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PubMed1997

Crocidolite asbestos induces apoptosis of pleural mesothelial cells: role of reactive oxygen species and poly(ADP-ribosyl) polymerase.

Mesothelial cells, the progenitor cells of the asbestos-induced tumor mesothelioma, are particularly sensitive to the toxic effects of asbestos, although the molecular mechanisms by which asbestos induces injury in mesothelial cells are not known. We asked whether asbestos induced apoptosis in mesothelial cells and whether reactive oxygen species were important. Rabbit pleural mesothelial cells were exposed to crocidolite asbestos or control particles (1-10 micrograms/cm2) over 24 hr and evaluated for oligonucleosomal DNA fragmentation, loss of membrane phospholipid asymmetry, and nuclear condensation. Asbestos fibers, not control particles, induced apoptosis in mesothelial cells by all assays. Induction of apoptosis was dose dependent; crocidolite (5 micrograms/cm2) induced apoptosis (15.0 +/- 1.1%, mean +/- SE; n = 12) versus control particles (< 4%), as measured by appearance of nuclear condensation. Apoptosis induced by asbestos, but not by actinomycin D, was inhibited by extracellular catalase, superoxide dismutase in the presence of catalase, hypoxia (8% oxygen), deferoxamine, and 3-aminobenzamide (an inhibitor of the nuclear enzyme, poly(adenosine diphosphate-ribosyl) polymerase). We conclude that asbestos induces apoptosis in mesothelial cells via reactive oxygen species. We speculate that escape from this pathway could allow the abnormal survival of mesothelial cells with asbestos-induced mutations.

Animals↗

PubMed1988

The relationship between lung cancer and asbestos exposure.

This study supports the theory that asbestos exposure may be implicated in a recent upsurge of terminal lung cancer cases in Kure, Japan. The number of asbestos bodies found in the lung during autopsy of 158 subjects from 1984 to 1986 suggests that 70.4 percent of the 51 diagnosed lung cancer cases could be attributed to asbestos exposure. Of the 107 subjects in whom death was not caused by cancer, 38.4 percent had significant asbestos exposure. Types of asbestos bodies found in diagnosed lung cancer cases were analyzed using scanning electron microscopy and x-ray analyzer. Chrysotile was the most widely found component, but amphiboles such as crocidolite and amosite also were detected. Residents of Kure had high exposure to the inhalation of asbestos bodies, possibly related to the upsurge in lung cancer deaths. In our earlier report, asbestos exposure was implicated in the increased incidence of malignant mesothelioma in Kure, an active Japanese ship-building port since the 1920s. Our current findings indicate that asbestos exposure may be a pathogenic factor in lung cancer in world seaports where asbestos exposure has been prevalent.

Asbestos↗

PubMed1993

[A survey on physiological strains of asbestos abatement work wearing protective clothing in summer].

Since the health hazard of asbestos fibers has been widely recognized, the number of asbestos abatement projects in schools has increased rapidly. Most of these projects were planned during summer vacation from school. However, in Japan, it is hot and humid in summer. Moreover, the workers have to wear impermeable protective clothing because of the asbestos exposure risk. The purpose of this survey is to study the workload of asbestos abatement work by measuring physiological reactions. Physiological strains of 12 male workers and working conditions during asbestos abatements work in two schools were measured in August in 1988 and in 1989. Body weight loss by the work of all workers was measured, and heart rate, rectal temperature and skin temperatures at five sites of some of them were measured every minute. In both workplaces, the workers wore disposable coveralls with hoods and shoes covers and protective masks. Air temperature in the workplaces was between 24.6 degrees C and 28.8 degrees C, and air humidity was between 85% and 96%. The high humidity was result of covering the floor, ceiling and wall of the workplaces were covered with vinyl seats, and sprinkling the asbestos fibers with water to lower the amount of asbestos in the air. Working hours of asbestos abatement were between 46 minutes and 95 minutes. Sweat rates were between 217 g/h and 605 g/h. These values were greater compared to the estimate values when work was done wearing commonly used light clothing. Heart rates during asbestos abatement work did not exceed 150 beats/min in one school where the temperature was 25 degrees C-27 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Asbestos and health in the Third World: the case of Brazil.

Almost all of the asbestos used in Brazil is mined by an enterprise wholly owned by two European multinational companies, which also produce and market over two-thirds (by weight of asbestos) of the products made from asbestos. About 80 percent of the asbestos used in Brazil is finally consumed in the form of asbestos cement: for roof tiles and roofing panels, wall-board, and domestic and industrial water tanks. A survey of consumer literature and advertising printed by Eternit, S.A., and Brasilit, S.A., disclosed no mention of a potential danger from exposure to asbestos dust, and no recommendations for cutting down exposure to that dust. The situation at smaller, Brazilian-owned firms is reputed to be disastrous from the standpoint of workers' exposure to asbestos dust at the point of production. At a large asbestos-cement manufacturing plant owned by Eternit, however, exposure to asbestos dust (according to company records) seemed to be kept under 2.0 fibers per cc., the present standard for the United States.

Air Pollutants, Occupational↗

PubMed2001

Cigarette smoke and asbestos activate poly-ADP-ribose polymerase in alveolar epithelial cells.

BACKGROUND: Cigarette smoke augments asbestos-induced bronchogenic carcinoma in a synergistic manner by mechanisms that are not established. One important mechanism may involve alveolar epithelial cell (AEC) injury resulting from oxidant-induced DNA damage that subsequently activates poly (ADP-ribose) polymerase (PARP), an enzyme involved in DNA repair that can deplete cellular energy stores. We previously showed that whole aqueous cigarette smoke extracts (CSE) augment amosite asbestos-induced DNA damage and cytotoxicity to cultured AEC in part by generating iron-induced free radicals. We hypothesized that CSE increase asbestos-induced AEC injury by triggering PARP activation resulting from DNA damage caused by iron-induced free radicals. METHODS: Aqueous CSE were prepared fresh on the day of each experiment. PARP activity in WI-26 (a type I-like cell line) and A549 (a type II-like cell line) cells was assessed by the uptake of labeled NAD over 4 hours and confirmed on the basis of the reduction of PARP levels in the presence of a PARP inhibitor, 3-aminobenzamide (3-ABA). Cell survival was assessed by trypan blue dye exclusion. RESULTS: Hydrogen peroxide (H2O2; 1-250 microM), CSE (0.4-10 vol%), and amosite asbestos (5-250 micrograms/cm2) each caused PARP activation in WI-26 and A549 cells. The combination of asbestos (5 micrograms/cm2) and CSE (0.04-10%) induced WI-26 and A549 cell PARP activation without evidence of synergism. 3-ABA significantly attenuated WI-26 and A549 cell PARP activity and cell death after exposure to H2O2, CSE, and asbestos. Phytic acid, an iron chelator, catalase, and superoxide dismutase each decreased WI-26 cell PARP activation caused by asbestos and CSE. CONCLUSIONS: CSE and asbestos induced PARP activation in cultured AEC in a nonsynergistic manner. These data provide further support that asbestos and cigarette smoke are genotoxic to relevant lung target cells and that iron-induced free radicals in part cause these effects.

Antioxidants↗

PubMed2002

Apportionment in asbestos-related disease for purposes of compensation.

Workers' compensation systems attempt to evaluate claims for occupational disease on an individual basis using the best guidelines available to them. This may be difficult when there is more than one risk factor associated with the outcome, such as asbestos and cigarette smoking, and the occupational exposures is not clearly responsible for the disease. Apportionment is an approach that involves an assessment of the relative contribution of work-related exposures to the risk of the disease or to the final impairment that arises for the disease. This article discusses the concept of apportionment and applies it to asbestos-associated disease. Lung cancer is not subject to a simple tradeoff between asbestos exposure and smoking because of the powerful biological interaction between the two exposures. Among nonsmokers, lung cancer is sufficiently rare that an association with asbestos can be assumed if exposure has occurred. Available data suggest that asbestos exposure almost invariably contributes to risk among smokers to the extent that a relationship to work can be presumed. Thus, comparisons of magnitude of risk between smokers and nonsmokers are irrelevant for this purpose. Indicators of sufficient exposure to cause lung cancer are useful for purposes of establishing eligibility and screening claims. These may include a chest film classified by the ILO system as 1/0 or greater (although 0/1 does not rule out an association) or a history of exposure roughly equal to or greater than 40 fibres/cm3 x y. (In Germany, 25 fibres/cm3 x y is used.) The mere presence of pleural plaques is not sufficient. Mesothelioma is almost always associated with asbestos exposure and the association should be considered presumed until proven otherwise in the individual case. These are situations in which only risk of a disease is apportioned because the impairment would be the same given the disease whatever the cause. Asbestosis, if the diagnosis is correct, is by definition an occupational disease unless there is some source of massive environmental exposure; it is always presumed to be work-related unless proven otherwise. Chronic obstructive airways disease (COAD) accompanies asbestosis but may also occur in the context of minimal parenchymal fibrosis and may contribute to accelerated loss of pulmonary function. In some patients, particularly those with smoking-induced emphysema, this may contribute significantly to functional impairment. An exposure history of 10 fibre x years is suggested as the minimum associated with a demonstrable effect on impairment, given available data. Equity issues associated with apportionment include the different criteria that must be applied to different disorders for apportionment to work, the management of future risk (eg. risk of lung cancer for those who have asbestosis), and the narrow range in which apportionment is really useful in asbestos-associated disorders. Apportionment, attractive as it may be as an approach to the adjudication of asbestos-related disease, is difficult to apply in practice. Even so, these models may serve as a general guide to the assessment of asbestos-related disease outcomes for purposes of compensation.

Asbestos↗

PubMed2004

Malignant pleural mesothelioma in parts of Japan in relationship to asbestos exposure.

Malignant pleural mesothelioma is induced by asbestos exposure. Many reports have described this situation in America and European countries, but a few have been published in Japan. In this study malignant pleural mesothelioma cases in hospitals located in an area facing the Seto Inland Sea were evaluated. A total of 106 patients were examined with 100 patients having had occupational exposure to asbestos and 6 patients without such histories of asbestos exposure. Ninety seven were male and 9 were female. Ages ranged from 41 to 87 yr with mean of 64.8+/-5.3 yr. Thirty seven cases showed epithelial type of tumor, 25 biphasic type and 15 showed sarcomatous. The remaining 23 cases had insufficient evidence for typing the tumor. The mean survival rate for all cases was 9.2+/-11.6 months. Fifty-one patients had occupational histories of shipyard work, 16 patients worked in asbestos cement piping, and the remainder were employed in miscellaneous jobs related asbestos exposure. The duration of asbestos exposure ranged up to 20 yr or longer with the mean of 17.2+/-8.9 yr and the average latent period for the occurrence of malignant pleural mesothelioma was more than 31 yr with the mean of 37.0+/-13.3 yr. Quantification of asbestos bodies in the lungs indicated a high concentration in most patients and the major types of asbestos fibers were crocidolite and amosite. Six cases appeared after exposure to chrysotile. These results indicated that ninety four percent of malignant pleural mesothelioma appeared due to the exposure to asbestos including crocidolite and amosite. The remainder may be blamed on exposure to chrysotile.

Adult↗

PubMed1988

Cigarette smoke potentiates asbestos-induced airflow abnormalities.

It has been suggested that exposure to both asbestos and cigarette smoke can produce worse parenchymal lung disease than exposure to asbestos alone. Using a guinea pig model of asbestos administration that produces primarily airway disease and associated airflow abnormalities, we showed previously that the combination of asbestos and smoke acts synergistically to produce more marked increases in tissue collagen, fibrosis of airway walls, and early interstitial fibrosis than are seen with asbestos alone. To investigate the functional effects of these morphological and biochemical abnormalities, pulmonary function tests for volumes and flows, including lung volumes, pressure-volume curves, and flow-volume curves, were performed. By themselves, both smoke and asbestos produced increases in total lung capacity (TLC), residual volume (RV), and functional residual capacity (FRC); the two agents together made all these changes worse than either one alone. Both smoking and asbestos moved the pressure-volume curve upward, and the effects of the two agents together were again greater than either alone. Similarly, both smoke and asbestos decreased flows, and the two agents produced more severe impairment than either one by itself. The changes in volumes, pressure-volume curve, and flows correlated with both increased thickness of small airway walls and increases in airspace size. These observations indicate that, at least in this guinea pig model, cigarette smoke can potentiate the functional consequences of asbestos exposure.

Asbestos↗

PubMed1996

Mechanisms of carcinogenesis and clinical features of asbestos-associated cancers.

Exposure to asbestos, particularly members of the amphibole subgroup (crocidolite, amosite), is associated with the development of malignant mesothelioma and lung cancer. Although management of asbestos in buildings and increased regulation of asbestos in workplace settings are viable approaches to the prevention of disease, the prognosis of asbestos-associated tumors is generally dismal. Moreover, although a vast amount of information is available on the responses of cells and tissues to fibers, understanding the pathogenesis of asbestos-associated malignancies is hampered by the complexity of and differences between various fiber types. Multiple interactions between components of cigarette smoke and asbestos may be important in the development of lung cancer. In this article, the general properties of asbestos fibers will be discussed with an emphasis on chemical and physical features implicated in tumorigenesis. We will then provide a brief overview of the clinical features and treatment of cancers associated with exposure to asbestos. Finally, we will review recent experimental data providing some insight into the cellular and molecular mechanisms of carcinogenesis by asbestos.

Asbestos↗

PubMed1999

[Mineralogical analysis and exploration of asbestos diseases].

Several tools are available for the evaluation of the exposure to asbestos, particularly occupational questionnaire and mineralogical analysis of biological samples. These analysis allow quantification of the level of retention of asbestos fibres in the respiratory tract. Two groups of analysis may be used: quantification of asbestos bodies in sputum, bronchoalveolar lavage fluid or lung tissue samples using light microscopy; quantification and identification of asbestos fibres in bronchoalveolar lavage fluid or lung tissue using analytical electron microscopy. Profiles of lung retention of asbestos bodies or asbestos fibres have been described in various asbestos-related disorders, and reference values are available in control populations mainly for asbestos bodies using light microscopy. Mineralogical analysis of biological samples is not required for compensation of occupational asbestos-related diseases. However, this type of analysis may prove to be useful to the chest physician when looking for the etiology of some nonspecific respiratory diseases (interstitial pulmonary fibrosis, lung cancer), particularly when the occupational questionnaire is not contributive. As they are quite easier and less expensive, analysis using light microscopy will be performed first.

Asbestos↗

PubMed1999

[Assessment of exposure to asbestos].

The aim of the study is to present the principles of assessing asbestos exposure in two different contexts: that of a patient suffering from pleuropulmonary pathology that could be attributed to asbestos and that of a group possibly exposed to asbestos. In the first case this evaluation concerns past exposure and depends typically on information obtained during the course of an interview with the patient. In the second case, the exposure is assessed by atmospheric analysis. Jobs in which occupational exposure to asbestos occurs should be examined, the tasks which entail this exposure and objects containing asbestos are discussed in the first part of the article. The accent is placed on the source of exposure, and the use of materials containing asbestos outside the asbestos industry. Some guidelines enabling the appreciation of the intensity of asbestos exposure as a function of the jobs involved and the objects handled are suggested. Regulations and the principle of quantifying asbestos in the atmosphere during direct exposure in the working environment on the one hand and during the course of passive exposure in the environment on the other are discussed in the second part of the article.

Air Pollution, Indoor↗

PubMedDate not supplied

Carcinogenicity of asbestos: convincing evidence, conflicting interests.

In spite of hard epidemiological and clinical evidence associating asbestos fibre with asbestosis and cancer, the issue is controversial and likely to remain so. The focus is now shifting to non-occupational exposure, differential risk to various asbestos fibre types and the relatively low level of carinogenicity of the chrysotile form. This creates further space for scientific debate and the opportunity to form a considered opinion. However, the situation may take a worrisome turn if some of these scientific inquiries are used by market forces to their advantage. A look at the history of corporate activities in asbestos-related research reveals a disturbing trend. Information that was made available, through legal interventions, clearly shows how for half a century the asbestos industry in collaboration with some academic leaders of occupational medicine successfully suppressed evidence against asbestos. In developing countries, extensive and aggressive marketing continues by chrysotile producers, mainly Canadian companies. There is renewed pressure on this part of the world since new use of asbestos has been almost completely discontinued in the developed countries as a result of public pressure and state prohibitions. In this scenario, relaxation of public health control over any form of asbestos should be opposed. It is extremely dangerous and scientifically untenable to say that chrysotile asbestos can be used without risk. It has been identified as a potent human carcinogen, and remains so. However, some restraint must be exercised while dealing with asbestos that has already been released into the environment. Disturbing it unnecessarily may cause more harm than good.

Asbestos↗

PubMedDate not supplied

[Incidence of malignant mesothelioma (1980-1999) and asbestos exposure in 190 cases diagnosed among residents of the province of Brescia].

Several cases of malignant mesothelioma (MM) previously unknown to the Occupational Health and Safety Service were recognised in the Province of Brescia after an active surveillance program carried out during the first nineteen years of operation; a large proportion of the cases involved workers occupationally exposed to asbestos. A local Mesothelioma Register was subsequently set up in 1993 and by the end of 1999, 190 MM cases had been collected. The annual incidence ratio (standardized on the Italian population, census 1981, x100,000 person-years) was calculated in the 1980-1999 period and showed an increasing trend for location in the pleura in both sexes; in the 1996-1999 period the incidence ratio was 2.95 for males and 1.35 for females. In the same period, this trend was not observed for peritoneal location, with an incidence ratio of 0.17 and 0.37 for males and females respectively. 161 pleural MM (84.7%) and 28 peritoneal MM (14.7%) are described; histopathologic diagnosis was performed in 161 cases (84.7%). Anamneses were collected for 88% of the cases but with direct information from patients only in 65% of these in the recent period. Only 7 cases of asbestosis were diagnosed in the MM cases, whereas 31 cases of pleural abnormalities were observed but only 17 of these were observed in workers occupationally exposed to asbestos. Occupational asbestos exposure was evaluated as certain, probable or possible in 45% of total cases and in 54% of recently (1996-1999) observed cases, which were ten times more frequent in males. Exposure occurred in sectors works where asbestos was not used as raw material, such as construction, iron and steel and metal working. MM's from environmental and non-occupational exposure to asbestos were very few, 1.5% and 0.5% respectively. In 65 MM's asbestos exposure was unknown (34.2%); 50% of these concerned females; for whom the industry and jobs are discussed. The distribution of histologic types of MM was similar in asbestos exposed and non exposed cases. No association between peritoneal mesotheliomas and heavy exposure to asbestos was observed. Ten cases of MM were diagnosed in subjects under 45 years old (5.2%) with only one case occupationally exposed. 2 cases were exposed to radiation therapy (1%) and 2 cases to thoracic trauma (1%). Although in Italy MM has been included in the list of compensatable occupational diseases by law since 1994, a large number of cases occupationally exposed to asbestos are still not recognised by the National Insurance Institute (INAIL). A number of problems limiting work of the Mesothelioma Register and its usefulness are discussed. The Lombardy Mesothelioma Register set up in January 2000 should be able to overcome the limits identified in the past.

Adult↗

PubMed2002

[Effects of exposure to asbestos on plasma activity of glutathione S-transferases].

OBJECTIVE: To understand the effects of exposure to asbestos and GSTM1 genotypes on plasma activity of glutathione S-transferases (GSTs). METHODS: Ninety-four workers exposed to asbestos and 51 controls were selected, and their general information, occupational history and personal behavior were collected by questionnaire. Venous blood specimen was collected from each of them and plasma was separated for detection of GSTs activity and lymphocytes for DNA extraction and GSTM1 genotyping. RESULTS: Plasma activity of GSTs in the asbestos-exposed workers (23.0 +/- 6.9) U/L was significantly lower than that in the controls (32.6 +/- 11.8) U/L, which declined with the length of employment in asbestos industry and the increase of cumulated dose of asbestos. Stratification of workers by GSTM1 genotypes showed that plasma activity of GSTs in asbestos-exposed workers with GSTM1+/+ or GSTM1-/- were (24.0 +/- 6.1) and (22.5 +/- 7.3) U/L, respectively, lower than those in the controls with the same genotypes (38.1 +/- 13.2) and (26.8 +/- 6.6) U/L. Plasma activity of GSTs in the control workers with GSTM-/- was significantly lower than in those with GSTM+/+, and, so did in asbestos-exposed workers, but without statistically significant difference. CONCLUSION: Exposure to asbestos could significantly decrease plasma activity of GSTs, and GSTM1 genotypes could affect on the activity of GSTs in the control workers, which was not so obvious in asbestos-exposed workers.

Adult↗

PubMed2002

[Asbestos-related carcinogenic risk].

Exposure to asbestos containing dust and its health effects are underestimated in many countries throughout the world, particularly in Poland. Asbestos has been proved to be carcinogenic to humans. The most specific health effect of asbestos exposure is pleural, pericardial and peritoneal mesothelioma. The relationship between asbestos exposure and primary lung cancer has been also documented. The association between pleural mesothelioma and asbestos exposure can be estimated by assessing the number of asbestos fiber in the lung tissue, or by checking the history of significant asbestos exposure. Minimum latency is 10 years, but in most cases it ranges between 20 and 40 years. Asbestos-related lung cancer occurs at varied frequency, depending on the country. The lung cancer risk is underestimated, but the frequency of its diagnosis is increasing owing to better detectability, despite the asbestos-use limitation. Lung cancer is distinctly more frequent in patients with asbestosis. In case of heavy occupational exposure, lung cancer can occur already after 1 year of work, but as mentioned earlier its minimum latency period is 10 years.

Asbestos↗

PubMed1991

Experimental studies in rats on the effects of asbestos inhalation coupled with the inhalation of titanium dioxide or quartz.

Rats were exposed for 1 year, with a 2-year follow-up, to dust clouds consisting of a mixture of amosite or chrysotile asbestos with either titanium dioxide or quartz. The addition of titanium dioxide to asbestos did not increase levels of pulmonary fibrosis above the amounts produced by chrysotile or amosite alone. Quartz, however, greatly increased fibrosis above that produced by the asbestos types alone. Both particulate dusts caused an increase in the numbers of pulmonary tumours and mesotheliomas compared to asbestos alone but while tumours in animals treated with asbestos and quartz tended to occur earlier than tumours with asbestos alone, in animals treated with dusts containing titanium dioxide, tumour production occurred later than with asbestos alone. In animals treated with mixtures of asbestos and quartz, there was evidence of increased transport of fibres across the visceral pleural surface and this may be associated with the finding of a higher proportion of pleural mesotheliomas than previously reported in experimental inhalation studies from any laboratory using the main asbestos varieties. The presence of particulate dusts made little difference to the amounts of amosite fibre retained in the lung tissue but, with chrysotile, titanium dioxide appeared to increase retention while quartz reduced it.

Animals↗

PubMed1991

[Asbestos content in bronchoalveolar lavage fluid].

The concentration and size distribution of bronchoalveolar lavage (BAL) asbestos fibers (AF) longer than 2 microns was determined by analytical transmission electron microscopy (TEM). The concentration of asbestos bodies (AB) was measured by TEM and light microscopy (LM). The study group consisted of 110 patients. 27 patients had no occupational asbestos exposure, 44 patients had occupational exposure to asbestos but no asbestos related disease and 39 patients had asbestos related diseases, either asbestosis (n = 34) or malignant mesothelioma of the pleura (n = 5) following long time asbestos exposure at the working place. Occupational asbestos exposure was reflected by increased asbestos fiber concentration in the BAL samples. Mean fiber concentration and size was different between the groups, but the scatter was large.

Asbestos↗

PubMed1989

[Morphologic studies of asbestos-cement surfaces].

A scanning electron microscopic procedure was used for the investigation of asbestos-cement surfaces. The samples of uncoated asbestos-cement sheets were up to 50 years old, coated asbestos-cement materials were 16 years old in maximum. Our results demonstrate that suitable coating systems effectively protect the asbestos-cement surface. On the other hand uncoated asbestos-cement shows a release of asbestos fibres locked up in cement. Therefore uncoated asbestos-cement sheets are emission sources of asbestos fibres. Wether the weathered material coursed a increase of asbestos fibre concentration in ambient air will be a subject of further investigations.

Asbestos↗