospective occupational cohort mortality studies of the hardmetal industry. METHODS: Job-exposure matrices (JEMs) were constructed for cobalt, tungsten, and nickel over the time period 1952 to 2014. The JEMs consisted of job class categories, based on job titles and processes performed, and exposure estimates calculated from available company industrial hygiene measurements. RESULTS: Exposure intervals of one-half order magnitude were established for all three agents. Eight job classes had significantly decreasing time trends for cobalt exposure; no significant time trends were detected for tungsten or nickel exposures. CONCLUSIONS: The levels of exposures determined for this study were similar to or lower than those previously reported for the hardmetal industry during the 1952 to 2014 study period.

Mortality Among Hardmetal Production Workers: German Historical Cohort Study.

OBJECTIVE: The aim of this study was to investigate a cohort in German hardmetal industry, especially relationship between exposures to cobalt, with and without tungsten, and risks of total and cause-specific mortality. METHODS: The cohort comprises blue-collar workers at three German plants who were employed in hardmetal processing. Individual cumulative exposures and long-term average concentrations were estimated for cobalt, nickel, tungsten, respirable, and inhalable dust. Standardized mortality ratios (SMRs) were calculated for external comparisons. Time-dependent multivariable Cox models were performed for internal analyses. RESULTS: Elevated SMRs were found for all-cause, heart diseases, and nonmalignant respiratory diseases mortality, but not for lung cancer. Internal analyses did not show increased risks for any endpoints, and no exposure-response relationship was indicated. CONCLUSIONS: This study does not provide evidence for elevated lung cancer risks. Methodologic limitations, incomplete ascertainment of death causes in particular, impede conclusions about exposure effects.

Mortality Among Hardmetal Production Workers: US Cohort and Nested Case-Control Studies.

OBJECTIVES: To evaluate total and cause-specific mortality among hardmetal production workers with emphasis on lung cancer. METHODS: Subjects were 7304 workers ever employed in one of eight US plants from 1952 to 2008. Vital status through 2012 was determined for 97% of subjects and cause of death for 98.3% of 1087 deaths. We computed standardized mortality ratios (SMRs) and evaluated exposure-response via relative risk regression analysis. RESULTS: We observed overall deficits in deaths for total mortality, all cancers, and lung cancer and found no evidence of any exposure-response relationships for lung cancer. CONCLUSIONS: We found no evidence that exposure to tungsten, cobalt, or nickel, at levels experienced by the workers examined, increases lung cancer mortality risks. We also found no evidence that work in the US hardmetal industry increases mortality risks from any other causes of death.

Mortality Among Hardmetal Production Workers: UK Cohort and Nested Case-Control Studies.

OBJECTIVE: The aim of this study was to characterize the mortality at two hardmetal production factories in the United Kingdom as part of an international study. METHODS: Standardized mortality ratios (SMRs) were calculated on the basis of mortality rates for England and Wales, and local rates. A nested case-control study of lung cancer was undertaken. RESULTS: The cohort comprised 1538 workers, with tracing complete for 94.4%. All-cause mortality was statistically significantly low for all cancers and nonmalignant respiratory disease, and for lung cancer was nonsignificantly low. The SMR for lung cancer for maintenance workers was elevated, based on only six deaths. The odds ratio for lung cancer per year of exposure to hardmetal was 0.93 (0.76 to 1.13). CONCLUSIONS: In this small study, there is no evidence to support that working in the UK hardmetal manufacturing industry increased mortality from any cause including lung cancer.

Mortality Among Hardmetal Production Workers: Pooled Analysis of Cohort Data From an International Investigation.

OBJECTIVES: Based on a pooled analysis of data from an international study, evaluate total and cause-specific mortality among hardmetal production workers with emphasis on lung cancer. METHODS: Study members were 32,354 workers from three companies and 17 manufacturing sites in five countries. We computed standardized mortality ratios and evaluated exposure-response via relative risk regression analysis. RESULTS: Among long-term workers, we observed overall deficits or slight excesses in deaths for total mortality, all cancers, and lung cancer and found no evidence of any exposure-response relationships for lung cancer. CONCLUSIONS: We found no evidence that duration, average intensity, or cumulative exposure to tungsten, cobalt, or nickel, at levels experienced by the workers examined, increases lung cancer mortality risks. We also found no evidence that work in these facilities increased mortality risks from any other causes of death.

Mortality patterns among workers in a US pharmaceutical production plant.

PURPOSE: To examine mortality among workers in a pharmaceutical production plant and to address community concerns about 1980 to 1990 increases in local county cancer mortality rates. METHODS: Subjects were 1999 workers with some full-time employment during the period between 1970 and 1996. We identified deaths through the year 2000 and reconstructed exposures to nine chemical agents with available exposure measurements. Data analyses included standardized mortality ratios (SMRs) and time trends in local cancer mortality rates. RESULTS: We observed deficits in deaths from all causes combined, all cancers combined, and most cause of death categories examined. Male workers with potential plant exposure had excesses in deaths from all lymphatic-hematopoietic tissue cancers (LHTC), in particular non-Hodgkin's lymphoma (NHL), and respiratory system cancers (RSC) that were larger among long-term workers, but the pattern of findings suggested the excesses were probably not related to occupational factors at the plant. The increase in local county cancer mortality rates was simply the upward cycle of a periodic trend that peaked in 1990 and returned to 1980 levels in 2000. CONCLUSIONS: With the possible exceptions of LHTC, in particular NHL, and RSC, this study provided no evidence of elevated total or cause-specific cohort mortality risks. It does not appear that plant factors played a role in the 1980 to 1990 increases in local county cancer mortality rates.

Determinants of exposure to volatile organic compounds in four Oklahoma cities.

To begin to develop generalized models for estimating personal exposure to ambient air pollutants within diverse populations, the design of the Oklahoma Urban Air Toxics Study incorporated eight dichotomous macroenvironmental and household factors that were hypothesized to be potential determinants of exposure. Personal, indoor, and outdoor samples of volatile organic compounds (VOCs) were collected over 24-h monitoring periods in 42 households, together with activity diaries and data on the participants' residences. The distributions of the VOC concentrations were moderately to highly left-censored, and were mostly bimodal. The ATSDR minimal risk level (MRL) was exceeded in a small number of the samples. Personal and indoor concentrations tended to be higher than outdoor concentrations, indicating that indoor exposures were dominated by indoor sources. However, indoor concentrations were not correlated with the permeability of the residence, suggesting that the observed indoor concentrations reflected mostly localized, short-term emissions. The influence of the eight dichotomous factors and of the presence of an attached garage was evaluated using the Wilcoxon rank-sum test and by comparison of "excursion fractions", that is, the fractions of each distributions exceeding 10% of the MRL. Dry weather and absence of children in the household were found to be associated with higher exposures in personal or indoor exposures. Given the small sample size, it is possible that these factors were confounded with unidentified household characteristics or activities that were the true determinants of exposure.

Long-term health experience of jet engine manufacturing workers: VII: occupational exposures.

OBJECTIVE: To reconstruct agent-specific occupational exposures for a cohort of jet engine manufacturing workers for use in an epidemiological mortality study. METHODS: Potential chemical and physical exposures at eight jet engine manufacturing and overhaul/repair plants were evaluated for the period 1952 to 2001. Eleven agents were selected for detailed examination, and a job-exposure matrix was constructed. RESULTS: Quantitative exposure estimates were generated for metalworking fluids, nickel, cobalt, chromium, solvents, and incomplete combustion aerosol from metalworking fluids. Qualitative exposure estimates were assigned for ionizing radiation, electromagnetic fields, polychlorinated biphenyls, and lead-cadmium. All exposures showed decreasing trends over the study period. CONCLUSIONS: The quantitative exposure levels generated in this study were lower than early contemporaneous professional practice recommendations and were similar to or lower than published data from other industries.

Long-term health experience of jet engine manufacturing workers: IX. further investigation of general mortality patterns in relation to workplace exposures.

OBJECTIVE: To evaluate mortality rates among a cohort of jet engine manufacturing workers. METHODS: Subjects were 222,123 workers employed from 1952 to 2001. Vital status was determined through 2004 for 99% of subjects and cause of death for 95% of 68,317 deaths. We computed standardized mortality ratios and modeled internal cohort rates. RESULTS: Mortality excesses reported initially no longer met the criteria for further investigation. We found two chronic obstructive pulmonary disease-related mortality excesses that met the criteria in two of eight study plants. CONCLUSIONS: At the total cohort level, chronic obstructive pulmonary disease-related categories were not related to any factors or occupational exposures considered. A full evaluation of these excesses was limited by lack of data on smoking history. Occupational exposures received outside of work or uncontrolled positive confounding by smoking cannot be ruled out as reasons for these excesses.