Occupational exposures to fibers and quartz at 19 crushed stone mining and milling operations.

From 1979 to 1982, the National Institute for Occupational Safety and Health (NIOSH) conducted a cross-sectional exposure assessment and mortality study of selected crushed stone facilities in the United States. This study was undertaken in part to address concerns that asbestos exposures could be occurring in some crushed stone operations due to the presence of amphibole and serpentine minerals. The investigation was also designed to characterize exposures to crystalline silica and other mineral compounds. Nineteen crushed stone operations, mining limestone, granite, or traprock were surveyed to assess exposures to respirable and total dusts, mineral compounds including crystalline silica, asbestos, and mineral fibers. At the initiation of the study, crushed stone operations were selected from a Mine Safety and Health Administration (MSHA) listing of the active industry in 1978. With the exception of requiring inclusion of the traprock operation in Maryland where asbestos fibers were initially discovered, a stratified sample of operations was randomly selected by rock type (granite, limestone, traprock, or sandstone). However, because of reluctance or refusal of some companies to participate and because of the closures of some of the selected operations, replacements were randomly selected. Some replacement selections were likewise replaced due to lack of cooperation from the companies. The studied sample included only 10 of the 27 randomly selected operations in the original sample. Asbestos fibers were detected at one traprock facility, the Maryland operation where asbestos was originally found. Measured personal exposures to fibers exceeded the NIOSH Recommended Exposure Limit (REL) for two out of 10 samples. All of the samples were below the MSHA Permissible Exposure Limit (PEL), which was in effect at the time of the survey. However, due to the presence of nonasbestos mineral fibers in the environment, it could not be stated with certainty that all of the fibers counted by phase contrast microscopy were asbestos. A variety of silicate mineral fibers (other than those classified by NIOSH as asbestos) were detected in the traprock operations and at one granite operation. Crystalline silica was detected at 17 of the 19 surveyed crushed stone operations. Overexposures to crystalline silica were measured at 16 of the crushed stone operations; approximately one in seven personal-respirable dust samples (14%) exceeded the MSHA PEL for crystalline silica. Approximately 25% of the respirable dust samples exceeded the NIOSH REL for crystalline silica. Mill operators and mill laborers consistently had the highest and most frequent overexposures to crystalline silica.

Statistical model for prediction of retrospective exposure to ethylene oxide in an occupational mortality study.

Since direct measures of individual exposure seldom exist for the entire period of an occupational mortality study, retrospective exposure estimates are necessary. This is often done in a subjective manner involving a consensus of opinion from a panel of epidemiologists and industrial hygienists. An alternative method utilizing a statistical model provides a more objective procedure for retrospective exposure assessment. The development of a weighted multiple regression model is presented for estimation of exposure levels to ethylene oxide (ETO) for inclusion in a cohort mortality study of workers in the sterilization industry. Three steps in development of the model are described: (1) data acquisition and assessment, (2) model building, and (3) evaluation of the model. The final model explained a remarkable 85% of the variability in 205 average measurements of ETO levels. Exposure factors included in the model were exposure category, product type, size of the sterilization unit, selected engineering controls, days after sterilization, and calendar year. The model was evaluated in two ways: against a set of measurement data not used to develop the model and a panel of 11 industrial hygienists representing the sterilization industry. The model predicted ETO exposures within 1.1 ppm of the validation data set with a standard deviation of 3.7 ppm. The arithmetic and geometric means of the 46 measurements in the validation data set were 4.6 and 2.2 ppm, respectively. The model also outperformed the panel of industrial hygienists relative to the validation data in terms of both bias and precision.

Influence of the dose levels of cocarcinogen ferric oxide on the metabolism of benzo[a]pyrene by pulmonary alveolar macrophages in suspension culture.

The concurrent administration of a cocarcinogenic carrier particle such as ferric oxide (Fe2O3) and the polycyclic aromatic hydrocarbon lung carcinogen benzo[a]pyrene (BaP) results in a decreased latency and an increased incidence in the production of lung tumors in hamsters compared to the administration of BaP alone. The pulmonary alveolar macrophage (AM), the primary lung defense cell, has been shown to endocytize BaP, metabolize BaP to a more biologically active form, and then release the metabolites. Therefore, a study was undertaken to determine in a dose-response manner the effect of AM phagocytosis of a carrier particle (Fe2O3) on the metabolism of a carcinogen (BaP) and on the production of reactive oxygen. The AM were lavaged from hamsters and cultured in suspension (2.5 x 10(6) cells/vial) with BaP (62.5 nmol, 14C labeled) alone or adsorbed onto 0.5, 1.0, or 2.0 mg Fe2O3 in the presence of cytochrome c. Following separate ethyl acetate extractions of the AM and medium, the metabolites were isolated by high-performance liquid chromatography (HPLC) and quantified by liquid scintillation spectrometry. The production of superoxide anions was monitored by the reduction of cytochrome c. Concurrent exposure of AM to BaP-coated Fe2O3 resulted in a significant increase in the amount of BaP metabolites and superoxide anions produced with dose of Fe2O3. The following metabolites were identified in both the medium and the AM: 9,10-dihydrodiol, 7,8-dihydrodiol, 4,5-dihydrodiol, 9-hydroxy, 3-hydroxy, and 3,6-quinone. In general, the 7,8-dihydrodiol, which is considered to be the precursor of the ultimate carcinogenic metabolite of BaP, and superoxide anions, which have been shown to produce localized lipid peroxidation and edema in vivo, were significantly enhanced (p = .05, Duncan's multiple comparison test) in AM exposed to all doses of Fe2O3 when compared to AM exposed to BaP alone. This Fe2O3 dose-related enhancement of superoxide anion production is indicative of increased endocytic capacity resulting in a greater amount of total metabolites being produced, in particular, the dihydrodiols of BaP, which are considered to be products of the active metabolic pathway of BaP.

Cancer mortality in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

BACKGROUND: In both animal and epidemiologic studies, exposure to dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, or TCDD) has been associated with an increased risk of cancer. METHODS: We conducted a retrospective cohort study of mortality among the 5172 workers at 12 plants in the United States that produced chemicals contaminated with TCDD. Occupational exposure was documented by reviewing job descriptions and by measuring TCDD in serum from a sample of 253 workers. Causes of death were taken from death certificates. RESULTS: Mortality from several cancers previously associated with TCDD (stomach, liver, and nasal cancers, Hodgkin's disease, and non-Hodgkin's lymphoma) was not significantly elevated in this cohort. Mortality from soft-tissue sarcoma was increased, but not significantly (4 deaths; standardized mortality ratio [SMR], 338; 95 percent confidence interval, 92 to 865). In the subcohort of 1520 workers with greater than or equal to 1 year of exposure and greater than or equal to 20 years of latency, however, mortality was significantly increased for soft-tissue sarcoma (3 deaths; SMR, 922; 95 percent confidence interval, 190 to 2695) and for cancers of the respiratory system (SMR, 142; 95 percent confidence interval, 103 to 192). Mortality from all cancers combined was slightly but significantly elevated in the overall cohort (SMR, 115; 95 percent confidence interval, 102 to 130) and was higher in the subcohort with greater than or equal to 1 year of exposure and greater than or equal to 20 years of latency (SMR, 146; 95 percent confidence interval, 121 to 176). CONCLUSIONS: This study of mortality among workers with occupational exposure to TCDD does not confirm the high relative risks reported for many cancers in previous studies. Conclusions about an increase in the risk of soft-tissue sarcoma are limited by small numbers and misclassification on death certificates. Excess mortality from all cancers combined, cancers of the respiratory tract, and soft-tissue sarcoma may result from exposure to TCDD, although we cannot exclude the possible contribution of factors such as smoking and occupational exposure to other chemicals.