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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 increasing use of high-resolution computed tomography in formerly asbestos-exposed workers requires valid diagnostic criteria for the findings which have to be reported as suspicious for being asbestos-related in surveillance programmes and for the assessment of causal relationships between former asbestos exposure and findings in computed tomography. The present article gives examples for asbestos-related findings in HR-CT and discusses the specificity of parenchymal and pleural changes due to asbestos fibres., (Georg Thieme Verlag KG Stuttgart New York.)

Asbestos-related diseases still play an important role in occupational medicine. The detection of benign asbestos-related diseases is one condition for the compensation of asbestos-related lung cancer in Germany. Due to the increasing use of computed tomography, asbestos-related diseases are more frequently detected in the early stages. The present article proposes recommendations for the findings which have to be reported as suspicious for being asbestos-related based on a) chest X-rays and b) computed tomography using the International Classification System for Occupational and Environmental Respiratory Diseases (ICOERD)., (Georg Thieme Verlag KG Stuttgart-New York.)

The classification of pneumoconiosis according to ILO standard - comparing a X-ray of the lung with ILO radiographs - is well established in Germany. The extension of digital imaging is a challenging task in occupational medicine as well as in pneumology. Technical requirements are not known sufficiently and the necessary equipment is not well distributed. This paper describes the current position on recording, assessment and documentation of digital imaging of the lung and pleura.

The ILO (1980) Classification has been revised during recent years. The new version is now available as the International Classification of Radiographs of Pneumoconioses (Revised edition 2000). The Guidelines booklet is currently available only in English. Those involved felt it was important to maintain continuity with the ILO (1980) edition, in particular to retain the standard radiographs, despite their restricted quality, so as to ensure comparability with earlier national and international data sets. The standard films illustrating pleural abnormalities, and 'u'-shadows, have been modified and reconstituted. The most important changes relate to assessment of film quality, pleural abnormalities, and additional symbols. In Germany, film quality is characterised as "+", "+-", "+--" and "u" according to whether the ability to assess pneumoconiosis is judged to be unimpeachable ("+") to unusable ("u"). If a film is not classified as "+", then written comments regarding defects are required. For "diffuse" pleural thickening, the ILO (2000) edition now requires the presence also of obliteration of the costophrenic angle. This was not required in the earlier (1980) edition and, as previously, is also not stipulated in the German version. A minimum width of 3 mm (previously 0-5 mm), coded "a", is required both for plaques as well as for the margin to the lateral chest wall. Congruence is thus achieved for criteria, which, in German practice, lead to an indication of suspect occupational disease. Plaques on the diaphragm are not considered for measurement of extent; they are only coded as present or absent. If calcification is identified, then this must also be classified and measured as a localised plaque. Extent of calcification on its own, previously coded "0" to "3", is no longer specified. The following new symbols, illustrated by new diagrams, have been introduced: aa = atherosclerotic aorta; at = apical thickening; cg = calcified granuloma (or other non-pneumocononiotic nodules); me = mesothelioma (already previously differentiated from "ca" on the German record sheet); pa = plate atelectasis; pb= parenchymal bands; ra = rounded atelectasis; od = other disease. (Examples of the latter are illustrated diagrammatically by lobar pneumonia, aspergilloma, goiter and hiatal hernia.) Earlier national differences (ILO 1980/German Federal Republic) on particular issues have also been agreed among German "double-readers" ["Zweitbeurteiler"]. However, conformity between the original (ILO 2000) text and the national (German) modified text has been retained in large measure. The detailed descriptions of the standard films differ in certain respects from the German (1980) definitions. Some revision of individual descriptions of the films are proposed. Except for a few differences, agreement was reached here too. The definitive date for the change in Germany is expected to be in early 2004. The standard films are already available now through ILO offices in Geneva or Bonn (addresses in appendix.)

Background and Objective: Laryngeal diseases caused by exposure to asbestos are listed in the current German list of occupational diseases under number 4104. Parallel to a multicenter study to evaluate whether a CT scan should be included in the examinations for occupational diseases according to the German surveillance guidelines, an additional ENT examination was evaluated., Patients and Methods: One hundred workers with a mean exposure time to asbestos of 20.9 years were given a complete ENT examination in 4 consecutive years (1993-1996). Radiological signs for asbestosis were observed in 21 cases and 58 participants had pleural affections caused by asbestos. Significant nicotine abuse was reported by 15 persons: 61 participants were ex-smokers and 24 had never smoked. Regular alcohol consumption was reported by 90% (11% more than 80 g/day)., Results: As documented in the literature, we found a high prevalence of laryngitis, especially in smoking patients. One patient had early laryngeal cancer (T1)., Conclusion: The integration of an ENT examination into the German surveillance guidelines for occupational diseases should be discussed for patients with a high exposure to asbestos.

In the preceding paper [B. Marczynski, P. Rozynek, T. Kraus, St. Schlösser, H.J. Raithel, X. Baur, Levels of 8-hydroxy-2'-deoxyguanosine in DNA of white blood cells from workers highly exposed to asbestos in Germany, Mutat. Res. (2000) submitted] we described significant increases (p<0.001) in the levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) adducts in the DNA of white blood cells (WBC) of workers highly exposed to asbestos fibers at the workplace relative to those found in the control group in all three study years (period between 1994 and 1997). The results show that the oxidative DNA damage in exposed individuals is between 1.7 times and twice that found in control samples for all 3 years of the study (p<0.001). The aim of this study was to examine the association between the 8-OHdG levels in WBC DNA of workers highly exposed to asbestos fibers at the workplace and clinical data, occupational and non-occupational confounding factors, and cancer. There is no obvious correlation between the steady-state levels of 8-OHdG in the circulating WBC DNA of asbestos workers and possible confounding factors, such as the presence of benign asbestos-associated diseases, the duration of asbestos exposure, the latency period, the fixed cumulative fibrous dust dose ("fiber years"), age, smoking status, acute febrile infections, medicines, aspirin, calcium (Ca(2+)), magnesium (Mg(2+)), and the hormone and vitamin intake. This indicates that previous inhalation of asbestos fibers is the major factor responsible for the difference observed in oxidative DNA damage between asbestos workers and controls. For patients suffering from respiratory cancer, cancer of the gastrointestinal tract, mouth/pharynx/larynx, and urogenital tract the mean DNA-adduct level was significantly higher (p<0.01) than that found in controls, but not significantly higher (p>0.05) than that for asbestos-exposed patients without tumours. The formation of 8-OHdG adduct levels in WBC DNA of patients with hematopoietic cancer, chondrosarcomas and multiform glioblastomas was not significantly higher than that found in the control group (p>0.05). Our results support the hypothesis that oxidative DNA damage in man caused by asbestos fibers plays a role in the formation of malignant tumours.

Asbestos fibers have genotoxic effects and are a potential carcinogenic hazard to occupationally exposed workers. The ability of inhaled asbestos fibers to induce the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the DNA of white blood cells (WBC) of workers highly exposed at the workplace has been studied. The 8-OHdG adduct level of asbestos-exposed workers was significantly increased (p<0.001) compared to that in the control group in all three years of the study. Asbestos-exposed individuals showed a mean value of 2.61+/-0.91 8-OHdG/10(5) dG (median 2.49, n=496) in 1994-1995, 2.96+/-1.10 8-OHdG/10(5) dG (median 2.76, n=437) in 1995-1996 and 2.55+/-0.56 8-OHdG/10(5) dG (median 2.53, n=447) in 1996-1997. For the control subjects, a mean of 1.52+/-0.39 (median 1.51, n=214) was determined. The results indicate that human DNA samples from exposed individuals contain between 1.7 times and twice the level of oxidative damage relative to that found in control samples in all 3 years of the study. The studies presented here show that asbestos exposure can result in oxidative DNA damage. Our data confirm that oxidative DNA damage occurs in the WBC of workers highly exposed to asbestos fibers, thus supporting the hypothesis that asbestos fibers damage cells through an oxidative mechanism. These in vivo findings underline the importance of oxidative damage in asbestos-induced carcinogenesis and highlight the need for exploring the molecular basis of asbestos-induced diseases, and for more effective diagnosis, prevention and therapy of mesothelioma, lung cancer and pulmonary fibrosis. In addition, preventive and therapeutic approaches using antioxidants may be relevant.

Controversy exists as to whether occupational asbestos dust exposure is responsible, or at least partially responsible, for the development of laryngeal carcinoma. The aim of this study is to present the current scientific knowledge on this subject based on a comprehensive literature research and to critically review the epidemiological investigations published. The results of 31 cohort studies and 24 case-control studies, and the conclusions in 11 more recent reviews are contradictory. In most studies there was no statistically significant indication of a casual relationship. It is noteworthy that an increased risk of laryngeal carcinoma among persons exposed to asbestos dust was observed mostly in older studies in which smoking habits and/or alcohol consumption as the most important nonoccupational risk factors were usually not taken into account. In addition, since most of the calculated positive associations are very weak, no reliable conclusion can be reached. While there may be a causal relationship between occupational exposure to asbestos dust and the occurrence of laryngeal carcinoma, this cannot be regarded as certain on the basis of the evidence reviewed.

According to the current regulations pertaining to occupational diseases lung cancer and mesothelioma can be compensated as asbestos-related malignomas under certain circumstances. For several years there has been controversial discussion as to whether laryngeal carcinomas can also be caused by occupational asbestos exposure and should therefore be added to the list of occupational diseases. Critical evaluation of the available scientific knowledge with the scope of currently applicable regulations does not warrant adding asbestos-related laryngeal carcinomas to the list of occupational diseases at present. Further investigations are urgently necessary and may possibly bring new insights.

Nickel (Ni) and chromium (Cr) and some of its compounds may be able to induce cancer in the lungs as well as in the nose and paranasal sinuses after occupational exposure. Latency periods amount to 20 years and more. Therefore objective exposure data are not available in the most cases and expert evaluation of the causal connection is often difficult. Recent investigations have shown, that Ni and Cr can cumulate in human lung tissue after occupational exposure. For the evaluation of "normal" Ni- and Cr-values a total of 495 human lung tissue samples of 30 occupationally non-exposed persons were analysed by AAS including ZEEMAN-compensation after wet oxidative digestion. Additional samples of 10 deceased persons who have been occupationally exposed to nickel in previous times by nickel-refining and welding, especially flame spraying have been investigated. The median Ni- and Cr- concentrations in the lungs of the non-exposed persons ranged between 20-40 resp. 133-277 ng/g (wet weight). In nickel refinery workers Ni- concentrations were found which exceeded the normal range about 1,000. In welders, especially flame sprayers, also values more than 100 times higher could be analysed for Ni and Cr. Partially these concentrations were found years after the end of the inhalative exposure.

The world-wide experience with millions of metallic implantations suggests the biocompatibility of modern alloys, commonly made of cobalt, chromium and nickel. There is, however, little information available on the internal metal exposure resulting from implants. In this study we assessed the metal concentrations in body fluids and tissue samples (muscle, bone) of patients who had undergone total hip replacement. Our patients were divided up into two groups. One group had firmly fixed implants two years after surgery. The other group had loose implants of the same Co-Cr-Mo alloy. Urine analyses revealed an increased renal elimination of nickel, chromium and cobalt. Cobalt and nickel exceeded the upper normal value. In serum the concentrations of nickel and chromium were normal or slightly elevated, the cobalt concentrations were significantly elevated. In some cases tissues adjacent to the implant showed extremely high concentrations of chromium and cobalt. This finding was also obtained in tissues that had no direct contact with the arthroplasty. The findings suggest that alloys of prostheses can undergo corrosion and release metal ions.

The two hepatitis B vaccines produced by gene technology that are presently available in Germany, were compared in respect of efficacy and tolerance in 80 nurses (female and male) who were under training. Both vaccines proved to be highly effective and well tolerated. In respect of the achieved anti-HBs titer, however, the two vaccines differed significantly from each other. Using the 20 micrograms HBs antigen, the antibody titers obtained were higher by a factor of 1.8. The article gives update recommendations in respect of hepatitis B vaccination as a preventive measure in risk groups.

Epidemiological studies have shown that occupational exposure to certain chromium and nickel compounds is followed by an increased lung cancer incidence. However, few data exist on the content of these metals in lung cancer patients in general. In the present study, central and peripheral lung tissue, bronchial tissue and hilar lymph nodes were collected from 20 patients with bronchial carcinoma and 21 control individuals, and the tissue concentration of chromium and nickel was measured by use of atomic absorption analysis. Increased levels of both metals were found in cancer patients as compared to controls. Lung tissue concentration of chromium was two-fold increased, while the bronchial wall content of nickel was three times the level in control individuals. Smokers showed a dose-related increase in the deposition of both chromium and nickel. Furthermore, in cancer patients an inverse relationship between smoking and the tissue level of chromium in regional lymph nodes was found, possibly indicating a depressive effect on pulmonary clearance mechanisms. Our results emphasize the possible role of small amounts of chromium and nickel as agents in bronchial carcinogenesis, unrelated to occupation and probably related to tobacco smoking.

In recent years reports on nickel-related diseases in the Federal Republic of Germany have been increasingly frequent. As a result, medical scientific institutions were called upon to clarify both the occupational medical and clinical, as well as the toxicological aspects of the situation. The main clinical finding was the increased incidence of malignant neoplasias in the respiratory tracts, in particular after many years of nickel exposure in refineries. Between 1967 and 1981, seven malignant neoplasms were legally recognized as occupation-related. Additionally, in the last two years, the existence of nickel-induced malignant neoplasms has been suspected in 16 cases, and the statutory procedure for the recognition of occupational diseases instituted. Our overview presents occupational-medical and clinical aspects. Among allergic nickel-induced conditions, eczematous skin diseases predominate. In addition, case reports of asthma have been published. Statistical evaluations showed that up to 17% of all occupational allergies may be related to occupational exposure to nickel. In this situation, preventive measure are of particular importance. To estimate exposure levels, both the measurement of the agent at the workplace and the quantitative determination of nickel in biological material can be used. The measurement of nickel excretion by the kidney has proved particularly useful in occupational medicine. In addition to clinical surveillance, it is recommended that this measurement should be performed on exposed persons at regular intervals.

Environmental pollution with carcinogenic substances, in addition to individual abuse, are discussed as important factors causing development of cancer. We must assume that certain nickel and chromium compounds, which are ubiquitous in our ecosystem, must have carcinogenic effects on humans too. The aim of this study is therefore to examine the extent to which the accumulation of the potentially carcinogenic metal ions nickel and chromium could be measured in tissue from tumour patients. We examined tumour and tumour-free tissue obtained from a total of 48 patients who had carcinomas of the stomach, bowel, or kidney. We also analyzed nickel and chromium content in whole blood and urine samples from these persons. The quantitative metal estimations were done using atomic absorption spectrophotometry. Differences between chromium and/or nickel content in tumour or tumour-free tissue were not observed. An accumulation of these metal ions in tumour tissue is therefore improbable. We were also unable to find differences in metal content with regard to chromium and nickel as related to the appearance of tumour in the organ. In contrast, tumour patients had a 5- to 7-fold increase over normal values for chromium and nickel in blood and urine. This was attributable to unavoidable contamination of tissue and body fluids with chromium- and nickel-containing instruments during major surgical procedures.

Since half a century the toxicity and carcinogenicity of nickel and its compounds is in discussion. Problems coming therefrom are of high relevance concerning occupational medicine. According to the new national and international literature the present findings are described and discussed. Starting from occurrence, refining and occupational hazards, in the first part, toxicologic mechanisms and characteristic symptoms are represented in detail. Inorganic and organic Ni-compounds are handled separately. In the second part of this study we are giving opinion to the questions of carcinogenicity. Experiences to occupationally nickel-exposed workers as well as a review about the topical findings in animal experiments are described. Of importance there are questions referring to the different carcinogenic potential of nickel and its compounds and the influence to techniques of application. Current results to the mechanism of carcinogenesis, which can be derived from animal experiments, are shown. The carcinogenicity for nickel and some especial water insoluble Ni-compounds in human beings must be seen as a fact. Malignoms in the respiratory tract are regarded by workers breathing dust/aerosols of metallic nickel, nickel subsulfide, Ni-oxide and in electrolysis. By critical review of the present literature a cancerogenicity of nickel-carbonyl has to be assumed too. According to this review measures in the field of occupational hygiene and medicine are required. Illness caused by nickel or its compounds should be included to the valid list of occupational diseases in the FRG.