Presence of tungsten-containing fibers in tungsten refining and manufacturing processes.

In tungsten refining and manufacturing processes, a series of tungsten oxides are typically formed as intermediates in the production of tungsten powder. The present study was conducted to characterize airborne tungsten-containing fiber dimensions, elemental composition and concentrations in the US tungsten refining and manufacturing industry. During the course of normal employee work activities, seven personal breathing zone and 62 area air samples were collected and analyzed using National Institute for Occupational Safety and Health (NIOSH) fiber sampling and counting methods to determine dimensions, composition and airborne concentrations of fibers. Mixed models were used to identify relationships between potential determinants and airborne fiber concentrations. Results from transmission electron microscopy analyses indicated that airborne fibers with length >0.5 microm, diameter >0.01 microm and aspect ratios > or =3:1 were present on 35 of the 69 air samples collected. Overall, the airborne fibers detected had a geometric mean length approximately 3 microm and diameter approximately 0.3 microm. Ninety-seven percent of the airborne fibers identified were in the thoracic fraction (i.e. aerodynamic diameter < or = 10 microm). Energy dispersive X-ray spectrometry results indicated that airborne fibers prior to the carburization process consisted primarily of tungsten and oxygen, with other elements being detected in trace quantities. Based on NIOSH fiber counting 'B' rules (length > 5 microm, diameter < 3 microm and aspect ratio > or = 5:1), airborne fiber concentrations ranged from below the limit of detection to 0.085 fibers cm(-3), with calcining being associated with the highest airborne concentrations. The mixed model procedure indicated that process temperature had a marginally significant relationship to airborne fiber concentration. This finding was expected since heated processes such as calcining created the highest airborne fiber concentrations. The finding of airborne tungsten-containing fibers in this occupational setting needs to be confirmed in similar settings and demonstrates the need to obtain information on the durability and associated health effects of these fibers.

Presence of airborne fibers in tungsten refining and manufacturing processes: preliminary characterization.

In tungsten refining and manufacturing processes, a series of tungsten oxides (WO(X)) are typically formed as intermediates in the production of tungsten powder. Studies in the Swedish tungsten refining and manufacturing industry have shown that intermediate tungsten refining processes can create WO(X) fibers. The purpose of the present study was to identify and provide a preliminary characterization of airborne tungsten-containing fiber dimensions, elemental composition, and concentrations in the U.S. tungsten refining and manufacturing industry. To provide the preliminary characterization, 10 static air samples were collected during the course of normal employee work activities and analyzed using standard fiber sampling and counting methods. Results from transmission electron microscopy analyses conducted indicate that airborne fibers with length > 0.5 microm, diameter > 0.01 microm, and aspect ratio > or = 3:1, with a geometric mean (GM) length of approximately 2.0 microm and GM diameter of approximately 0.25 microm, were present on 9 of the 10 air samples collected. Energy dispersive X-ray spectrometry results indicate that airborne fibers prior to the carburization process consisted primarily of tungsten and oxygen, with other elements being detected in trace quantities. Results from an air sample collected at the carburization process indicated the presence of fibers composed primarily of tungsten with oxygen and carbon, and traces of other elements. Based on National Institute for Occupational Safety and Health standard fiber counting rules, airborne fiber concentrations ranged from below the limit of detection to 0.14 f/cm(3). The calcining process was associated with the highest airborne fiber concentrations. More than 99% (574/578) of the airborne fibers identified had an aerodynamic diameter

DNA damage in leukocytes of workers occupationally exposed to 1-bromopropane.

1-bromopropane (1-BP; n-propyl bromide) (CAS No. 106-94-5) is an alternative to ozone-depleting chlorofluorocarbons that has a variety of potential applications as a degreasing agent for metals and electronics, and as a solvent vehicle for spray adhesives. Its isomer, 2-brompropane (2-BP; isopropyl bromide) (CAS No. 75-26-3) impairs antioxidant cellular defenses, enhances lipid peroxidation, and causes DNA damage in vitro. The present study had two aims. The first was to assess DNA damage in human leukocytes exposed in vitro to 1- or 2-BP. DNA damage was also assessed in peripheral leukocytes from workers with occupational exposure to 1-BP. In the latter assessment, start-of- and end-of-work week blood and urine samples were collected from 41 and 22 workers at two facilities where 1-BP was used as a solvent for spray adhesives in foam cushion fabrication. Exposure to 1-BP was assessed from personal-breathing zone samples collected for 1-3 days up to 8h per day for calculation of 8h time weighted average (TWA) 1-BP concentrations. Bromide (Br) was measured in blood and urine as a biomarker of exposure. Overall, 1-BP TWA concentrations ranged from 0.2 to 271 parts per million (ppm) at facility A, and from 4 to 27 ppm at facility B. The highest exposures were to workers classified as sprayers. 1-BP TWA concentrations were statistically significantly correlated with blood and urine Br concentrations. The comet assay was used to estimate DNA damage. In vitro, 1- or 2-BP induced a statistically significant increase in DNA damage at 1mM. In 1-BP exposed workers, start-of- and end-of-workweek comet endpoints were stratified based on job classification. There were no significant differences in DNA damage in leukocytes between workers classified as sprayers (high 1-BP exposure) and those classified as non-sprayers (low 1-BP exposure). At the facility with the high exposures, comparison of end-of-week values with start-of-week values using paired analysis revealed non-sprayers had significantly increased comet tail moments, and sprayers had significantly increased comet tail moment dispersion coefficients. A multivariate analysis included combining the data sets from both facilities, log transformation of 1-BP exposure indices, and the use of multiple linear regression models for each combination of DNA damage and exposure indices including exposure quartiles. The covariates were gender, age, smoking status, facility, and glutathione S-transferase M1 and T1 (GSTM1, GSTT1) polymorphisms. In the regression models, start-of-week comet tail moment in leukocytes was significantly associated with serum Br quartiles. End-of-week comet tail moment was significantly associated with 1-BP TWA quartiles, and serum Br quartiles. Gender, facility, and GSTM1 had a significant effect in one or more models. Additional associations were not identified from assessment of dispersion coefficients. In vitro and in vivo results provide limited evidence that 1-BP exposure may pose a small risk for increasing DNA damage.

Abrasive blasting agents: designing studies to evaluate relative risk.

Workers exposed to respirable crystalline silica used in abrasive blasting are at increased risk of developing a debilitating and often fatal fibrotic lung disease called silicosis. The National Institute for Occupational Safety and Health (NIOSH) recommends that silica sand be prohibited as abrasive blasting material and that less hazardous materials be used in blasting operations. However, data are needed on the relative risks associated with exposure to abrasive blasting materials other than silica. NIOSH has completed acute studies in rats (Hubbs et al., 2001; Porter et al., 2002). To provide dose-response data applicable to making recommendation for occupational exposure limits, NIOSH has collaborated with the National Toxicology Program (NTP) to design longer term studies with silica substitutes. For risk assessment purposes, selected doses will include concentrations that are relevant to human exposures. Rat lung burdens achieved should be comparable to those estimated in humans with working lifetime exposures, even if this results in "overloading" doses in rats. To quantify both dose and response, retained particle burdens in the lungs and lung-associated lymph nodes will be measured, as well as biochemical and pathological indices of pulmonary response. This design will facilitate assessment of the pulmonary fibrogenic potential of inhaled abrasive blasting agents at occupationally relevant concentrations.

Priorities for development of research methods in occupational cancer.

Occupational cancer research methods was identified in 1996 as 1 of 21 priority research areas in the National Occupational Research Agenda (NORA). To implement NORA, teams of experts from various sectors were formed and given the charge to further define research needs and develop strategies to enhance or augment research in each priority area. This article is a product of that process. Focus on occupational cancer research methods is important both because occupational factors play a significant role in a number of cancers, resulting in significant morbidity and mortality, and also because occupational cohorts (because of higher exposure levels) often provide unique opportunities to evaluate health effects of environmental toxicants and understand the carcinogenic process in humans. Despite an explosion of new methods for cancer research in general, these have not been widely applied to occupational cancer research. In this article we identify needs and gaps in occupational cancer research methods in four broad areas: identification of occupational carcinogens, design of epidemiologic studies, risk assessment, and primary and secondary prevention. Progress in occupational cancer will require interdisciplinary research involving epidemiologists, industrial hygienists, toxicologists, and molecular biologists.

Applying new biotechnologies to the study of occupational cancer--a workshop summary.

As high-throughput technologies in genomics, transcriptomics, and proteomics evolve, questions arise about their use in the assessment of occupational cancers. To address these questions, the National Institute for Occupational Safety and Health, the National Cancer Institute, the National Institute of Environmental Health Sciences, and the American Chemistry Council sponsored a workshop 8-9 May 2002 in Washington, DC. The workshop brought together 80 international specialists whose objective was to identify the means for best exploiting new technologies to enhance methods for laboratory investigation, epidemiologic evaluation, risk assessment, and prevention of occupational cancer. The workshop focused on identifying and interpreting markers for early biologic effect and inherited modifiers of risk.

Oxidative DNA damage is associated with intense noise exposure in the rat.

Increasing evidence suggests that noise-induced hearing loss may be reduced or prevented with antioxidant therapy. Biochemical markers of reactive oxygen species (ROS)-induced damage can help elucidate possible treatment timing constraints. This study examined the time course of ROS damage following a 2-h, broad-band noise exposure resulting in permanent threshold shift in 35 Long-Evans rats. Cochlea, brain, liver, serum and urine were analyzed at 1, 3, 8, 72, and 672 h (28 days) after exposure. Oxidative DNA damage was assessed by measuring 8-hydroxy-2'-deoxyguanosine (8OHdG) by high performance liquid chromatography with electrochemical detection. Lipid peroxidation was measured via the thiobarbituric acid-reactive substances (TBARS) colorimetric assay for detection of aldehydes (e.g., malondialdehyde). Auditory brainstem response and distortion product otoacoustic emission thresholds showed progressive elevation for the 3- and 8-h groups, then notable recovery for the 72-h group, and some worsening for the 672-h group. 8OHdG was significantly elevated in cochlea in the 8-h group, and in brain and liver for the 72-h group. TBARS were significantly elevated in serum for the 72-h group. Based upon oxidative DNA damage present in cochlea following intense noise, we postulate that the first 8 h following exposure might be a critical period for antioxidant treatment.

Effect of perchloroethylene, smoking, and race on oxidative DNA damage in female dry cleaners.

Perchloroethylene (PERC) is used widely as an industrial dry cleaning solvent and metal degreaser. PERC is an animal carcinogen that produces increased incidence of renal adenomas, adenocarcinomas, mononuclear cell leukemia, and hepatocellular tumors. Oxidative DNA damage and lipid peroxidation were assessed in 38 women with (dry cleaners) or without (launderers) occupational exposure to PERC. PERC exposure was assessed by collecting breathing zone samples on two consecutive days of a typical work week. PERC levels were measured in blood drawn on the morning of the second day of breathing zone sample collection in dry cleaners and before a typical workday in launderers. Blood PERC levels were two orders of magnitude higher in dry cleaners compared to launderers. A significant correlation was noted between time weighted average (TWA) PERC and blood PERC in dry cleaners (r=0.7355, P<0.002). 8-Hydroxydeoxyguanosine (8-OHdG), ng/mg deoxyguanosine (dG) in leukocyte nuclear DNA was used as an index of steady-state oxidative DNA damage. Urinary 8-OHdG, microg/g creatinine was used as an index of oxidative DNA damage repair. Urinary 8-epi-prostaglandin F(2alpha) (8-epi-PGF), ng/g creatinine was used as an index of lipid peroxidation. The mean+/-S.D. leukocyte 8-OHdG in launderers was 16.0+/-7.3 and was significantly greater than the 8.1+/-3.6 value for dry cleaners. Urinary 8-OHdG and 8-epi-PGF were not significantly different between dry cleaners and launderers. Unadjusted Pearson correlation analysis of log transformed PERC exposure indices and biomarkers of oxidative stress indicated a significant association in launderers between blood PERC and day 1 urinary 8-OHdG (r=0.4661, P<0.044). No significant associations between exposure indices and biomarkers were evident in linear models adjusted for age, body mass index, race, smoking (urinary cotinine, mg/g creatinine) and blood levels of the antioxidants Vitamin E and beta-carotene. The mean+/-S.D. leukocyte 8-OHdG value in control white women was 17.8+/-7.4 and was significantly greater than the 11.8+/-5.9 in control black women. No significant differences by race were evident for the other biomarkers. Smoking status was not significantly associated with any of the oxidative damage indices. Results indicate a reduction in oxidative DNA damage in PERC exposed dry cleaners relative to launderers, but PERC could not clearly be defined as the source of the effect.