Exposure assessment of carbon nanotube manufacturing workplaces.

Seven CNT (carbon nanotube) handling workplaces were investigated for exposure assessment. Personal sampling, area sampling, and real-time monitoring using an SMPS (scanning mobility particle sizer), dust monitor, and aethalometer were performed to characterize the mass exposure, particle size distribution, and particle number exposure. No workplace was found to exceed the current ACGIH (American Conference of Governmental Industrial Hygienists) TLVs (threshold limit values) and OELs (occupational exposure levels) set by the Korean Ministry of Labor for carbon black (3.5 mg/m(3)), PNOS (particles not otherwise specified; 3 mg/m(3)), and asbestos (0.1 fiber/cc). Nanoparticles and fine particles were most frequently released after opening the CVD (chemical vapor deposition) cover, followed by catalyst preparation. Other work processes that prompted nanoparticle release included spraying, CNT preparation, ultrasonic dispersion, wafer heating, and opening the water bath cover. All these operation processes could be effectively controlled with the implementation of exposure mitigation, such as engineering control, except at one workplace where only natural ventilation was used.

Recurrent exposure to welding fumes induces insufficient recovery from inflammation.

Previous studies on welding-fume-induced lung fibrosis have indicated that recovery is possible when the degree of exposure is short-term and moderate. However, this study investigated the recovery after recurrent exposure to welding fumes, as welders are invariably re-exposed to welding fumes after recovering from radiographic pneumoconiosis. Thus, to investigate the disease and recovery processes of welding-fume-induced pneumoconiosis in the case of recurrent welding-fume exposure, rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes with a total suspended particulate (TSP) concentration of 51.4 +/- 2.8 mg/m(3) (low dose) or 84.6 +/- 2.9 mg/m(3) (high dose) for 2 h/day in an inhalation chamber for 1 mo and then allowed to recover from the inflammation for 1 mo. Thereafter, the rats were exposed again to MMA-SS with a TSP concentration of 44.1 +/- 8.8 mg/m(3) (low dose) or 80.1 +/- 9.8 mg/m(3) (high dose) for another 30 d and then allowed to recover from the inflammation for 1 mo. The recovery from the first exposure was then compared with that from the second exposure. The first and second exposures to MMA-SS welding fumes were found to produce significant increases in the lung weights and inflammatory parameters, including total cell numbers, alveolar macrophages (AMs), polymorphonuclear cells (PMNs), lymphocytes, and lactate dehydrogenase (LDH) in the bronchoalveolar lavage fluid (BALF) when compared with the unexposed controls. Following the first and second recovery, a significant reduction in inflammatory parameters of BALF was observed between the exposure and recovery groups. Histopathological observations showed foamy or pigmented macrophage accumulation, cellular debris, or pigment from burst macrophages after the first or second exposure. Following the first or second recovery, cellular debris or pigment from burst macrophages was cleared away from the lungs and accumulation of foamy or pigmented macrophages was decreased when compared to previous exposure. Reactive hyperplasia was noticed after second exposure or either recovery. However, significant differences were observed between the first and second exposure or the first and second recovery. In particular, the number of PMNs was significantly higher after the second exposure than after the first exposure. Also, all cell types in the BALF were significantly elevated in the high-dose second recovery group than in the first recovery group, indicating an incomplete recovery from second exposure. In conclusion, these results indicated that the lung damage caused by the second welding-fume exposure was more difficult to recover from than the first exposure.

Comparison of lung asbestos fiber content in cancer subjects with healthy individuals with no known history of occupational asbestos exposure in Korea.

To evaluate the effects of environmental asbestos exposure on the inducement of lung cancer, pulmonary asbestos and non-asbestos fiber content was determined in 36 normal Korean subjects and 38 lung cancer subjects with no known occupational history of asbestos exposure. Pulmonary asbestos fiber content was measured by transmission electron microscopy (TEM) with energy-dispersive x-ray analysis after applying a low-temperature ashing procedure. Chrysotile fibers were the major fiber type found in the lungs of the Korean subjects. The asbestos fiber concentrations found in the lungs of normal males (25) and females (11) were 0.26 x 10(6) fibers/g of dry lung tissue and 0.16 x 10(6) fibers/g of dry lung tissue, respectively. The asbestos concentrations found in the lungs of cancer subjects were 0.16 x 10(6) fibers/g of dry lung tissue for 32 males and 0.44 x 10(6) fibers/g of dry lung tissue for 6 females. No statistical difference was found in pulmonary asbestos content between the normal and lung cancer subjects, whereas a statistical difference was noted between normal and lung cancer subjects with respect to lung non-asbestos content, indicating a potential role for non-asbestos fibers being associated with lung cancer.

High signal intensity on magnetic resonance imaging as a predictor of neurobehavioral performance of workers exposed to manganese.

INTRODUCTION: Using previously obtained cross-sectional data from a nationwide survey on workers exposed to manganese (Mn), we assessed the relation of high signal intensity with neurobehavioral effects, and reevaluated the preexisting cross-sectional data to get additional findings on the relation of high signals with other Mn-exposure indices. SUBJECTS AND METHODS: Subjects were the same as those in the previous study. The exposure status was reassessed based on similar exposure groups. The signal intensity of the globus pallidus (GP) relative to frontal white matter was subjectively evaluated as either with or without increased signals, and the increased signals were further graded into three categories. For quantitative evaluation of signal intensities of the GP we also calculated the pallidal index (PI). Neurobehavioral function was assessed using the World Health Organization Neurobehavioral Core Test Battery. In addition, computerized finger tapping speed was included to assess motor speed. RESULTS: The mean blood Mn for those with grade III was significantly greater than those without increased signals and those with grade I. Airborne Mn and PI also showed similar findings. PI paralleled subjective MRI gradings. The proportion of workers with increased signals increased with all the Mn-exposure variables, airborne and blood Mn, the duration of work, and cumulative exposure. The PI was significantly associated with a correct score of pursuit aiming II tests and finger tapping of the dominant hand after control of age and educational level among neurobehavioral performances. DISCUSSION: The present findings showed that signal index on T1-weighted MRI showed a dose-response relationship with all the Mn-exposure variables. The two neurobehavioral tests reflecting fine motor function were significantly decreased above 107.1 of PI, the cutoff point between those with and without increased signals. Hence, signal intensity on MRI is an effective predictor of the neurobehavioral performance of Mn exposed workers.

Pallidal index on MRI as a target organ dose of manganese: structural equation model analysis.

We have used a structural equation model (SEM) to analyze the interrelationships among exposure markers, magnetic resonance imaging (MRI) signal index, and neurobehavioral effects. Based on exposure groups, we assessed blood manganese, MRI measurements of pallidal index (PI), and neurobehavioral core test battery (WHO-NCTB) on 111 male workers occupationally exposed to manganese, including welders, smelter workers, and welding rod manufacturing workers. Latent variables were constructed to represent the neurobehavioral effects in an integrated way. The structural equation model revealed that airborne manganese and blood manganese contribute to PI significantly. Manganese exposure in the ambient air may lead to an increase in the internal dose, not only indirectly, by increasing blood manganese level, but also directly, independent of blood concentration. PI significantly contributed to a decrease in neurobehavioral test scores. We found that airborne manganese contributed to PI, and that PI is the most effective predictor of neurobehavioral performance, after adjusting for age and level of education. In conclusion, PI on MRI reflects target organ dose of occupational manganese exposure.