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PubMed1990

[Bronchial cancer and asbestos: comparison of anamnestic exposure to asbestos, detection of asbestos bodies in bronchoalveolar lavage and in lung tissue].

The histories of 19 surgical patients with carcinomas of the lungs were examined for exposure to asbestos, and the patients investigated with BAL and lung tissue analysis for the presence of AB. In 63% there was a history of occupational exposure to asbestos; in 47% there was an above-average asbestos load in the lung tissue. In 22% of the patients with exposure to asbestos, the BALF was positive. The asbestos content of lung tissue was appreciably higher than that of a published control group with no carcinoma of the lungs, on the basis of post-mortem material.

Adenocarcinoma↗

PubMed1986

Asbestos fibres in bronchoalveolar lavage fluid from asbestos workers: examination by electron microscopy.

The uncoated and coated fibre load in bronchoalveolar lavage (BAL) fluid was assessed using light microscopy, scanning electron microscopy, and x ray microanalysis in 15 subjects with previous, unprotected exposure to asbestos, including three with clinical and radiological evidence of asbestosis, and in 13 urban dwelling control subjects with no known occupational exposure to asbestos. The mean ferruginous body count per ml BAL fluid in asbestos exposed subjects as determined by light microscopy was 52 (range 0-333). No ferruginous bodies were detected in control subjects. The mean fibre count per ml BAL fluid in asbestos exposed subjects as determined by electron microscopy was 793 (133-3700), significantly greater than 239 (44-544) in controls (p less than 0.05). Electron microscopic counts correlated with duration of previous exposure to asbestos (r = 0.47, p less than 0.05) and with percentage neutrophil counts (r = 0.53, p less than 0.025). There was no relation between electron microscopic fibre counts and light microscopic ferruginous body counts. In 11 asbestos exposed cases x ray microanalysis confirmed the presence of asbestos and in six the asbestos fibre type was clearly identified. Of five subjects showing no asbestos bodies by light microscopy, all showed fibres by electron microscopy, and in three cases the presence of asbestos was confirmed by microanalysis. Among control subjects, fibres were either large organic fibres or smaller particles which microanalysis showed were not asbestos. In only one control case were a few fibres identified which were confirmed as asbestos fibres on microanalysis. Electron microscopic examination of BAL fluid may confirm past exposure to asbestos and probably gives a crude quantitative estimate of asbestos load.

Adult↗

PubMed1991

Carcinoma of the colon in asbestos-exposed workers: analysis of asbestos content in colon tissue.

Epidemiological studies have indicated an increased incidence of carcinoma of the colon in asbestos workers. The present study evaluated the colon tissue asbestos burden, by light and electron microscopic analytic techniques, in patients with a history of occupational asbestos exposure and colon cancer. Asbestos fibers and/or asbestos bodies were present in colon tissue from 14 of 44 (31.8%) asbestos workers with colon carcinoma (range 142,199 to 15,231, 543 fibers/g/wet weight, mean 2,517,823). Chrysotile was identified in 9 patients and amosite in 3 patients. Both amosite and chrysotile were found in the colonic wall in one individual. Other forms of asbestos (e.g., crocidolite, tremolite, or anthophyllite) were not found. Asbestos fibers and asbestos bodies were not found in colon tissue from 20 control patients (colon carcinoma and no asbestos exposure). Asbestos fibers frequently enter and reside in the wall of the colon and are often intimately associated with tumor tissue at the site of colon carcinoma in workers with asbestos exposure and colon carcinoma.

Asbestos↗

PubMed1985

[Evaluation of exposure of workers to asbestos dust in asbestos-processing plants].

Working environments have been tested in plants producing asbestos products, asbestos-cement products, textile asbestos products, asbestos-caoutchouc plates, asbestos boards and asbestos frictional materials for automotive industry, Measurements of total dust concentrations and concentrations of asbestos fibres 5 micron long supported workers' exposure investigations. Basing on literature data on the working environment at the Mining Metallurgical Plant in Szklary, the health risk for workers producing nickel from ores containing asbestos mixtures has been analysed. The asbestos-exposure in asbestos-processing plants has been found to be still considerable despite modernization of the plants. Particularly dangerous to health have been regarded the conditions at asbestos spinning-mills and the Mining-Metallurgical Plant at Szklary, where even average asbestos concentrations considerably exceed the threshold limit values.

Air Pollutants, Occupational↗

PubMed1992

[Concentration and form of asbestos fibers in tap drinking water contaminated from a water supply pipe with asbestos-cement].

The identification and concentration of asbestos fibers in tap drinking water supplied in a central area of Akita Prefecture, Japan, were determined by phase-contrast microscopy and a scanning electron microscope equipped with an energy-dispersive X-ray microanalyzer. The following results were obtained. 1. Asbestos fibers were found in the tap water from two areas in which an asbestos-cement pipe was used for public water supply. The concentrations of asbestos fibers in the tap water were 2.7 x 10(4) to 27.0 x 10(4) fibers per liter of water in area A and 10.0 x 10(4) to 21.0 x 10(4) in area B. On the other hand, no asbestos fiber contamination was observed in tap water of area C, which shared a common water source with area A. A vinyl chloride pipe was used over the entire length of the water supply in route C. 2. Crocidolite was the predominant type of asbestos fiber detected in the tap water. Chrysotile and a mixture of chrysotile and amosite were also observed. 3. Almost all asbestos fibers detected in the tap water possessed the form of thick or sheaved fibers with lengths ranging from ca. 5 to 10 microns. Their shapes were very different from those of asbestos fibers found in the atmosphere. The typical form of the latter is short (ca. 1 micron in length) and needle-like. 4. It was suggested that the contamination of asbestos fibers in the tap water was caused by erosion and peeling off of the inner wall of the asbestos-cement pipe used as a conduit. In order to evaluate the safety of drinking water in Japan, an extensive survey on asbestos-fiber contamination in tap water is necessary.

Asbestos↗

PubMed1989

On the release of asbestos fibers from weathered and corroded asbestos cement products.

The controversy on whether weathered and corroded asbestos cement products are emitting biologically significant asbestos fiber concentrations in ambient air has not been resolved. Nor is it known if the weathered and corroded asbestos cement products release asbestos fibers which have the same carcinogenic potency as "standard" chrysotile. The purpose of this research project was to develop a method for sampling and measuring asbestos fiber emissions from solid planar surfaces (i.e., roofs and facades) consisting of asbestos cement products and to develop methods for studying the physical and chemical changes and the carcinogenic potency of the emitted fibers. Using this method asbestos fiber emissions in ambient air have been measured in the FRG during 1984/1986. The emissions of asbestos fibers longer than 5 microns were in the range 10(6) to 10(8) fibers/m2.hr. The ambient air concentrations of these asbestos fibers were for the most part less than 10(3) fibers/m3. It was shown that the emitted asbestos fibers were chemically changed and it was shown with animal experiments that their carcinogenic potency did not differ from the carcinogenicity of "standard" chrysotile fibers.

Air Pollutants↗

PubMed1975

[The effect of asbestos cement, UICC asbestos samples and quartz on the peritoneum of the mouse].

Aqueous suspensions of asbestos cement powder injected experimentally into the peritoneal cavity of mice act as a fibrogenic agent, as do chrysotile asbestos or chrysotile asbestos-containing soil samples. The fibrotic nodules caused by the dust resemble morphologically silicosis granulomas. In addition, asbestos cement has a characteristically strong cytotoxic effect during the first 2 weeks of the experiment. It is suggested that this is due to the chrysotile asbestos and/or the calcite component of the powder. Amosite and crocidolite, on the other hand, induce a diffuse peritoneal fibrosis with the appearance of numerous foreign body giant cells and asbestos bodies. Dust particles displaced to the regional lymph nodes are frequent in the animals treated with quartz, asbestos cement and asbestos-containing soil samples. A spindle cell type sarcoma arising from the visceral peritoneum is observed in animals injected with crocidolite or asbestos cement. In addition, dusts containing chrysotile asbestos induce considerable amyloidosis of the liver and spleen.

Amyloidosis↗

PubMed1992

Human mesothelioma cells and asbestos-exposed mesothelial cells are selectively resistant to amosite toxicity: a possible mechanism for tumor promotion by asbestos.

To determine if asbestos exposure could contribute to mesothelial cell carcinogenesis by selection and/or expansion of an initiated cell population, we compared normal human pleural mesothelial cells to either human mesothelioma cell lines or mesothelial cells transfected with cancer-related genes for sensitivity to amosite fibers in vitro. Neither normal nor mesothelioma cells were directly stimulated to replicate or increase DNA synthesis by any of the asbestos exposure conditions tested. The potential selective effect of asbestos exposure was demonstrated by a differential sensitivity of normal mesothelial cells and mesothelioma cells to amosite: for example, up to 20-fold higher concentrations of amosite fibers were required to inhibit replication of mesothelioma cell lines than normal mesothelial cells. In addition, a significant resistance (4-fold) to amosite toxicity was observed for SV40 immortalized mesothelial cell lines that had previously been selected in vitro for resistance to asbestos. SV40 immortalized cells that have become tumorigenic after transfection with either Ha-ras or PDGF A-chain genes were not significantly more resistant to the cytotoxic effects of amosite than primary normal cells, and the primary cells were equally sensitive to amosite as mesothelial cells that were only immortalized by SV40. The sensitivity of normal mesothelial cells to asbestos does not appear to be simply a result of general fragility of the mesothelial cells, since similar levels of hydrogen peroxide and silica were cytotoxic for normal mesothelial cells and mesothelioma cell lines. Because mesothelioma cells have a greater resistance to asbestos cytotoxicity than normal mesothelial cells, we hypothesize that a differential resistance to cell killing by asbestos fibers in vivo may result in a selective expansion of an initiated or transformed cell population and thus contribute to the carcinogenesis process. Since tumorigenicity and asbestos resistance occur independently of one another in genetically altered mesothelial cell lines, genotypic and phenotypic alterations that lead to tumorigenic conversion may not be the same changes that provide resistance to cell killing by asbestos.

Asbestos↗

PubMed1987

Asbestos exposure during renovation and demolition of asbestos-cement clad buildings.

External asbestos cement (AC) claddings become weathered after many years by the gradual loss of cement from exposed surfaces; as a result, loosely bound layers enriched with asbestos fibers are formed. This effect usually appears pronounced with roof cladding but slight with wall cladding. Asbestos fibers on such weathered surfaces may be mixtures of chrysotile with amosite or crocidolite. Renovation and demolition of old AC clad buildings could cause asbestos fiber emission, but this has not been investigated in the past. The exposure of workers to asbestos dust during these operations and precautions to minimize exposure now have been investigated at several building sites. Asbestos dust concentrations during water jet cleaning or painting of weathered AC roofing were approximately 0.1 to 0.2 fibers per milliliter (f/ml.). Limited results suggest that concentrations may be reduced substantially by avoiding abrasion of surfaces. Concentrations during AC roof replacement averaged approximately 0.1 f/mL and were reduced markedly by employing more careful work procedures (e.g., by careful handling of sheets or by wet stacking of sheets). Asbestos dust concentrations during demolition by removal of whole sheets averaged 0.3 to 0.6 f/mL for roofs and less than 0.1 f/mL for walls, reflecting the significant differences in extent of weathering between these elements. Suppression of asbestos emissions from roof sheets by wetting or sealing of weathered surfaces was not predictable because of the occurrence of asbestos fibers in dust trapped under sheet laps. Precautions such as respiratory protection and clothing decontamination are considered to be essential for the demolition of roofing containing amosite or crocidolite by the procedures investigated.

Asbestos↗

PubMed1986

Asbestos content of lung tissue in asbestos associated diseases: a study of 110 cases.

Diseases associated with asbestos exposure include asbestosis, malignant mesothelioma, carcinoma of the lung, and parietal pleural plaques. In this study the asbestos content of lung tissue was examined in groups of cases representing each of these diseases and in several cases with non-occupational idiopathic pulmonary fibrosis. Asbestos bodies (AB), which are the hallmark of asbestos exposure, were present in the lungs of virtually everyone in the general population and present at increased levels in individuals with asbestos associated diseases. The highest numbers of AB occurred in individuals with asbestosis, all of whom had levels greater than or equal to 2000 ABs/g wet lung tissue. Every case with a content of 100,000 ABs/g or higher had asbestosis. Intermediate levels occurred in individuals with malignant mesothelioma and the lowest levels in patients with parietal pleural plaques. There was no overlap between the asbestos content of lung tissue from patients with asbestosis and those with idiopathic pulmonary fibrosis. Lung cancer was present in half the patients with asbestosis, and the distribution of histological patterns did not differ from that in patients with lung cancer without asbestosis. The asbestos body content in patients with lung cancer was highly variable. Control cases had values within our previously established normal range (0-20 ABs/g). There was a significant correlation (p less than 0.001) between AB counted by light microscope and AB and uncoated fibres counted by scanning electron microscopy. The previous observation that the vast majority of asbestos bodies isolated from human tissues have an amphibole core was confirmed.

Aged↗

PubMed1989

Asbestos and cancer: human natural killer cell activity is suppressed by asbestos fibers but can be restored by recombinant interleukin-2.

Inhalation of asbestos fibers is associated with a marked increase in the risk of developing pulmonary malignancy, particularly bronchogenic carcinoma. As natural killer (NK) cells are specialized lymphocytes that are considered to have an important in vivo role in the recognition and destruction of malignant cells, we examined the capacity of asbestos fibers (chrysotile, amosite, and crocidolite) to interfere with the NK activity of nylon wool-nonadherent, human blood lymphocytes (51Cr-release assay, K562 target cells, 14 h effector-to-target ratio = 50:1). Final asbestos concentrations used were 1 to 1,000 micrograms/ml. None of the fibers altered spontaneous target cell lysis or lymphocyte viability. All types of asbestos suppressed NK activity in a dose-dependent fashion. This effect was most marked with chrysotile, which exerted a profound inhibitory effect on blood NK cell activity; at 100 micrograms/ml, NK activity was inhibited 84 +/- 2% (p less than 0.001). The suppressive effects of asbestos were exerted directly on the NK cells (large granular lymphocytes, 91 +/- 2% inhibition at 100 micrograms/ml; p less than 0.001). Exposure of lymphocytes to recombinant interleukin-2 (IL-2, 150 units/ml) for 24 h prior to exposure to asbestos restored the level of activity to 99 +/- 6% of the original value (p less than 0.001), and lung lymphocytes that were exposed to IL-2 in vivo (active sarcoidosis) were resistant to suppression by asbestos. Similar results were observed in a group of patients with asbestosis. This suppression of NK activity may contribute to the increased susceptibility of asbestos-exposed persons to the development of pulmonary malignancy.

Asbestos↗

PubMed1991

Asbestos exposure and asbestos-related pleural and parenchymal disease. Associations with immune imbalance.

The study hypothesis was that asbestos exposure and asbestos-related pleural plaques and interstitial disease are associated with (1) immune imbalances favoring helper-inducer T-cell subsets in blood and bronchoalveolar lavage (BAL) and (2) T-lymphocyte accumulation in BAL. One hundred twenty-two asbestos-exposed subsets (AES), including 27 nonsmokers (NS), were evaluated and compared with 10 unexposed normal subjects. Data were collected on medical, smoking, and occupational histories, physical examination, spirometry, lung volumes, single-breath DLCO, chest films read by a "B" reader, and T-lymphocyte characterization in blood and BAL using flow cytometry analysis of monoclonal-antibody-treated cells. On average, AES were 47 yr of age and had 23 yr of asbestos exposure. Fifty-eight (48%) had pleural thickening, and seven (6%) had profusion greater than or equal to 1/0. In blood, asbestos-exposed NS had lower total and percent CD8 and lower total CD3 than did normal subjects. In BAL, asbestos-exposed NS had higher total CD3 than did normal subjects. Among AES, increased asbestos exposure was associated with increased percent CD8 in BAL and decreases in both percent lymphocytes and total CD8 in blood. Increase in CD4/CD8 ratio in BAL were associated with pleural thickening. In those seven with profusion greater than or equal to 1/0, there was increased percent CD4 in blood and decreased percent CD8 in BAL. These results suggest immune imbalance favoring helper-inducer T-cell subsets in association with asbestos exposure systemically and with pleural plaques in BAL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Asbestos exposure and retention as determinants of airway disease and asbestos alveolitis.

To evaluate the relationships of asbestos exposure, retention, airway response, and the asbestos alveolitis, we exposed 2 groups of sheep every 2 wk for 3 yr to either 100 ml phosphate-buffered saline (PBS) or 100 mg UICC chrysotile fibers in 100 ml PBS. The sheep were evaluated periodically by pulmonary function tests (PFT), chest radiograph (CR), bronchoalveolar lavage (BAL), and transbronchial lung biopsy (TLB). At Month 24 of the study, all asbestos-exposed sheep had significant increases in lung resistance and upstream resistance. However, only 9 of the 16 asbestos-exposed sheep had significant changes in TLB, CR, Cst, and VC, which clearly separated them from the other 6 sheep in these parameters. The 2 groups, however, had similar air-flow limitation. At lung biopsy, all asbestos-exposed sheep had significant peribronchiolar fibrosis, with significant alveolitis only in the group of 9 sheep with radiographic and functional changes of early asbestosis. The 9 sheep also had significant changes in BAL cellularity and biochemical profile, which differentiated them from the other 6 asbestos-exposed sheep. Analysis of BAL fiber content at that point revealed that despite identical exposure, the group with interstitial lung disease had significantly more fiber retention (p less than 0.01). The data demonstrate that whereas asbestos airway disease appears to be primarily an exposure-dose-related response, the lung response appears to be more closely related to alveolar retention of the dust.

Airway Resistance↗

PubMed1992

Effects of cigarette smoke on the clearance of short asbestos fibres from the lung and a comparison with the clearance of long asbestos fibres.

Long asbestos fibres are generally considered to have greater disease-producing potential than short asbestos fibres. However, recent reports have suggested that short fibre asbestos appears to be as effective an inducer of macrophage growth factors and toxic oxygen species as long fibre asbestos, but that short fibres are readily removed from lung and do not gain access to tissues. Because smoke is believed to impair the clearance of asbestos fibres from lung, we examined the clearance of a short (geometric mean length 1.3 microns) amosite preparation administered by intratracheal instillation to guinea-pigs. Half the animals in each group were exposed to the smoke of 10 cigarettes daily. Animals were sacrificed 1 day, 1 week, or 1 month later, the macrophages recovered by lavage, and fibre concentrations and sizes determined by analytical electron microscopy in macrophages and lung tissue. A 30-fold increase was seen in total numbers of fibres retained in macrophages in smokers compared to non-smokers by 1 month, and there was an eightfold increase in retention of short fibres in the lung tissue by 1 month. By contrast, a long fibre amosite preparation (geometric mean length 8.9 microns) showed approximately the same increase in fibre retention in macrophages, but only a twofold increase in tissue retention. We conclude that (1) cigarette smoke markedly impairs the clearance of short amosite fibres from the lung with enhanced retention of fibres in both macrophages and tissue; (2) the effects of smoke on short fibre tissue retention appear to be greater than those on long fibre retention; (3) with the long fibre preparation, smoke causes increased tissue retention of relatively shorter fibres; (4) for both fibre size experiments, the increase in total fibres in macrophages in smoke-exposed animals reflects an increase in the total number of fibre-containing macrophages, rather than an increase in the number of fibres phagocytized per macrophage; (5) enhanced short fibre retention markedly increases total fibre surface area, a parameter which has been suggested as a measure of fibre toxicity, to the point where short fibres might under some circumstances have roughly the same potential toxicity as long fibres. These observations suggest that short asbestos fibres could play an important role in the pathogenesis of some types of asbestos-related disease in cigarette smokers.

Animals↗

PubMed1990

Asbestos body formation and iron accumulation in mouse peritoneal granulomas after the introduction of crocidolite asbestos fibers.

This report describes the cell biology of the development of asbestos bodies after a single intraperitoneal injection of a suspension of crocidolite asbestos fibers into the mouse peritoneal cavity. The majority of the infected fibers were found in aggregates of peritoneal macrophages, exudate cells, and fibrous tissue. These aggregates developed into granulomas containing not only numerous asbestos fibers, but also cells of various types, including macrophages, multinucleated giant cells, fibroblasts, plasma cells, granulocytes, and mast cells. Cytoplasmic ferritin was abundantly present in macrophages and giant cells. In addition, iron-rich inclusion bodies were detected. The results of this study show that asbestos body formation can occur outside the pleural cavity. Asbestos body formation occurred in the granulomas after periods of 1 month and longer. On the basis of morphologic criteria, various types of asbestos body were distinguished. X-ray microanalysis showed that variations in the density of the coat could attributed to the presence of chemical elements in various concentrations. Evidence is presented that asbestos body formation is an extracellular phenomenon.

Animals↗

PubMed1986

Asbestos fibers and trace metals in the blood of cattle grazing in fields inundated by asbestos-rich sediments.

During a major storm in 1975, a pasture was inundated with serpentinitic sediments which are rich in asbestos fibers and trace metals. Little natural revegetation has occurred at the site and dairy and beef cattle which continue to graze in and around the contaminated site are exposed to asbestos fibers by inhalation and ingestion. The effect of this material on the cattle was investigated in this study by analyzing blood samples from exposed and control animals for asbestos fibers, trace metals, and general blood chemistry. The analysis showed that at the time of exposure Ni and Mn values were significantly higher in the exposed animals than in the controls, and in six out of seven samples asbestos fibers were present as determined by STEM analysis. Once the animals were removed from the site, trace metal levels returned to normal but asbestos fibers were still present in three out of seven animals. Two of the control animals unaffected by the sediments also showed asbestos fibers and there were no relationships between the magnitude of fibers and trace metal content. This suggests that the sediments influence the blood chemistry of animals but the presence and magnitude of asbestos fibers in the blood can be influenced by other factors as well.

Animals↗

PubMed1992

Fibres and asbestos bodies in bronchoalveolar lavage fluids of asbestos sprayers.

The alveolar content of fibres and asbestos bodies was assessed by bronchoalveolar lavage (BAL) in 21 asbestos sprayers. Transmission and scanning electron microscopy (TEM and SEM) and two light microscopical (LM) methods, cytocentrifugation, and Millipore filtration were used. The subjects had been exposed mainly to crocidolite asbestos for an average of 2.8 (range 0.2-13) years in 1950-75. The mean (median) total fibre count (of asbestos bodies and uncoated fibres) per ml of BAL fluid was 5500 (2800) by TEM and 2900 (1000) by SEM. The mean (median) count of asbestos bodies per ml with LM was 810 (500) with cytocentrifugation and 750 (480) with Millipore filtration, 840 (320) by TEM, and 1750 (420) by SEM. The mean proportion of coated fibres was 35% by TEM and 45% by SEM. The mean length of the coated fibres was 22 (range 4-65) microns by TEM and 34 (range 4.5-170) microns by SEM. The total fibre count exceeded 1000 fibres per ml in 70% of the cases by TEM. Asbestos body counts exceeded 1 per ml in 95% of the cases by LM. The fibre counts by SEM were in good accordance with counts by TEM except in a few cases in which the TEM result was considerably higher. In these cases the proportion of coated fibres was also low. All four counting methods appeared to give consistent results in heavily exposed cases when fibre load in the lungs was high. The counting of asbestos bodies may, however, underestimate the total alveolar fibre load in some cases.

Adult↗

PubMed1979

Analysis of the cores of asbestos bodies from members of the general population: patients with probable low-degree exposure to asbestos.

Asbestos bodies were isolated from the lungs of 21 patients who had 300 to 9,000 of such bodies/g of lung tissue, a concentration frequently found in manual laborers in the general population who are not primary asbestos workers. All of the 123 bodies examined by electron diffraction produced diffraction patterns consistent with amphibole varieties of asbestos. Electron microprobe analysis (energy dispersive x-ray spectroscopy) of 46 bodies revealed that 38 of the cores were composed of the commercial amphiboles, amosite and crocidolite, whereas only 8 were composed of the noncommercial amphiboles, anthophyllite and tremolite. Review of the occupations of these patients revealed that all but one had blue-collar jobs. For many of these persons, putative sources of asbestos exposure such as construction work could be defined, but for some, the source could not be determined. One woman was apparently exposed to asbestos in the practice of her hobby of ceramics, in which she used anthophyllite-contaminated clay. We concluded that commercial amosite/crocidolite asbestos forms the cores of most asbestos bodies in manual laborers in the general population and that the source is usually occupational.

Adult↗