Chrysotile, or “white”, asbestos is the dominant form of asbestos in international commerce today. It accounts for 99% of current world asbestos production of 2 million tonnes. Chrysotile is an extremely hazardous material. Clinical and epidemiologic studies have established incontrovertibly that chrysotile causes cancer of the lung, malignant mesothelioma of the pleura and peritoneum, cancer of the larynx and certain gastrointestinal cancers. Chrysotile also causes asbestosis, a progressive fibrous disease of the lungs. Risk of these diseases increases with cumulative lifetime exposure to chrysotile and rises also with increasing time interval (latency) since first exposure. Comparative analyses have established that chrysotile is 2 to 4 times less potent than crocidolite asbestos in its ability to cause malignant mesothelioma, but of equal potency of causation of lung cancer. The International Agency for Research on Cancer of the World Health Organization has declared chrysotile asbestos a proven human carcinogen. Sales of chrysotile asbestos have virtually ended in Western Europe and North America, because of widespread recognition of its health hazards. However, asbestos sales remain strong in Japan, across Asia and in developing nations worldwide. The claim has been made that chrysotile asbestos can be used “safely” under “certain conditions” in those nations. That claim is not accurate. The Collegium Ramazzini, an international learned society in environmental and occupational medicine, has called for an immediate worldwide ban on all sales and uses of all forms of asbestos, including chrysotile. The rationale for this ban is threefold: (1) that safer substitute materials are readily available, (2) that “controlled” use of asbestos is not possible, and (3) that the health risks of asbestos are not acceptable in either the industrialized or the newly industrializing nations.
This paper focuses on the prevention of IgE-mediated symptoms of the eyes and airways caused by exposure to acid anhydrides in the workplace. Acid anhydrides are widely used in the production of alkyd resins and as curing agents for epoxy resins. Heavy exposure to acid anhydrides causes severe irritation. However, reports of direct irritation of mucous membranes or skin are rare in recent years, since a package of multiple engineering controls has been introduced to reduce exposure. On the other hand, acid anhydrides are well-known industrial inhalant sensitizers and can cause occupational allergy even at very low exposure intensities. Therefore, safe use in industry demands both control of the level of exposure causing allergic diseases in the workshop and programmes for prevention of occupational allergy.
This study was conducted to determine if exposure to 50Hz magnetic field (MF) affects intracellular calcium ([Ca2+]i). We employed flow cytometry for real-time detection of possible changes in [Ca2+]i in a large number of cells. A solenoid coil for vertical MF exposure and a multiple-loop square-coil for horizontal MF were utilized. In the laboratory, background 50Hz MF was less than 0.08μT when all necessary equipment was powered. Rat thymocytes were exposed to 0.1mT horizontal or vertical field, or to 0.14mT circularly polarized field for 30min; the effects of consecutive exposures to vertical and horizontal MFs, or vice versa, for 20min each also were examined. In addition, intact thymocytes or lectin-activated thymocytes, splenocytes and peripheral blood lymphocytes were exposed to the 5mT vertical field for 30min. In all these experiments, no alteration in [Ca2+]i was evident. As a positive control, a calcium ionophore always was added to the medium following MF exposure to verify that the cells were capable of increasing [Ca2+]i and the system would record the response. The data indicate that MF exposure had no effect on [Ca2+]i under any of the conditions examined.
The purpose of this study was to clarify the effect of silica-induced cytosolic free calcium mobilization and cell injury in immortalized cell lines from transgenic mice kidney harboring SV40 T-antigen gene. The proximal convoluted tubule (S1)- and the inner medullary collecting tubule (IMCT)- originated cell lines were used. Cytosolic free calcium concentration ([Ca2+]i) was measured employing Fura-2 fluorescence and cell injury was evaluated by a vital dye exclusion procedure. Silica increased [Ca2+]i in a concentration-dependent manner in S1 (60μg/ml-600μg/ml) and IMCT (6μg/ml-600μg/ ml). Silica caused a biphasic increase in [Ca2+]i which was composed of an initial rapid rise and following sustained phase. Ca2+ removal from the medium resulted in abolishment of initial and sustained phase of silica (600μg/ml)-induced [Ca2+]i in both cell lines. Silica-induced cell injury was increased in a dose-dependent manner. This silica-induced cell injury was attenuated by the pretreatment with EGTA (100μM) and nifedipine (1μM). Cellular ATP content ([ATP]i) by silica also decreased in a concentration-dependent manner. The relationship between [Ca2+]i and [ATP]i showed that [ATP]i depletion caused [Ca2+]i to rise. This study suggests hat 1) the elevation of [Ca2+]i caused by silica is due mainly to influx through plasma membrane Ca2+ channel and non specific membrane damage (at high concentration) and 2) nephrotoxicity of silica shows site-specificity within the kidney.
A new tissue digestion method is proposed to recover man-made mineral fibers (MMMFs) from lungs, which is an improved Kjeldahl method using microwaves. Tissue digestion is carried out under five different conditions in this experiment, and the most suitable condition is found as follows; dried rat lung (0.5g of wet weight) is put into a flask with 0.1ml of H2SO4 and 2.0ml of HNO3, and treated by microwaves for 5min. After the treatment, 1.0ml of H2O2 is added immediately and the sample is treated again under the same condition. Pure samples of glass fibers and refractory ceramic fibers are treated by this proposed method. Numbers and sizes of the fibers are measured before and after the treatment on enlarged photos taking by a scanning electron microscope. As no significant changes are observed in fiber dimensions and numbers, the proposed method is shown to be applicable to recover these MMMFs from lungs.
The amount of airborne lead absorbed by the body during occupational exposure depends not only on lead concentration in workplace air, but also on the granulometric distribution of the aerosol. The Occupational Safety and Health Administration (OSHA) set the lead Permissible Exposure Limit (PEL) at 50μg/m3 on the basis of Bernard's model and a number of assumptions, including assumption “C”, which predicts that the first 12.5μg/m3 are made up of fine particles (aerodynamic diameter <1μm) whereas the remaining 12.5μg/m3 consist of particles >1μm. Occupational exposure to airborne lead at a concentration of 50μg/m3 and a granulometric distribution calculated according to the above mentioned assumption, leads, in the model, to a mean blood level of 40μg/dl. In the present study, we tested the validity of assumption “C” in the environmental air of a factory that manufactured crystal glassware containing 24% lead oxide. An 8-stage impactor was used to measure the particle size of airborne dust collected from personal and area samplings. Results indicate that, on the whole, assumption “C” cannot be considered valid in the work environment investigated in this study. As a result, lead absorption levels in exposed workers may be noticeably different from those predicted by the OSHA model. We therefore suggest that in order to make a correct evaluation of the risk of occupational exposure to lead, it is essential to integrate total airborne lead concentration with a measurement of the granulometric distribution of the aerosol.
Man-made mineral fibers (MMMF), most of which are referred to as man-made vitreous fibers (MMVF), are mostly amorphous silicates manufactured from glass, rock, or other minerals. Analysis for MMMF have been restricted largely to the measurement of total airborne mass concentrations, but more recently to the determination of airborne fiber levels by phase contrast optical microscopy. In Korea, many small factories are related with manufacturing and using MMMF without any special evaluation of environmental measurements. Though MMMF are known as the substitute of asbestos and their toxicity are regarded as very low, MMMF do not totally excluded from the respiratory and/or skin diseases now. Therefore, we evaluated the environments of many workplaces with total dust and fiber concentration. Most dust and fiber concentrations were below threshold limit value (TLV) at various industries and working processes. However, these data showed a slight relationship between total dust and fiber concentration.
To determine which parameters are useful for the risk assessment of man-made mineral fibers (MMMFs), we examined the gene expression of interleukin-1α (IL-1α), tumor necrosis factor α (TNFα), interleukin-6 (IL-6) and inducible nitric-oxide synthase (iNOS) in mineral fiber-exposed alveolar macrophages (AMs). Male Wistar rats were intratracheally exposed to saline or mineral fibers suspended in saline (2mg of crocidolite, chrysotile, alumina silicate refractory fiber (RF1) or potassium octatitanate whisker (TW)). Bronchoalveolar lavage was performed 4 weeks after the fiber-instillation, and the recovered AMs were stimulated by lipopolysaccharide for 2 or 6 hours. Expression of IL-1α, TNFα, IL-6 and iNOS from AMs was observed using reverse transcription-polymerase chain reaction (RT-PCR). The levels of IL-1α and IL-6 mRNA induced by mineral fiber exposure were greatest in AMs exposed to TW, crocidolite, chrysotile and RF1 in that order. However, both gene expression of iNOS and TNFα were not elevated in both crocidolite and TW exposure, despite their high pathological potential. These data suggested that IL-1α and IL-6 may be useful indicators for the risk assessment of MMMFs.
This study was performed to determine whether chromium exposure increased 8-hydroxydeoxyguanosine levels in respiratory epithelial and white blood cells of chromate pigment workers. The subjects of this study were 22 chromium pigment workers and 16 controls in a chromate pigments factory. To estimate the level of exposure, hexavalent chromium concentrations in the factory air were measured. Chromium concentrations of venous blood and spot urine, and 8-hydroxydeoxyguanosine levels in DNA extracted from sputum and white blood cells were determined. Correlation coefficients were calculated between them and their statistical significance was tested. Hexavalent chromium concentration in the factory air ranged from below limit of detection to 0.5150 mg/m3. Chromium levels in blood and 8-hydroxydeoxyguanosine levels in DNA extracted from venous blood and sputum were not statistically different between the two groups. Urine chromium level was significantly higher among workers. Among the correlation coefficients between blood chromium concentration, urine chromium concentration, blood 8-OH-dG level, and sputum 8-OH-dG level, none was statistically significant for workers, controls, and total subjects. Duration of employment did not show any significant correlation with those four variables, either. These results suggest that neither the hydroxyl radical nor 8-hydroxydeoxyguanosine is formed by the reduction of hexavalent chromium, or that one or both of these is formed and then effectively removed by oxygen free radical scavengers or 8-hydroxydeoxyguanosine repair enzymes. Since increased exposure to hexavalent chromium did not result in increased 8-hydroxydeoxyguanosine levels, it is unlikely that hexavalent chromium induces lung cancer through 8-hydroxydeoxyguanosine formation.
In order to study and compare genetic damage induced by 10 kinds of man-made mineral fibers (JFM fibers) in cells, human lung epithelial cells (A549) were exposed to JFM fibers and chrysotile for 1h, then single-cell gel electrophoresis (SCGE) assay was used to detect DNA strand breaks, DNA-DNA interstrand crosslink and the ability of DNA to repair; The results showed that all 10 JFM fibers could induce DNA strand breaks, DNA-DNA interstrand crosslinks and inhibit the ability of DNA repair. When human embryo lung (HEL) cells were exposed to JFM fibers and chrysotile for 24h respectively, the chromosomal aberration was analyzed and the results showed that chrysotile and most of JFM fibers at 5.0μg/ml induced structural chromosomal aberration, but all of these effects were lower than that of chrysotile and were different among them, suggesting that 10 types of JFM fibers had genotoxicity with different degree in vitro, but all of them were lower than that of chrysotile.
Asbestos fibers have been used in industry for decades. Deleterious effect of asbestos on the lungs has been documented. However, the mechanism of asbestos related diseases has not been fully explained yet. Numerous papers suggest there is a role of reactive oxygen intermediates (ROI) in asbestos-induced lung disease development. The excess ROI produced can be removed from the lungs by enzymatic and nonenzymatic antioxidants. The aim of our study was to compare the levels of antioxidants (ascorbic acid, retinol, α-tocopherol, glutathionperoxidase) as well as some markers of lung injury (lipid peroxides, total amount of protein, alkaline phosphatase) in asbestos treated Wistar-rats both 24hr and 3 months after exposure to those in the controls, and to find out if the changes in antioxidant levels could affect impairment of the lungs. Decreased levels of antioxidants and increased values of lung tissue injury parameters in exposed groups suggest involvement of ROI in the mechanism of asbestos lung disease development, resulting in lung tissue injury, both 24 hr and 3 months after exposure.