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PubMed1987

[Risk of cancer in locations containing asbestos: myth or reality?].

The risk of cancer induced by asbestos is proportional to the 'dose' inhaled (level X duration of exposure). Airborne asbestos fibre concentrations in buildings with sprayed asbestos insulation are very low. The estimation of life-long risk of cancer for people working continuously in this kind of buildings was made according to the Hughes and Weill's model. The lung cancer and mesothelioma mortality increase, attributable to asbestos, would be less than 0.1%, which means less than one death by century for all employees working in these buildings, in Switzerland. On the other hand, maintenance employees lying electric cables, pipes, etc., inside the asbestos-containing sprayed insulation, or workers transforming or pulling down these buildings, may be exposed to high asbestos fibre levels and should wear protective equipment.

Adult↗

PubMedDate not supplied

Lung asbestos bodies and pleural plaques at autopsy.

Examination for lung asbestos bodies and pleural plaques was made in 996 consecutive unselected autopsies in Torino. The prevalence of asbestos bodies was 12.4% and that of pleural plaques 19.1%. Both findings were found with significantly greater frequency in men, and in the age group above 50 years. In addition, their occurrence increased with age up to 70 years, then decreased thereafter. A significant association between the severity of plaque lesions and the presence of asbestos bodies was found, whereas the number of asbestos bodies was not related to the presence of pleural plaques. It is suggested that pleural plaques are more reliable markers of asbestos exposure started many years earlier, and that lung asbestos bodies are more reliable indicators of more recent exposure.

Age Factors↗

PubMed1999

Presence of asbestos in peritoneal malignant mesotheliomas in women.

Heller DS, Gordon RE, Clement PB, Turnnir R, Katz N. Presence of asbestos in peritoneal malignant mesotheliomas in women. Asbestos plays a causal role in pleural mesotheliomas. The role in peritoneal mesotheliomas is less clear, particularly in women, who are less likely to have an exposure history. Seven peritoneal malignant mesotheliomas in women with no recorded asbestos exposure were analyzed in this report. Tissue digestion was performed on paraffin blocks of tumor. Transmission electron microscopy, energy-dispersive spectroscopy, and electron diffraction were performed for tissue fiber burden and fiber identification. Asbestos fiber burdens were present in 6 cases. Two showed crocidolite, 2 showed chrysotile, one showed chrysotile and amosite, and one showed chrysotile and tremolite. Fiber burdens ranged from 56,738 to 1,963,250 fibers per gram wet weight tissue. All fibers counted were between 1 and 5 microns. This study demonstrates asbestos in peritoneal mesotheliomas in women. Asbestos may play a role in the development of these tumors.

Journal Article↗

PubMed1990

Influence of smoking on radiographic profusion and pleural changes in asbestos-exposed subjects.

The influence of smoking on pleural and parenchymal radiographic changes, particularly in asbestos-exposed cohorts, has been debated. We studied this issue in 440 asbestos-exposed subjects referred for evaluation between 1981 and 1985. Information was obtained on age, exposure, and smoking. Chest radiographs were independently read by three "B" readers under blind conditions and it was determined that 80.5% of the subjects had a history of smoking. The odds ratio for smoking and parenchymal opacities greater than or equal to 1/0 was 1.98 (95% confidence interval, 1.2 to 3.3); this association was not affected by adjustment for asbestos exposure and/or age. A dose-response pattern emerged between increasing pack-years and parenchymal opacities greater than or equal to 1/0; the effect between asbestos exposure and smoking appeared to be additive. No associations were found between smoking and pleural abnormalities. The findings in this investigation are consistent with prior studies showing an influence of smoking on radiographic parenchymal, but not pleural, changes, at least in asbestos-exposed groups. The anatomical equivalent of these radiographic changes and their impact, if any, on the natural history of asbestos-associated disease remains unclear.

Aged↗

PubMed1988

Asbestos-related pleural and parenchymal fibrosis: detection with high-resolution CT.

Twenty-nine subjects with occupational asbestos exposure and clinical asbestosis were examined with high-resolution computed tomography (HRCT) to determine its sensitivity, relative to that of conventional computed tomography (CT), for detection of benign asbestos-related disease. Thin-section HRCT scans were obtained at five discrete levels through the mid and lower thorax in both prone and supine positions. The same technique was used in 34 age-similar control patients. Parenchymal abnormalities were seen most frequently in the posterior portion of the lung bases in the asbestos-exposed subjects. HRCT prone scans enabled basal structural abnormalities to be reliably distinguished from gravity-related physiologic phenomena in 25 asbestos-exposed subjects. HRCT was more sensitive than CT in detection of both pleural and parenchymal fibrosis. In subjects with clinical asbestosis, HRCT demonstrated parenchymal abnormality in 96%, compared with 83% for CT. Similarly, pleural thickening was shown in 100% of subjects at HRCT, compared with 93% at CT. HRCT could be an important adjunct in the evaluation of asbestos-related pleuroparenchymal fibrosis. An HRCT study including prone scans is a sensitive, reliable means of detecting thoracic abnormalities in asbestos-exposed individuals.

Adult↗

PubMed2001

Surface of localized pleural plaques quantitated by computed tomography scanning: no relation with cumulative asbestos exposure and no effect on lung function.

To evaluate if there is a relation between the size of asbestos plaques and the level of past exposure and pulmonary function, we measured the surface of localized pleural plaques found on high-resolution (HR) CT scan, using a computerized video display unit-imaging system, in 73 workers (mean age, 43.5 yr) who had worked from 23 to 27 yr in an asbestos-cement factory. Their estimated cumulative exposure to asbestos ranged from 16.4 to 98.7 fiber-years/ ml (mean, 26.3 fiber-years/ml). Lung function measurements included lung volumes, maximal expiratory flows, and diffusing capacity. A control group of 21 workers was examined by the same procedures. Plaques were detected by CT in 51 (70%) asbestos-exposed subjects and in none of the control subjects. The average calculated plaque surface was 47.9 +/- 61.7 cm2 (median, 22.1 cm2; range, 0 to 278.4 cm2). There was no relation between plaque surface and cumulative asbestos exposure (p = 0.24). In the 51 subjects with pleural plaques, the surface of the pleural lesions was not related to cumulative asbestos exposure, or to smoking history or time since first exposure. Neither the presence nor the extent of the plaques was correlated with lung function parameters.

Asbestosis↗

PubMed1987

Changes in autacoid and neuropeptide contents of lung cells in asbestos-induced pulmonary fibrosis.

The purpose of this study was to determine if asbestos-induced pulmonary fibrosis in the rat can affect the levels of autacoids and peptides in freshly isolated lung cells. Lung fibrosis was experimentally induced in rats by a single intratracheal instillation of 5 mg UICC Canadian chrysotile B fibers. Isolated lung cells were prepared from normal and from asbestos-exposed rats. These cells were also fractionated on bovine serum albumin (BSA) gradients. The contents of serotonin (5-HT), histamine (HIST), vasoactive intestinal peptide (VIP), and bombesin (BN) were measured in isolated total cell preparations as well as in density-fractionated cell populations from normal and from asbestos-exposed rats. Analysis of total lung cell preparation showed the presence of heterogeneous populations in normal rat lung. After asbestos exposure, there were significant changes in these cell populations as evidenced by significant increases in lymphocyte and mast cell numbers. In addition, increased levels of 5-HT, HIST, and VIP were observed in isolated lung cells obtained from rats exposed to asbestos 1, 3, and 6 months after instillation. BN content was unchanged 3 months after treatment, but was significantly increased at the 6 month-interval, suggesting a different pattern of response for this neuropeptide. Density fractionation of various cell populations further showed selective changes in specific cell fractions of lung after asbestos exposure. At 6 months, increased levels of 5-HT, HIST, and VIP were associated with cell fraction 7, whereas changes in BN content were found in cell fractions 2 and 3. Similarly, there was a significant increase of mast cells in fraction 7 at the 6-month interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Idiopathic pulmonary fibrosis in asbestos-exposed workers.

Diffuse interstitial lung disease in asbestos-exposed workers is presumed to represent asbestosis. Among 176 asbestos-exposed persons for whom lung tissue was available, we found nine with clinical features consistent with asbestosis, but histologic sections failed to demonstrate asbestos bodies, the usual requirement for pathologic diagnosis of asbestosis (Group I). These nine were compared by analytic electron microscopy with nine persons with idiopathic pulmonary fibrosis (Group II), and with nine persons with all the criteria of asbestosis (Group III). The three groups did not differ significantly with respect to lung burden of chrysotile or tremolite and actinolite, but Group III had a lung burden of amosite and crocidolite that was three orders of magnitude greater than in Groups I and II, with no overlap. We conclude that (1) the American Thoracic Society criterion of "a reliable history of exposure" is sometimes difficult to define; (2) asbestos bodies are seen in tissue sections only when exposure has been reasonably high, and given the proper clinical setting, the presence of diffuse fibrosis and asbestos bodies in tissue sections are sensitive and specific criteria for a diagnosis of asbestosis; and (3) the prevalence here of 5.1% nonasbestos-induced interstitial lung disease among asbestos-exposed persons is artefactually high because of atypical case selection. However, because asbestosis is a disappearing disease, such cases will become more frequent. The identification of these other diseases is important because therapy and prognosis may differ from that of asbestosis.

Aged↗

PubMed1986

Cytokine regulation of lung fibroblast proliferation. Pulmonary and systemic changes in asbestos-induced pulmonary fibrosis.

A complex series of interactions between immunocompetent cells and fibroblasts exists. Because pulmonary fibrosis may result from an increased number of collagen-producing fibroblasts, we studied the production of fibroblast growth factors derived from alveolar macrophages (AM) and peripheral blood mononuclear leukocytes (PBML) during the development of asbestos-induced fibrosis. Three groups of rats received, respectively, a single intratracheal injection of saline (control), 5 mg of asbestos, and 10 mg of asbestos. Bronchoalveolar lavage (BAL) and PBML isolation were performed on each animal 1, 3, and 6 months after instillation. Differential cell analyses revealed no significant change in the BAL cell populations except for a small but significant increase in the proportion of lymphocytes in the 10-mg group at 1 month and in both asbestos groups at 3 months. Similar analyses of PBML revealed only a small reduction in total PBML in the 10-mg group at 6 months. Bronchoalveolar cells (98% AM) from control rats spontaneously released a fibroblast growth factor (FGF), whereas Con-A-stimulated PBML of the same animals produced fibroblast growth inhibitory activity (FGIF). One month after asbestos exposure, when fibrotic lesions were apparent, AM production of FGF was significantly enhanced, and such increase persisted for as long as 6 months. By contrast, no significant change in FGIF production by Con-A-stimulated PBML was seen at the 1-month interval. However, 3 months after exposure, there was a significant suppression of FGIF production by PBML from rats in the 10-mg group and at 6 months by PBML from rats in both asbestos groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Occupational Exposures to Asbestos in Brazil.

European and Canadian asbestos companies have long taken advantage of the lack of regulation of the asbestos industry in developing countries. Their activities exploit vulnerable workers whose lack of medical care may result in a silent epidemic of asbestos-related diseases. At this time, virtually all cases of asbestosis and asbestos-related cancers are not identified, reported, or compensated in developing countries. Brazil provides a compelling example of this growing problem. To stem the epidemic of asbestos-related diseases, Brazil, and many other countries, must adopt the total ban on asbestos use now in effect in more developed countries. Obstacles to accomplishing this in developing countries are daunting.

Journal Article↗

PubMed2005

Exposure and risks from wearing asbestos mitts.

BACKGROUND: Very high fibre inhalation exposure has been measured while people were wearing personal protective equipment manufactured from chrysotile asbestos. However, there is little data that relates specifically to wearing asbestos gloves or mitts, particularly when used in hot environments such as those found in glass manufacturing. The aim of this study was to assess the likely personal exposure to asbestos fibres when asbestos mitts were used. RESULTS: Three types of work activity were simulated in a small test room with unused mitts and artificially aged mitts. Neither pair of mitts were treated to suppress the dust emission. The measured respirable fibre exposure levels ranged from <0.06 to 0.55 fibres/ml, with no significant difference in fibre exposure between aged and unused mitts. The use of high localised ventilation to simulate convective airflows from a furnace reduced exposure levels by about a factor of five. Differences between tasks were statistically significant, with simulated "rowing" of molten glass lowest and replacement of side seals on the furnace highest. Estimated lifetime cancer risk from 20 years exposure at the upper end of the exposure range measured during the study is less than 22 per 100,000. CONCLUSION: People who wore asbestos mitts were likely to have been exposed to relatively low levels of airborne chrysotile asbestos fibres, certainly much lower than the standards that were accepted in the 1960's and 70's. The cancer risks from this type of use are likely to be very low.

Journal Article↗

PubMed2005

ROS-mediated genotoxicity of asbestos-cement in mammalian lung cells in vitro.

Asbestos is a known carcinogen and co-carcinogen. It is a persisting risk in our daily life due to its use in building material as asbestos-cement powder. The present study done on V79-cells (Chinese hamster lung cells) demonstrates the cytotoxic and genotoxic potential of asbestos-cement powder (ACP) in comparison with chrysotile asbestos. A co-exposure of chrysotile and ACP was tested using the cell viability test and the micronucleus assay. The kinetochore analysis had been used to analyse the pathway causing such genotoxic effects. Thiobarbituric acid-reactive substances were determined as evidence for the production of reactive oxygen species. Both, asbestos cement as well as chrysotile formed micronuclei and induced loss of cell viability in a concentration- and time-dependent way. Results of TBARS analysis and iron chelator experiments showed induction of free radicals in ACP- and chrysotile exposed cultures. CaSO4 appeared to be a negligible entity in enhancing the toxic potential of ACP. The co-exposure of both, ACP and chrysotile, showed an additive effect in enhancing the toxicity. The overall study suggests that asbestos-cement is cytotoxic as well as genotoxic in vitro. In comparison to chrysotile the magnitude of the toxicity was less, but co-exposure increased the toxicity of both.

Journal Article↗

PubMed1986

Asbestos bodies in rat lung following intratracheal instillation of chrysotile.

Asbestos bodies in rat lung have rarely been reported, and just one previous record of their formation from chrysotile fibres in the rat is known. This paper illustrates the production of numerous true asbestos bodies in the lungs of Lister hooded rats after a single small intratracheal dose of lightly milled chrysotile. The demonstration of these bodies is particularly useful because uncoated chrysotile fibres in lung tissue cannot normally be visualized by light microscopy; the detection of asbestos bodies, and therefore of asbestos fibres, provides a means of directly relating asbestos exposure to observed tissue lesions. The asbestos bodies detected in the present study were nearly always associated with small pulmonary fibrotic lesions. The bodies ranged in length from 5 to 80 micron and were up to 5 micron in diameter. Small spheres, rods and bodies the shape of a comma were common; larger beaded structures were somewhat rarer. The bodies were visible in tissue sections stained routinely with modified Azan stain and with haematoxylin and eosin, but their detection and localization was enhanced by the use of Perls' Prussian blue stain in association with a pale eosin counterstain.

Animals↗

PubMed1983

Biochemical mechanisms in asbestos toxicity.

The alarming hazardous nature of asbestos makes it the foremost among toxic fugitive dusts. The biochemical mechanisms responsible for the diverse biological effects of asbestos, such as fibrosis, asbestos bodies, pleural plaques, respiratory difficulty, cancer, and cytotoxicity, are being studied in this laboratory. As asbestosis progresses in guinea pigs, along with reticulum formation, lysosomal enzymes are released from membrane-bound latent state to active free form, initiating degradative changes. Considerable alterations take place in the pulmonary metabolic machinery. Mitochondria in lung cells were found to be important loci for the toxic effect of asbestos. A profile of mitochondrial activity, in control and asbestotic animals, revealed specific enzymic changes such as increased cytochrome c oxidase during the disease. The functional organization of mitochondria was also altered, since the organelles from asbestotic lungs were swollen as measured by spectrophotometry. Glutamate dehydrogenase activity of mitochondria became exposed in asbestosis. The maleate dehydrogenase shunt which is involved in transport of the redox potential across the membrane was enhanced in cytosol and mitochondria. The involvement of microsomal enzymes in asbestosis was indicated by alterations in glucose-6-phosphatase and tyrosine transaminase and aniline hydroxylase. Changes in the biotransformational capacity of lung, due to asbestos, could be an important aspect in toxicity, especially the carcinogenic effect. Considerable alterations were encountered in the levels of different phospholipids and in mucopolysaccharide constituents. On the basis of the above, the molecular mechanisms in asbestos toxicity are explained as an integrated model. Interactions of dust constituents with those of membranes and the ensuing metabolic adjustments are thus important in the etiology of asbestosis.

Acid Phosphatase↗

PubMed1992

Association between neutrophil concentration in bronchoalveolar lavage fluid and recent losses in diffusing capacity in men formerly exposed to asbestos.

It has been observed widely that some individuals exposed to asbestos will experience continued losses of lung function after asbestos exposure ceases. Unfortunately, there are few data on factors that determine clinical course, limiting the clinician's ability to determine prognosis in an individual case and restricting the possibility for testing or targeting any potential intervention to alter the course among the millions at risk. In an attempt to address this question, we studied a volunteer population of 50 such men from among a stable, heterogeneous population of asbestos-exposed workers who had been continuously followed in our occupational medicine clinics for up to 12 years (mean, 6.3 years); most had some clinical or roentgenographic sign of asbestos effect, pleural or parenchymal. Each subject was reexamined clinically, functionally, and roentgenographically. Asbestos and tobacco exposure histories were carefully reviewed with the subjects and quantified based on these reports and available data regarding the various work environments from which they came. Subsequently, each underwent a bronchoalveolar lavage to assess cellularity and levels of various proteins. The levels of risk factors, clinical findings, and biologic parameters from lavage were examined for their relationship to serial changes in lung function during the period over which they had been previously followed. Results of the study demonstrate that serial changes in lung function were not closely related to level or length of prior exposure, smoking behavior, chest roentgenographic findings, or lung volumes. Progressive loss of diffusing capacity for carbon monoxide (Dco) was significantly associated with two factors: level of neutrophil concentration in lavage fluid (0.043 +/- 0.016 ml/min/mm Hg/yr drop for each 0.1 x 10(4) neutrophils per milliliter, p = 0.02) and the level of Dco itself (0.17 +/- 0.07 ml/min/mm Hg/yr drop for each 10 percent decrease in percent Dco predicted, p = 0.01). The relationship with neutrophil concentration was statistically independent of the association with Dco itself and stronger; it persisted when loss of Dco was adjusted for baseline value. Lung volume changes were not associated with any predictor variables, alone or in combination. We conclude that the presence of neutrophils in bronchoalveolar lavage fluid is associated with recent disease progression that may have implications in studies of the mechanisms of asbestos-associated disease and in clinical treatment of patients at risk.

Asbestosis↗

PubMed1990

Pulmonary functional impairment associated with pleural asbestos disease. Circumscribed and diffuse thickening.

To define the pulmonary functional impairment associated with pleural asbestos signs (PAS), we compared 738 men with only circumscribed (plaques) or diffuse pleural thickening on chest roentgenograms but no irregular opacities by ILO pneumoconiosis criteria (1980) with 738 age-matched asbestos-exposed men without any roentgenographic signs and with 228 men unexposed to asbestos. All men were white. Spirometry and total thoracic gas volumes (TGV) were measured and expressed as percentage of predicted of white Michigan men who have been modeled for spirometric values thereby adjusting for height, age, and in current and ex-smokers for duration of smoking. Asbestos-exposed men who never smoked had reduced FEF75-85 (p less than 0.01) and increased TGV (p less than .0001) as compared with unexposed men. The 155 men with PAS who had never smoked had reduced flows (p less than .0001), FVC (p less than 0.0056), and TGV (p less than .0001) when compared with 155 age-matched asbestos-exposed men. The 325 asbestos-exposed current smokers with normal chest roentgenograms compared with unexposed smokers had reduced expiratory airflows (p less than 0.0001), reduced FEV1 (p less than 0.004), and increased TGV (p less than 0.0001). The 325 current smokers with PAS had additional air trapping that further reduced vital capacity. Thus, PAS were associated with significant pulmonary dysfunction in men who never smoked, and current and ex-smokers had additional dysfunction even after adjustment for duration of smoking.

Asbestosis↗

PubMed1994

Asbestos hazard evaluation in South Korean textile production.

The manufacture and use of asbestos-containing products has become the object of restrictive environmental and occupational health regulation in the United States and many European countries. World production, however, has not declined, but rather shifted to developing countries. Our knowledge of the working conditions in these countries is limited. This article describes an investigation conducted in 1991 into the conditions and work practices in asbestos textile manufacturing in South Korea. The findings are based on site visits to several asbestos textile manufacturing facilities, meetings with industrial safety experts, and labor and industry representatives. The authors describe the current status of exposure control technology and industrial hygiene practices, and the results of personal asbestos dust monitoring at five representative textile production workstations. In general, manufacturers and regulatory agencies have not taken the precautions necessary to adequately protect employee health and meet international standards. Worker exposure to asbestos dust well above U.S. and German standards is commonplace in South Korea. International cooperation of health and safety experts with experience in asbestos-related problems should be promoted to improve the level of industrial safety in developing countries.

Air Pollutants, Occupational↗

PubMed1999

[Screening of diseases associated with asbestos. On-going activities, synthesis].

Medical screening requires always assessment. On the basis of ongoing studies on occupational health asbestos programs, we suggest some recommendations for asbestos screening after occupational exposure. The proposal for asbestos workers post-exposure surveillance should take into account the medical but also the social aspects of the problem. Post-exposure screening of asbestos workers includes an evaluation of occupational exposure, compulsory basis medical check-up, the characteristics of the radiological investigations and schedule of the medical surveillance. In conclusion, we suggest some general recommendations for asbestos screening after occupational exposure, particularly the necessity to obtain a concerted approach of asbestos screening with regional and national networks, the concern of their assessment and the implementation of specific research studies.

Asbestosis↗