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PURPOSE: This study evaluated the pulmonary risk caused by possible respirable dust of Al2O3 and SiO(x) resulting from chairside tribochemical sandblasting procedures in a dental office. MATERIALS AND METHODS: Dust was collected using a trap near the working field, and quantitative morphologic determination and identification were performed with SEM and EDAX. Forty blasting processes (total time 20 minutes) were aimed at a dummy to obtain maximum pollution of the workplace. Respirable dust fraction was measured using personal air samplers with an 8-microm cellulose-nitrate filter and a volume flow rate of 2 L/min. Mass of the respirable dust fraction was determined, and respirable free crystalline silica was identified with the help of infrared spectroscopy. RESULTS: Blasting of metal or ceramic surfaces with tribochemical agents produces respirable and potentially harmful SiO(x) and Al2O3 particles with a diameter of less than 5 microm, showing a total concentration in the air of less than 0.3 mg/m3. With and without dental suction, the concentration of the respirable free crystalline silica was smaller than 0.02 mg/m3. CONCLUSION: Concern regarding the risk of chairside tribochemical methods and possible impairment of health of patients and dental staff is unfounded, even under extreme conditions or without protective measures, since the concentrations of SiO(x) found in the air of the workplace were far below the current threshold value of 0.15 mg/m3. [ABSTRACT FROM AUTHOR]

The aim of the study is to examine the cancer-predictive values of SMRP (soluble mesothelin-related peptides), CA125, and CYFRA21-1 as potential tumor markers for lung cancer and malignant mesothelioma in a cohort of workers formerly exposed to asbestos. A voluntary surveillance program has been established for German workers with former asbestos exposure. A subgroup of 626 subjects with a mean age of 63 years (range 53-70 years) at baseline was enrolled in an extended health examination program with high-resolution computer tomography (HRCT) of the chest and blood drawing between 1993 and 1997. Serum concentrations of SMRP, CA125, and CYFRA21-1 were measured in archived serum samples in 2005 and 2006. A mortality follow-up was conducted through 2007. So far, 12 cases with lung cancer and 20 cases with malignant mesothelioma have been observed in this cohort. The average time between sample collection and diagnosis was 4.7 years. Analyzed biomarkers showed low sensitivities (5-25%) and positive predictive values (4-30%) for both cancer sites. Marker combinations resulted in sensitivities between 5 and 50% and positive predictive values ranging from 3 to 14%. Even in those cases, where biomarker concentrations were available within 36 months before diagnosis, no trend for increasing biomarker levels was observed. The analyzed tumor markers were characterized by high specificities, but low sensitivities. SMRP, CA125, and CYFRA21-1 alone or in combination were less suitable to serve as predictors for the diagnosis of lung cancer or malignant mesothelioma. However, a prospective study with annual sampling might reveal a better predictive value of these markers. [ABSTRACT FROM AUTHOR]

Presents a study that correlated the prevalence of respiratory tract symptoms and diseases with dust and fibre exposure in the soft tissue producing industry in Germany. Methods; Results; Conclusions.

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Objective: The aim of this study was to determine low molecular weight (LMW)-DNA fragmentation changes after white blood cell (WBC) incubation in lysis buffer followed by constant-field gel electrophoresis (CFGE). WBCs were isolated from blood samples of workers highly exposed to asbestos fibres at the workplace in Germany, and were compared with those from healthy adults. This study was conducted parallel to the study presented in our preceding paper (Marczynski et al. 2000b) in which we described significant increases in the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG) adducts in the DNA of white blood cells from the same highly exposed workers relative to the levels found in the control group in all three study years (1994 to 1997). Method: We found that 15-h incubation in lysis buffer of WBCs embedded in agarose-plugs from healthy control donors with 2% SDS, proteinase K and Na2-EDTA at 42 °C followed by 0.5 h at 4 °C produced a characteristic DNA fragmentation pattern below 23 kbp using CFGE. Results: In the 1st year of the study (1994–1995) changes were found in LMW-DNA fragmentation in 54.8% of the asbestos workers studied, compared with the DNA fragmentation pattern of controls. Interestingly, in the 2nd year of the study (1995–1996) changes in DNA fragmentation were found in only 39.9% of exposed subjects. In the 3rd year of the study (1996–1997) the highest number of workers exposed to asbestos (67.3%) with changes in the LMW-DNA fragmentation pattern was found. The Chi-square test for each year of the study revealed significant changes (P < 0.001). These changes may be due to the presence of hydrogen peroxide (H2O2), as has been shown in vitro. It is likely that a Fenton reaction involving the heterolytic reduction of H2O2 by traces of reduced transition metals such as Fe2+ and Cu+ is involved in the fragmentation of DNA. No difference was found in the changes in DNA fragmentation between asbestos-exposed subjects with and without benign asbestos-associated diseases (asbestosis, asbestos-associated pleural plaques). Significant correlations were not found after analysis of the changes in DNA fragmentation in relation to different possible occupational and non-occupational confounding factors, such as the duration of asbestos exposure, the latency period, estimated cumulative fibrous dust dose (“fibre-years”), and non-occupational confounding factors, such as age, smoking status, acute febrile infections, the intake of medicines, aspirin, Ca2+, Mg2+ and/or hormones, the intake of vitamins, and cases of cancer. Conclusions: Our data confirm that oxidative stress occurs in the WBCs of workers highly exposed to asbestos fibres, thus supporting the hypothesis that asbestos fibres damage cells through an oxidative mechanism. Oxidative stress and oxidative DNA damage may be induced by long-term exposure to asbestos. The new insights into the oxidative effects of asbestos fibres are of great importance because they provide a way forward for new preventive strategies. Preventive and therapeutic approaches using antioxidants should be taken into consideration. [ABSTRACT FROM AUTHOR]

The ILO classification of pneumoconiotic changes in the lungs and pleura has become a standardized and widely accepted method of documentation in occupational medicine. Recently a classification system for computed tomography/high-resolution computed tomography (CT/HRCT) findings in the lung has been proposed as well. For both classification systems, computed-assisted programs have been developed that allow the storage and archiving of the results as well as further statistical processing. The programs are compatible with usual hardware configurations, have a comprehensible and transparent structure, and are easy to learn and adaptable to individual needs. The use of the computer-assisted classification systems is presented in the example of an insulator exposed to asbestos. The system of data documentation and processing has proved to be very practicable in the more than 2000 patients studied thus far. [ABSTRACT FROM AUTHOR]

The standard ILO classification for pneumoconiotic changes using conventional X-ray films has become well established. In recent years computed tomography has played an increasing role in occupational medicine and above all in the assessment of pneumoconiosis. Therefore a standardised method of classification for CT also seems necessary. A system of classification developed by occupational hygienists and radiologists allows a detailed description of parenchymal and pleural changes and the use of 28 additional symbols. Furthermore, special diagnoses relevant to occupational medicine and additional comments can be made. The classification system was tested in practice in the research project 'Early diagnosis of asbestos-related diseases' ( Frühdiagnostik asbestverursachter Erkrankungen). It was shown to be both practicable and easily reproducible, intra-individually and interindividually. [ABSTRACT FROM AUTHOR]

Forty manual metal arc welders welding stainless steel (SS) were monitored for 1-7 workdays measuring total chromium (Cr), water-soluble hexavalent Cr, and nickel (Ni) in the working atmosphere, and Cr and Ni in blood and urine. The mean daily increase was 1.0 μg Cr/l in plasma and 5.6 μg Cr/g creatinine in urine. There were significant correlations between total Cr and Cr in air and the total Cr in biologic fluids. This was not the case for the corresponding correlations for Ni. The observed correlations between urinary and plasma Cr levels may permit interchange of these body fluids for biologic monitoring at high exposures. The results indicate that urine sampled after work is a body fluid versatile for routine monitoring of Cr in SS welders. Smokers had higher levels of Cr in biologic fluids than did nonsmokers at equivalent levels of air Cr. The results also indicate that filter masks provide better protection against uptake of Cr in the airways than air-stream helmets. [ABSTRACT FROM AUTHOR]

After inhalative occupational exposure to certain compounds containing nickel and chromium (mostly over many years), an accumulation of these metals may occur in the lung tissue. This is of particular importance, both from a toxicological point of view and with regard to expert reports, since certain nickel and chromium compounds may induce lung cancers. In the context of this study, samples of pulmonary tissue from 34 deceased persons from the Bergen area (Norway) were analysed by atomic absorption spectrometry with regard to their content of chromium and nickel. The deceased comprised 21 men and 13 women. In 15 cases, death resulted from lung cancer; in the other 19 deceased, there was no indication of a malignant disease of the airways. The concentrations of nickel found in the lung tissue do not differ between patients with lung cancer and patients with healthy lungs. On the other hand, the concentration of chromium in the pulmonary tissue in the patients who had died of lung cancer and who had all been inhalative smokers, are higher (statistically significant) than in the nonsmokers or in those with healthy lungs. An accumulation of these two metals in the tumor matrix could not be detected. Both the average nickel and the average chromium concentrations were higher in the persons who had probably been exposed occupationally. Considering the present state of scientific knowledge, the aspects relevant to expert reports which result from the analyses of metals in the pulmonary tissue are discussed. [ABSTRACT FROM AUTHOR]

For the period from 1973 to the end of 1986, 70656 data sets on occupational preventive medical examinations in employees exposed occupationally to asbestos dust (G 1.2) were made available to us by the Central Registry for Employees Exposed to Asbestos Dust (ZAS). On the basis of this data, an analysis of asbestosis risk was to be made in relation to specific areas of work, taking into consideration the beginning and duration of exposure. Proceedings for declaratory appraisal in accordance with occupational disease no. 4103 were instituted in 1760 cases in the report period. In accordance with the character of the available data, the X-ray findings in the lungs were available from the persons investigated as parameters of possible asbestosis risk on the basis of coding consistent with the International Pneumoconiosis Classification (ILO U/C 1971 and/or ILO 1980 West Germany). The major result of the statistical analyses on the mainframe macrocomputer of the University of Erlangen-Nuremberg was that the relatively highest risk of asbestosis was present in persons whose exposure began before 1955. On the other hand, with increasing duration of exposure, an unequivocal rise of the asbestosis risk could not be detected on the basis of the overall population. In relation to the individual fields of work, the relatively highest risk of asbestosis was shown to be in the asbestos textile and paper industry, as well as in the asbestos cement industry. No detectable risk of asbestosis was present in the fields of mining, traffic and health service and for women in the industrial sectors of building material, gas and water, catering trade, building, commerce as well as banking and insurance. Accordingly, it can be assumed that certain fields of work are or were exposed to such a small extent or not at all that a risk of asbestosis which is relevant in terms of occupational medicine is no longer to be assumed or was not to be assumed. This applies above all to certain work in the frictional coating (brake lining) and asbestos paper industry. Furthermore, the analysis of the data material did not provide any unequivocal indications that inhalative smoking habits have a negative effect on the risk of asbestosis. In prinicple, it can be stated that the occupational preventive medical investigations according to G 1.2 are effective. However, irrespective of this, the analysis has shown that a regular exchange of experience on the part of authorized physicians should be institutionalized and the second X-ray appraisal should be retained in order to ensure a high measure of reliability and diagnostic relevance of the available investigation data. Besides this, all expert appraisal results from patients with recognized occupational diseases according to subparagraphs, 4103, 4104 and 4105 BeKV (no. 4103: asbestosis, no. 4104: asbestosis in connection with lung cancer, no. 4105: mesothelioma of the pleura or peritoneum) should be centrally registered both in persons exposed to asbestos dust and in persons with asbestosis and accompanying malignant diseases, would then be possible. [ABSTRACT FROM AUTHOR]

Nickel (Ni) and some of its relatively insoluble compounds as well as chromates may be able to induce cancer in the region of the lungs, as well as in the nose and paranasal sinuses after occupational exposure. Latency periods may amount to 20 years and more. The results of recent investigations have shown that these metals cumulate in the lung tissue after inhalation of relatively insoluble chromium and nickel compounds. The quantitative detection of these heavy metals in samples of pulmonary tissue hence permits the amount of past exposure to be estimated. To establish the normal values, samples of pulmonary tissue from 30 normal subjects were investigated for chromium and nickel content. The samples were taken from different segments and lobes of the lungs, taking topographical anatomical criteria into consideration. In addition, 15 persons who had formerly been exposed to nickel and/or chromium (11 nickel refinery workers, of whom 10 had died of lung cancer, 2 stainless steel welders, 1 foundry worker, 1 electrical technician) were also investigated. From the results of 495 tissue samples from the normal group, median chromium concentrations between 130 and 280 ng/g were calculated, with median nickel concentrations of 20-40 ng/g (wet weight). If these values are related to the nickel concentrations measured in refinery workers, values 112-5,860 times higher were found. The concentrations were about 500 times higher than normal for nickel, and about 60 times higher than normal for chromium in the stainless steel welders. For the foundry workers who died of lung cancer, chromium and nickel concentrations in the normal range were calculated, with the exception of the nickel concentrations in the upper and lower lobes of the right lung. The very high nickel concentrations found in the samples of lung tissue from former nickel refinery workers should be regarded as a guideline with regard to the appraisal of the causal relationship between lung cancer and occupational exposure to relatively insoluble nickel compounds. This result is also supported by epidemiological investigations on this subgroup and must thus be considered etiologically conclusive. For the welders, chromium and nickel concentrations were found that were markedly above normal, but as yet there is no epidemiologically reliable verification for the increased occurrence of malignancies in this occupational group. On the basis of present scientific knowledge, no indications were found of relevant chromium and/or nickel exposure of the lung tissue that might be able to induce lung cancer in either foundry workers or for electric technicians. [ABSTRACT FROM AUTHOR]

Thallium and its compounds have a high toxic potency. For the production of particularly resistant sorts of cement, additives containing thallium, among other things, are employed. In conformity with our present toxicological knowledge, the determination of the concentration of thallium in the urine must be considered a suitable parameter for the assessment of the presence of thallium in the body. Occupational-medical preventive examinations were carried out in a total of 128 male employees from all areas of production in three cement factories. An exposure of these employees to thallium was objectified by analyses of the roasted pyrites employed and the dust from the electric filter. The study included the questioning of the employees with respect to their previous history of health, and also a physical examination aimed at detecting clinical symptoms of a possible effect of thallium. The analysis of thallium was carried out in samples of 'spontaneous' urine. The analytical method employed was flameless atomic absorption spectroscopy (carbon-rod atomizer). In part, the group of persons investigated revealed excretions of thallium slightly or moderately above the normal level (range: < 0.3-6.3 μg/g creatinine). As the upper normal limit of thallium excretion, we computed a value of 1.1 μg/g creatinine. In no case, however, did the case history data or the findings of the physical examination reveal any indication of the symptoms characteristic of thallium poisoning. [ABSTRACT FROM AUTHOR]

Neutralizing selenic acid with caustic soda caused a hyperintensive exothermic reaction, with about 450 1 of the reaction mixture erupting in a factory hall. A 44-year-old industrial worker was fatally intoxicated, suffering from second-degree skin burns, necrosis of oral mucous membranes and hemorrhagic lung edema. He died 90 min later. Analysis of body fluids and tissue samples showed high selenium concentrations in blood serum, urine, stomach content and lungs. The analytical results are discussed in comparison with normal selenium levels of non-exposed groups. [ABSTRACT FROM AUTHOR]