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PubMed1985

Detection of chrysotile asbestos in workers' urine.

Urinary asbestos concentrations were evaluated as an indicator of occupational exposure to chrysotile asbestos via inhalation and ingestion. Detection of asbestos in the urine represents the first step in developing a biological indicator of exposure. Such an indicator could be used to supplement exposure data from workplace air sampling. A biological indicator would be particularly valuable in evaluating workers with intermittent airborne asbestos exposures and in determining if airborne exposure results in penetration of asbestos through the lung or gastro-intestinal tract. Transmission electron microscopy was selected as the most sensitive technique for identification of all sizes of asbestos fibers which might appear in the urine. First morning void urine samples were obtained from six workers (occupationally exposed to chrysotile asbestos in a factory producing roof coatings) and from a control group (six individuals with no occupational exposure). The levels of chrysotile asbestos detected in the urine of five workers were significantly greater than the asbestos concentrations in matched field blanks (both on a number and mass basis). Field blanks were designed to detect asbestos in the urine samples due to contamination which might occur during urine collection. Also, the workers' urinary asbestos levels were significantly greater than the concentrations found in the control group (both on a number and mass basis). Finally, the levels of chrysotile asbestos detected in the urine of two of six controls were significantly greater than those in matched field blanks (both on a number and mass basis). Although the project was not specifically designed to correlate urinary and airborne asbestos concentrations, preliminary data indicated that a correlation did not exist between these factors.

Air Pollutants, Occupational↗

PubMedDate not supplied

Asbestos-related malignancy.

Asbestos-associated malignancies have received significant attention in the lay and medical literature because of the increasing frequency of two asbestos-associated tumors, lung carcinoma and mesothelioma; the wide distribution of asbestos; its status as a prototype environmental carcinogen; and the many recent legal compensation proceedings, for which medical testimony has been required. The understanding of asbestos-associated carcinogenesis has increased through study of animal models, human epidemiology, and, recently, the application of modern molecular biological techniques. However, the detailed mechanisms of carcinogenesis remain unknown. A wide variety of malignancies have been associated with asbestos, although the strongest evidence for a causal association is confined to lung cancer and mesothelioma. Epidemiological studies have provided evidence that both the type of asbestos fiber and the industry in which the exposure occurs may affect the rates of asbestos-associated cancers. It has been shown that asbestos exerts a carcinogenic effect independent of exposure to cigarette smoking that, for lung cancers, is synergistically enhanced by smoking. Other questions remain controversial, such as whether pulmonary fibrosis necessarily precedes asbestos-associated lung cancer and whether some threshold level of exposure to asbestos (including low-dose exposures that may occur in asbestos-associated public buildings) may be safe. Mesothelioma, the most closely asbestos-associated malignancy, has a dismal natural history and has been highly resistant to therapy. However, investigational multi-modality therapy may offer benefit to some patients. A description of the processes through which compensation claims for asbestos-associated malignancies are evaluated illustrates for physicians the legal system's approach to possible injury from toxic substances. The differences between scientific and legal reasoning about the causes of diseases with long latency, especially when they are imputed to toxic exposures are substantial, and may impede the application of toxicological evidence to legal disputes.

Asbestos↗

PubMed2006

Chrysotile asbestos exposure associated with removal of automobile exhaust systems (ca. 1945-1975) by mechanics: results of a simulation study.

For decades, asbestos-containing gaskets were used in virtually every system that involved the transport of fluids or gases. Prior to the mid-1970s, some automobile exhaust systems contained asbestos gaskets either at flanges along the exhaust pipes or at the exhaust manifolds of the engine. A limited number of automobile mufflers were lined with asbestos paper. This paper describes a simulation study that characterized personal and bystander exposures to asbestos during the removal of automobile exhaust systems (ca. 1945-1975) containing asbestos gaskets. A total of 16 pre-1974 vehicles with old or original exhaust systems were studied. Of the 16 vehicles, 12 contained asbestos gaskets in the exhaust system and two vehicles had asbestos lining inside the muffler. A total of 82 samples (23 personal, 38 bystander, and 21 indoor background) were analyzed by Phase Contrast Microscopy (PCM) and 88 samples (25 personal, 41 bystander, and 22 indoor background) by Transmission Electron Microscopy (TEM). Only seven of 25 worker samples analyzed by TEM detected asbestos fibers and 18 were below the analytical sensitivity limit (mean 0.013 f/cc, range 0.001-0.074 f/cc). Applying the ratio of asbestos fibers:total fibers (including non-asbestos) as determined by TEM to the PCM results showed an average (1 h) adjusted PCM worker exposure of 0.018 f/cc (0.002-0.04 f/cc). The average (1 h) adjusted PCM airborne concentration for bystanders was 0.008 f/cc (range 0.0008-0.015 f/cc). Assuming a mechanic can replace four automobile single exhaust systems in 1 workday, the estimated 8-h time-weighted average (TWA) for a mechanic performing this work was 0.01 f/cc. Under a scenario where a mechanic might repeatedly conduct exhaust work, these results suggest that exposures to asbestos from work with automobile exhaust systems during the 1950s through the 1970s containing asbestos gaskets were substantially below 0.1 f/cc, the current PEL for chrysotile asbestos, and quite often were not detectable.

Air Pollutants, Occupational↗

PubMed2005

Asbestos exposure, pleural mesothelioma, and serum osteopontin levels.

BACKGROUND: We investigated the presence of osteopontin in pleural mesothelioma and determined serum osteopontin levels in three populations: subjects without cancer who were exposed to asbestos, subjects without cancer who were not exposed to asbestos, and patients with pleural mesothelioma who were exposed to asbestos. METHODS: A group of 69 subjects with asbestos-related nonmalignant pulmonary disease were compared with 45 subjects without exposure to asbestos and 76 patients with surgically staged pleural mesothelioma. Tumor tissue was examined for osteopontin by immunohistochemical analysis, and serum osteopontin levels were measured by an enzyme-linked immunosorbent assay. RESULTS: There were no significant differences in mean (+/-SE) serum osteopontin levels between age-matched subjects with exposure to asbestos and subjects without exposure to asbestos (30+/-3 ng per milliliter and 20+/-4 ng per milliliter, respectively; P=0.06). In the group with exposure to asbestos, elevated serum osteopontin levels were associated with pulmonary plaques and fibrosis (56+/-13 ng per milliliter) but not with normal radiographic findings (21+/-5 ng per milliliter), plaques alone (23+/-3 ng per milliliter), or fibrosis alone (32+/-7 ng per milliliter) (P=0.004). Serum osteopontin levels were significantly higher in the group with pleural mesothelioma than in the group with exposure to asbestos (133+/-10 ng per milliliter vs. 30+/-3 ng per milliliter, P<0.001). Immunohistochemical analysis revealed osteopontin staining of the tumor cells in 36 of 38 samples of pleural mesothelioma. An analysis of serum osteopontin levels comparing the receiver-operating-characteristic curve in the group exposed to asbestos with that of the group with mesothelioma had a sensitivity of 77.6 percent and a specificity of 85.5 percent at a cutoff value of 48.3 ng of osteopontin per milliliter. Subgroup analysis comparing patients with stage I mesothelioma with subjects with exposure to asbestos revealed a sensitivity of 84.6 percent and a specificity of 88.4 percent at a cutoff value of 62.4 ng of osteopontin per milliliter. CONCLUSIONS: Serum osteopontin levels can be used to distinguish persons with exposure to asbestos who do not have cancer from those with exposure to asbestos who have pleural mesothelioma.

Aged↗

PubMed1990

Effects of cigarette smoke dose and time after smoke exposure on uptake of asbestos fibers by rat tracheal epithelial cells.

We have previously shown that exposure of excised rat tracheal segments to cigarette smoke followed by exposure to a solution of amosite asbestos increases uptake of asbestos fibers compared to exposure to air followed by asbestos. To learn more about the mechanism of smoke-enhanced fiber uptake, we evaluated the effects of amount of smoke and time delay between smoke exposure and asbestos exposure on fiber penetration into the epithelium. To determine whether amount of smoke exposure affected this process, we exposed tracheal segments to 1, 3, or 6 puffs of smoke and subsequently to 5 mg/ml amosite asbestos for 1 h. The segments were then maintained in organ culture for up to 7 d. Asbestos uptake was evaluated by counting fibers in the epithelium by light microscopy. Exposure to increasing numbers of puffs of smoke produced a dose-related increase in fiber uptake at 1 d, 3 d, and 7 d after exposure. To determine whether asbestos exposure needed to occur immediately after smoke exposure for enhanced uptake of fibers to occur, we exposed tracheal segments to 6 puffs of smoke and then delayed exposure to asbestos for 0 (immediate exposure), 3, 18, or 48 h. Tracheas were again maintained in organ culture for up to 7 d after asbestos exposure. Delayed exposure to asbestos after 6 puffs of smoke produced an increase in fiber uptake, even with an interval as long as 48 h between smoke and asbestos exposure; however, the absolute magnitude of fiber uptake was less than that seen with immediate postsmoke asbestos exposure. If catalase was added to the asbestos solution, the smoke-enhanced uptake was abolished, no matter what the time delay.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

A review of environmental and occupational exposure to asbestos in Israel.

The case for a total ban on manufacture and use of asbestos products is stated by the history of asbestos use, exposures, and risks in Israel. Manufacture and use of asbestos began in Israel in the 1950s, rising to a peak in the mid-1970s, and dropping gradually thereafter until reaching minimal levels in the 1990s. Following heightened public concern regarding the carcinogenic effects of asbestos products, there were reductions in use, manufacture, and persons exposed. Since the 1960s, asbestos-related diseases have been diagnosed in hundreds patients nationwide, including asbestos workers and users, as well as individuals living proximally to the manufacturing facilities. Exposures to asbestos in place remain, and patients with asbestos-related disease from environmental exposure are expected to appear for at least another 20-30 years. In the 1980s, an advisory committee appointed by the Ministry of Health of Israel outlined a comprehensive approach towards prevention, control, management, and compensation for health risks from asbestos exposures. As certain areas are still contaminated with asbestos waste and as environmental exposure persists, continued and improved medical monitoring and compensation programs are urgently needed in order to reduce the suffering of exposed individuals and their families. The ban on asbestos prevents risks from new exposures, but does not undo the damage from past manufacture, use, disposal, and dumping. In this paper, we review the history of Israel's import and use of asbestos, and the management of occupational and environmental exposures. We also address policy, practice, and the need to protect future victims of asbestos-related disease.

Asbestos↗

PubMed2005

[Wonder matter and assassin. The perception of the asbestos danger as a mirror of the time 1930-1990].

In the seventies and eighties of the twentieth century the ideas of the dangers concerning the use of asbestos changed dramatically. The mineral, which had, more than half a century before been introduced in the Netherlands as a miraculous mineral, was completely banned from use. Asbestos became known as a 'silent killer' and 'the blue sand of death', and as a symbol of the hidden hazards of a deteriorating environment caused by unscrupulous companies and indolent authorities. Asbestos seems to fit perfectly into the ubiquitous hazards which Ulrich Beck defines in his concept of the 'risk society' as the dangerous side effects of industrial production. Yet the perception of the risk associated with asbestos depended more on socio-cultural characteristics than on scientifically risk assessments. In the first half of the twentieth century the use of asbestos was limited and therefore did not cause any concern. Economic crisis and war silenced the first alarming signals of asbestos related disease from foreign experts and a handful of Dutch physicians. The asbestos workers themselves were held responsible for their own health and safety. In the 1951 asbestosis became recognised as an industrial disease. Preventive measures with regard to the industrial use of asbestos were prescribed by law. Workers shared the responsibilities for a safe use with employers and authorities. However, during this period, all the attention was directed towards economic growth. Supervision by the labour inspection was scarce and workers and employers were not very interested in upholding the safety measures. Among asbestos workers the use of protective clothes and dust masks was generally seen as unmanly. In the sixties the foreign literature on the connection between the exposure to asbestos and the occurrence of lung cancer and mesothelioma became known among Dutch specialists. The results of these studies were confirmed by research among Dutch insulation workers. At the same time the trade unions rejected the idea of a shared responsibility and formulated the unilateral 'right to a safe working environment', with the implication that, in their view, all unhealthy and unsafe procedures should unconditionally be banned from the workshops, including the use of asbestos. Concerned civilians, environmental lobbyists, progressive political parties and concerned scientists transformed this idea into a 'right to a safe living environment', while mass media spread the message. Asbestos was pointed out as a threat to the public health, tracked down all of its hiding places and ultimately removed. The ban on asbestos was one of the results of democratisation and emancipation movement of the late sixties and seventies. The emancipation expressed itself in an increasing intolerance to risks brought about by powerful companies and bureaucratic authorities.

Asbestos↗

PubMed1985

Cocarcinogenic and tumor promoting properties of asbestos and other minerals in tracheobronchial epithelium.

Epidemiologic and experimental studies document a synergistic effect of asbestos and smoking in the induction of bronchogenic carcinoma. Whereas the increased risk of these cancers in nonsmoking asbestos workers is 4-fold or less in comparison to nonsmokers in the general population, individuals who smoke and are exposed to asbestos occupationally have a 80-90 fold increased risk. The observations summarized above provide substantial insight into the interactions between asbestos and chemical carcinogens in cigarette smoke at the cellular level (Fig. 8). On the one hand, asbestos fibers and other particulates appear to act as condensation nuclei for PAH in the occupational setting or environment. They then facilitate the transfer of these chemical carcinogens into target cells, i.e., those destined to develop into tumor cells. As a result, the adduct formation of PAH to DNA is encouraged, an event linked intrinsically to initiation of transformation. Alternatively, asbestos appears to enhance and modulate the further development of initiated cells to neoplastic cells by a process resembling tumor promotion in mouse skin. In this regard, the most dramatic example illustrating the importance of asbestos in two-stage carcinogenesis is an experiment by Topping and Nettesheim. These investigators inserted the PAH, 7,12-dimethyl-benz(a)anthracene (DMBA) into the lumen of rat trachea which then were implanted on syngeneic animals. Subsequently, chrysotile asbestos was introduced, and grafts were removed for histology when palpable tumors occurred. At non-tumorigenic (i.e., initiating) amounts of DMBA, asbestos promoted the development of malignancies, although two neoplasms were observed with use of asbestos alone. Asbestos was not carcinogenic at these amounts, but a low incidence (5%) of squamous cell carcinoma was observed with use of chrysotile alone at much higher concentrations. These results suggest that asbestos is a weak carcinogen, but more importantly a promoter of carcinogenesis in the respiratory tract. Studies in this laboratory show striking effects of asbestos fibers on cell proliferation and differentiation although these responses appear to occur also after exposure of tracheobronchial cells to nonasbestos fibers including fiberglass.

Adsorption↗

PubMedDate not supplied

[Significance of bronchoalveolar lavage in demonstrating previous exposure to asbestos].

A study was made via a clinical approach in the absence of environmental data with the aim of demonstrating a possible past exposure to asbestos in a working population that had never been examined before nor had ever undergone any specific health checks. It was deemed useful to compare this working population with a control population not exposed to asbestos. The population under study consisted of 126 employees of a single (thermonuclear) department of a metal engineering industry who reported having used asbestos as insulation material in all heat processes up to the beginning of the 1980's. Pleural plaques were observed in 13 workers that were also confirmed by high resolution TC (HRTC) except in one case. The control group consisted of subjects seen at the Clinica del Lavoro of Milan for non-asbestos related diseases in whom a fibrobronchoscopy with broncho-alveolar lavage (BAL) was performed for diagnostic purposes. In each group asbestos bodies were counted in the BAL liquid using a method with a detection limit of 0.1 bodies/ml. The asbestos bodies detected in the alveolar liquid of subjects in the control group were between a maximum of 0.25 and a minimum of 0 bodies/ml of liquid (mean = 0.03; SD = 0.64) whereas in the sample of subjects from the population under study who underwent BAL the results gave a concentration of asbestos bodies in the BAL liquid between a maximum of 9.0 and a minimum of 0.15 bodies/ml of liquid (mean = 2.38; SD = 2.72). In order to obtain a statistically significant difference between the control population, which was certainly not exposed, and the sample of subjects undergoing BAL from the population for which an occupational exposure was assumed, we applied the non-parametric Wilcoxon-Mann-Whitney test for independent samples in view of the asymmetric distribution of the values of asbestos body concentration in the alveolar liquid: the result was a statistically significant difference (p < 0.001) between the two populations. We also calculated the total asbestos bodies recovered in the BAL liquid of subjects from both populations. In the control group total asbestos bodies were between a maximum of 15 and a minimum of 0 (mean = 1.8; SD = 3.9) while in the group under study the concentration of total asbestos bodies recovered in BAL liquid was between a maximum of 990 and a minimum of 12.7 (mean = 206.5; SD = 270). The Wilcoxon-Mann-Whitney test was also applied to these data, the result of which was that the difference in exposure between the two populations was statistically significant (p < 0.001). Concluding, the study demonstrates the importance of asbestos body count in BAL liquid as an objective indicator of past occupational exposure to asbestos, thus providing documented proof that overcomes any doubts arising from case history and any lack of environmental data that could prove exposure.

Adult↗

PubMed1984

Detection of chrysotile asbestos in workers' urine.

Urinary asbestos concentrations were evaluated as an indicator of occupational exposure to chrysotile asbestos via inhalation and ingestion. Detection of asbestos in the urine represents the first step in developing a biological indicator of exposure. Such an indicator could be used to supplement exposure data from workplace air sampling. A biological indicator would be particularly valuable in evaluating workers with intermittent airborne asbestos exposures and in determining if airborne exposure results in penetration through the lung or gastrointestinal tract. Transmission electron microscopy was selected as the most sensitive technique for identification of all sizes of asbestos fibers which might appear in the urine. First morning void urine samples were obtained from six workers (occupationally exposed to chrysotile asbestos in a factory producing roof coatings) and from a control group (six individuals with no occupational exposure). The levels of chrysotile asbestos detected in the urine of five workers were significantly greater than the asbestos concentrations in matched field blanks (both on a number and mass basis). Field blanks were designed to detect asbestos in the urine samples due to contamination which might occur during urine collection. Also, the workers' urinary asbestos levels were significantly greater than the concentrations found in the control group (both on a number and mass basis). Finally, the levels of chrysotile asbestos detected in the urine of two of six controls were significantly greater than those in matched field blanks (both on a number and mass basis). Although the project was not specifically designed to correlate urinary and airborne asbestos concentrations, preliminary data indicated that a correlation did not exist between these factors.

Adult↗

PubMed1998

Asbestos-induced lung epithelial permeability: potential role of nonoxidant pathways.

Asbestos fibers are an important cause of lung fibrosis; however, the biological mechanisms are incompletely understood. The lung epithelium serves an important barrier function in the lung, and disrupting the epithelial barrier can contribute to lung fibrosis. Lung epithelial permeability is increased in patients with asbestosis, and asbestos fibers increase permeability across cultured human lung epithelium. However, the mechanism of this increased permeability is not known. Many of the biological effects of asbestos are postulated to be due to its ability to generate oxidants, and oxidants are known to increase epithelial permeability. However, we previously reported that altering the iron content of asbestos (important in oxidant generation) had no effect on its ability to increase permeability. For that reason, we undertook these studies to determine whether asbestos increases epithelial permeability through nonoxidant pathways. Both extracellular (H2O2) and intracellular (menadione) oxidants increase paracellular permeability across human lung epithelial monolayers. Extracellular catalase but not superoxide dismutase prevented increased permeability after both oxidant exposures. However, catalase offered no protection from asbestos-induced permeability. We next depleted the cells of glutathione or catalase to determine whether depleting normal cellular antioxidants would increase the sensitivity to asbestos. Permeability was the same in control cells and in cells depleted of these antioxidants. In addition to generating oxidants, asbestos also activates signal transduction pathways. Blocking protein kinase C activation did not prevent asbestos-induced permeability; however, blocking tyrosine kinase with tyrophostin A25 did prevent asbestos-induced permeability, and blocking tyrosine phosphatase with sodium vanadate enhanced the effect of asbestos. These data demonstrate that asbestos may increase epithelial permeability through nonoxidant pathways that involve tyrosine kinase activation. This model offers an important system for studying pathways involved in regulating lung epithelial permeability.

Amitrole↗

PubMed1986

In vitro biologic responses to native and surface-modified asbestos.

A comparative study was made of in vitro biologic responses to native chrysotile, amosite, and crocidolite and corresponding asbestos fibers whose surfaces were modified by metal oxides. Interferon induction by influenza virus was depressed by approximately 50% by all native asbestos whereas corresponding surface modified asbestos minimally affected this nonspecific cellular defense mechanism. The release of the cytoplasmic enzyme, lactate dehydrogenase (LDH), and lysosomal enzymes, beta-N-acetylglucosaminidase (beta-NAG) and beta-glucuronidase (beta-Gluc), by rat alveolar macrophages after exposure to either native or surface-modified asbestos (which is indicative of membrane damage) was monitored. Although both native and surface-modified asbestos induced significant leakage of LDH, generally, lesser amounts of the enzyme were released as a result of exposure to the latter than to native asbestos. Whereas all forms of native asbestos caused significant release of beta-NAG and beta-Gluc, leakage of these enzymes from macrophages exposed to surface-modified asbestos was minimal. In contrast to native asbestos which induced irritation of cell membranes, as indicated by hemolysis of sheep erythrocytes, surface-modified asbestos exhibited minimal hemolytic activity. The findings indicate that surface modification of different asbestos by metal oxides generally lessened the adverse effect of the native mineral on the aforementioned biologic entities.

Animals↗

PubMedDate not supplied

Cytopathology of asbestos-associated pulmonary disease.

The goal of this investigation was to determine the practical role of cytopathology in the clinical and laboratory diagnosis of asbestos-related pulmonary diseases. For this purpose, sputum, bronchial washings, lung tissues, and pleural fluids were obtained from asbestos workers and controls. The asbestos-associated pulmonary diseases studied were: (1) asbestosis, (2) carcinoma, and (3) mesothelioma. The cytology smears were prepared with both Papanicolaou and iron stains. Lung tissues were digested by the Chlorox (5.25% sodium hypochlorite solution) technique for quantitation of asbestos bodies. Asbestos bodies within the sputum were found to be highly specific markers for past asbestos exposure, indicating a heavy residual pulmonary asbestos load (greater than 900 asbestos bodies/g wet lung weight). Asbestos bodies in sputum were also found to have a highly significant relationship (P less than 0.001) with the degree of accompanying atypia of bronchial epithelial cells. Bronchial washings appeared to be more sensitive than sputum for the detection of asbestos bodies. Asbestos bodies were not found within the pleural fluids of malignant mesotheliomas. It is concluded that sputum cytology screening represents a practical, noninvasive, and inexpensive approach to the diagnosis and study of asbestos exposure.

Asbestos↗

PubMed1994

Mesothelial cell injury caused by pleural leukocytes from rats treated with intratracheal instillation of crocidolite asbestos or Corynebacterium parvum.

The pleural and peritoneal mesothelium is a major target in asbestos exposure where mesothelial cell proliferation, exfoliation, and neoplasia have been reported in workers and experimental animals. The objective of this study was to determine the role of pleural leukocytes in mesothelial cell damage caused by asbestos exposure. We therefore investigated detachment and lysis injury to mesothelial cells in vitro induced by leukocytes lavaged from the pleural space of rats exposed, by intratracheal instillation, to crocidolite asbestos. Our studies revealed that normal pleural leukocytes were composed of macrophages, lymphocytes, eosinophils, and mast cells. This population showed a small but significant recruitment of mast cells and eosinophils 3 to 14 days after instillation of crocidolite asbestos; there were also modestly increased levels of macrophages present 30 days after low doses of asbestos. One day after intratracheal instillation of 5 mg crocidolite asbestos, the pleural leukocytes caused detachment injury to mesothelial cells in vitro. This injury was markedly reduced 3 days after asbestos exposure and was undetectable by Day 14. One month after instillation of asbestos, despite doses of asbestos from 0.5 to 5 mg, pleural leukocytes showed no ability to injure mesothelial cells in vitro. In a parallel study, pleural inflammation was induced by intratracheal instillation of heat-inactivated Corynebacterium parvum. Transient mesothelial cell-detaching injury was again expressed by pleural leukocytes 1 day after C. parvum instillation. This was likely related to an increase in the percentage of neutrophils present on this day. These results show that a single administration of crocidolite asbestos, intratracheally, leads to transient activation of pleural leukocytes in terms of the ability of these cells to detach mesothelial cells from matrix. This finding implies that mesothelial cell proliferation and exfoliation found in individuals exposed to asbestos may result from persistent stimulation of pleural leukocytes caused by the continuous presence of asbestos in the lung.

Animals↗

PubMed2000

Role of occupational asbestos exposure in Hungarian lung cancer patients.

OBJECTIVE: What is the frequency of occupational asbestos exposure among patients suffering from malignant respiratory tumours and how many of these tumours are associated with asbestos in Hungary? METHODS: An internationally established questionnaire with 29 questions, covering the most characteristic activities of asbestos exposure at the workplace was completed for 300 patients with respiratory malignancies, i.e. 297 patients with lung cancer and three with mesothelioma of the pleura. From the questionnaire, the smoking habits were estimated and cumulative asbestos exposure was assessed in fibre-years. Additionally, lung X-rays were classified and the national data on the incidence of malignant pleura mesothelioma were analysed. RESULTS: A cumulative asbestos exposure of 25 fibre-years or more was detected in 11 patients with lung cancer (4%) and in each of the three patients with pleural mesothelioma (100%). In a further 72 patients (24%), cumulative occupational asbestos exposure was assessed as below 25 fibre-years (between 0.01 and 23.9 fibre-years). In this group, car and truck mechanics, and installation and construction workers using asbestos-cement were registered. Among patients with an asbestos exposure of 25 fibre-years or more, six asbestos-cement production workers were observed, among them the three mesothelioma cases. A weak but significant association between positive X-ray findings and exposure estimates could be demonstrated. Additionally, results of the lung tissue fibre counts by scanning transmission electron microscopy were available for 25 of the lung cancer patients. A good correlation was observed between the asbestos fibre counts and the assessment of cumulative asbestos exposure. In Hungary, 84 cases of pleural mesothelioma were registered in 1997 and 73 in 1998. These numbers correspond to an annual incidence of about one new case per 100,000 inhabitants older than 15 years. CONCLUSIONS: The annual incidence of lung cancer in Hungary is about 6,000. Since in our series of lung cancer patients about 4% were observed, which could be accepted as representing occupational disease because of a cumulative exposure to 25 fibre-years or more, the annual asbestos related lung tumour incidences may be estimated to be approximately 150 or more. The proportion of nearly two estimated cases of lung cancer per case of pleural mesothelioma corresponds to international experience. Up to now, lung cancer cases only exceptionally have been registered as occupational diseases, i.e. they were seriously under-diagnosed in Hungary. For improving this situation, diagnostic assistance by a self-interview with a questionnaire covering the working history for all newly diagnosed lung cancer patients would be helpful.

Adolescent↗

PubMed1992

The role of free radicals in asbestos-induced diseases.

Asbestos exposure causes pulmonary fibrosis and malignant neoplasms by mechanisms that remain uncertain. In this review, we explore the evidence supporting the hypothesis that free radicals and other reactive oxygen species (ROS) are an important mechanism by which asbestos mediates tissue damage. There appears to be at least two principal mechanisms by which asbestos can induce ROS production; one operates in cell-free systems and the other involves mediation by phagocytic cells. Asbestos and other synthetic mineral fibers can generate free radicals in cell-free systems containing atmospheric oxygen. In particular, the hydroxyl radical often appears to be involved, and the iron content of the fibers has an important role in the generation of this reactive radical. However, asbestos also appears to catalyze electron transfer reactions that do not require iron. Iron chelators either inhibit or augment asbestos-catalyzed generation of the hydroxyl radical and/or pathological changes, depending on the chelator and the nature of the asbestos sample used. The second principal mechanism for asbestos-induced ROS generation involves the activation of phagocytic cells. A variety of mineral fibers have been shown to augment the release of reactive oxygen intermediates from phagocytic cells such as neutrophils and alveolar macrophages. The molecular mechanisms involved are unclear but may involve incomplete phagocytosis with subsequent oxidant release, stimulation of the phospholipase C pathway, and/or IgG-fragment receptor activation. Reactive oxygen species are important mediators of asbestos-induced toxicity to a number of pulmonary cells including alveolar macrophages, epithelial cells, mesothelial cells, and endothelial cells. Reactive oxygen species may contribute to the well-known synergistic effects of asbestos and cigarette smoke on the lung, and the reasons for this synergy are discussed. We conclude that there is strong evidence supporting the premise that reactive oxygen species and/or free radicals contribute to asbestos-induced and cigarette smoke/asbestos-induced lung injury and that strategies aimed at reducing the oxidant stress on pulmonary cells may attenuate the deleterious effects of asbestos.

Asbestos↗

PubMed2004

The epidemiology of asbestos-related diseases.

Asbestos has been recognised as a potential health hazard since the 1940s. Of the two major species of asbestos; white asbestos (chrysotile) and blue asbestos (crocidolite), both of which are hazardous. The workers at extraction facilities are at the greatest risk of exposure to asbestos and, therefore, the development of asbestos-related diseases, commonly mesothelioma. However, other individuals at a high risk of exposure include asbestos-cement workers, insulation workers and ship-yard workers. Environmental exposure to asbestos can occur as a result of living in areas either characterised by natural outcrops of asbestos or asbestos-related materials, or those close to asbestos-producing or -using plants. Unfortunately, man-made fibre alternatives to asbestos, such as rock and slag-wool and glass wool, have also been shown to have a detrimental effect on human health. A characteristic of mesothelioma is that there is a long latency period (20-30 years) before the signs and symptoms of the disease become apparent. In addition, diagnosis of the disease can be difficult. The use of biological markers, such as tissue polypeptide antigen, may play a useful role in the early detection of the disease in individuals at risk.

Asbestos, Crocidolite↗

PubMed1998

Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer.

BACKGROUND: Heavy industrial exposure to asbestos causes lung cancer and mesothelioma, but it remains unknown whether much lower environmental exposure to asbestos also causes these cancers. Nevertheless, regulatory agencies, including the Environmental Protection Agency (EPA), have assessed the risk of lung cancer by extrapolating known risks from past industrial exposure to asbestos to today's much lower environmental asbestos levels (roughly 100,000 times lower). We also tested the EPA's model for predicting the risk of asbestos-induced lung cancer in a population of women with relatively high levels of nonoccupational exposure to asbestos. METHODS: Mortality among women in 2 chrysotile-asbestos-mining areas of the province of Quebec was compared with mortality among women in 60 control areas, and age-standardized mortality ratios were derived. With the help of an expert panel, we estimated past exposure to asbestos among women in the mining areas and used these data with the EPA's model to predict the relative risk of lung cancer. We then compared this prediction with the observed mortality ratios. RESULTS: On the basis of the estimated exposure in the asbestos-mining areas, a relative risk of death due to lung cancer of 2.1 was predicted by the EPA's model, amounting to about 75 excess deaths from lung cancer in this population. By contrast, we calculated a standardized mortality ratio of 1.0 and a standardized proportionate mortality ratio of 1.1 (P> 0.05), suggesting that there were between 0 and 6.5 excess deaths from lung cancer among the women with nonoccupational exposure to asbestos. Seven deaths from pleural cancer were observed (relative risk=7.63; P<0.05). CONCLUSIONS: We found no measurable excess risk of death due to lung cancer among women in two chrysotile-asbestos-mining regions. The EPA's model overestimated the risk of asbestos-induced lung cancer by at least a factor of 10.

Adult↗