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PubMed1985

Lung function studies of asbestos workers.

Pulmonary function tests have been conducted on 155 asbestos workers and 130 referents. It was found that the lung function impairment in asbestos workers is predominantly a restrictive ventilatory defect appearing even when radiographic changes are not detectable. There was, however, no evidence of airway obstruction. As the disease progressed, all the pulmonary function indices, including vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), maximal ventilation volume (MVV), total lung capacity (TLC), and pulmonary diffusing capacity (DLCO), were reduced dramatically, with the exception of FEV1.0/FVC(%). It is suggested that both radiographic examination and pulmonary function tests should be used as early detection measures of asbestos-induced lung disorders. VC, FVC, and FEV1.0 are the simplest, most reproducible, and most valid indices for the health surveillance of asbestos workers, while the FVC test is the most valuable for epidemiologic study. With stepwise regression analysis a quantitative relationship between dust exposure and pulmonary function was demonstrated. There was no significant difference in the small airway function of the exposed workers and the referents. Further study is needed to investigate the possibility of asbestos-induced small airway obstruction and to estimate the roles played by cigarette smoking and air pollution.

Adult↗

PubMed1985

Epidemiological investigations of decreased employees of the asbestos cement industry in the Federal Republic of Germany.

An epidemiological study of the causes of death was performed covering the entire German asbestos cement industry (10 plants). Of 376 workers who had died in the period of 1 January 1976 - 31 December 1980 and who had been employed for a minimum of 10 years, 314 were included; 307 of these were men. Special consideration was given to the asbestos-related diseases asbestosis, asbestosis in combination with lung cancer, and mesothelioma of the pleura or peritoneum. The relationship between lung cancer with asbestosis and lung cancer without asbestosis is nearly 1:1. From this the conclusion can be drawn that a causal relationship between asbestos exposure and lung cancer can be assumed in only half of the lung cancer cases. This is, however, an upper approximation, since 15 cases of lung cancer were found which is 1/3 less than the expected number in comparison with the normal population. This documents the relatively small excess (SPMR = 1.2) of all cases of lung cancer detected in the asbestos cement industry as compared to the expected lung cancer cases not due to asbestos.

Aged↗

PubMed1981

[Host factors in asbestos-associated disease. A study in twins (author's transl)].

Observations in two pairs of identical twins illustrate the importance of genetic factors in determining the outcome of exposure to asbestos in relation to pleural plaques and bronchogenic carcinoma. The first pair of twins, laggers with french railroad (S.N.C.F.), were discovered fortuitously, after only several years exposure, to have bilateral pleural plaques and calcification at the same site on the axillary and diaphragmatic surfaces. The second set of twins developed epidermoïd bronchial carcinoma : one at the right hilum, the other postero-basally on the right in 1969 and 1977 respectively. Both were in ship-building and each had been exposed to asbestos in the same yard for 20 years between 1945 and 1965. Radiographs showed left sided pleural calcification and reticular shadowing at the bases in the two cases. These observations show the role of the host in the generation of asbestos disease. They are in keeping with studies on the presence of certain tissue types (HLA B27, and HLA B8) in those with asbestosis and of non-specific auto-antibodies (anti-nuclear factor, rheumatoid factor) in asbestosis, silicosis and the idiopathic pulmonary fibrosis. The relation between genetic factors and asbestos-induced cancer is suggested by the variable susceptibility of different kinds of animals to carcinogenesis in response to asbestos and by the increased inductibility of the enzyme system Aryl-hydrocarbon-hydroxylase in subjects exposed to this air-born contaminant who develop pleural tumours and/or bronchitis. There are only two other publications of bronchial carcinoma in twins in the literature.

Adult↗

PubMed1998

[Asbestos-related diseases].

The growing use of asbestos in France like in other industrialized countries since the beginning of the century is the reason of the increase of asbestos-related diseases, which occur after long latency periods. From asymptomatic benign pleural plaques up to malignant mesothelioma of poor prognosis, the fibrogenic and carcinogenic properties of asbestos mainly concern occupationally exposed subjects. The Institut national de la santé et de la recherche médicale (INSERM) expert committee concluded that about 1,950 deaths due to asbestos-related cancers occurred in France in 1996. Reinforcement of French legislation aims at reducing all kinds of asbestos exposure.

Asbestosis↗

PubMed1992

An environmental survey in chrysotile asbestos milling processes in India.

Environmental monitoring to determine airborne asbestos fiber levels has been carried out in four different mills processing chrysotile asbestos in the Cuddapah District (Andhra Pradesh) of India. The "membrane filter method" comprising standard asbestos sampling techniques, acetone-triacetin method for sample preparation, fiber counting, and sizing using the phase contrast optical microscope were adopted in the study. Fiber concentrations both with respect to personal exposures and processing areas were found in most of the cases to be much higher than the prescribed Threshold Limit Value (TLVs) of the developed and developing countries for chrysotile asbestos. By optical microscopy, fiber length distribution showed 70% of fibers in the milling processes were in size range > 5-10 microns, whereas in > 10-20 and > 20 microns, 20% and 8%, respectively. Fiber identification for major elemental content, also done by using scanning electron microscope equipped with an energy dispersive X-ray analyzer, indicated the presence of tremolite along with chrysotile. The study stresses the urgent need to adopt suitable engineering controls at the dust generating sources to reduce the fiber level in the mill environment below the threshold limit.

Air Pollutants, Occupational↗

PubMed1998

Regulation of nitric oxide synthase induction by iron and glutathione in asbestos-treated human lung epithelial cells.

Treatment of human lung epithelial (A549) cells with crocidolite asbestos resulted in the induction of the inducible form of nitric oxide synthase (iNOS), production of NO, and a dramatic decrease in intracellular reduced glutathione (GSH). Iron, mobilized from the crocidolite fibers (27% iron by weight), and the formation of NO were required for the formation of 2'-deoxy-7-hydro-8-oxoguanosine in the DNA of the A549 cells, but not for the decrease in GSH. Therefore, we investigated the role of GSH and iron in the induction of iNOS in A549 cells by crocidolite. Iron was required for the induction of iNOS by crocidolite. A fivefold higher amount of chrysotile asbestos (3% iron by weight) was required to cause a similar decrease in intracellular GSH and induction of iNOS. In the absence of asbestos, treatment with either buthionine sulfoximine (BSO), an inhibitor of gamma-glutamylcysteine synthetase, or ferric ammonium citrate (FAC), a soluble form of iron, did not result in induction of iNOS. However, iNOS was induced when A549 cells were treated simultaneously with BSO and FAC. The presence of 5 mM N-acetylcysteine prevented induction of iNOS in crocidolite-treated A549 cells. These observations suggest that the induction of iNOS resulted from a decrease in intracellular GSH and the presence of iron from the asbestos fibers.

Asbestos↗

PubMed1992

Asbestos-related pleural thickenings in Japanese sake brewers.

Asbestos was long used as an additive material for the filtration of many kinds of alcoholic beverages. There has been, however, only one case report of a distiller in Italy showing pleural thickenings and lung parenchymal fibrosis due to exposure to asbestos. We report a retired Japanese sake brewer who showed bilateral calcified pleural plaques on chest X-ray films. X-ray diffraction analysis and energy disperse X-ray microanalysis demonstrated the additive material used for sake filtration to be almost pure chrysotile. Furthermore, 17 cases showing probably asbestos-related pleural thickenings were found on examination of 235 chest X-ray films of male workers at different sake breweries. These findings indicate that Japanese sake brewers should be listed as workers at possible risk of asbestos-related health problems.

Aged↗

PubMed1984

Measurement of beta-glucuronidase in effluent of perifused alveolar macrophages challenged with chemically modified chrysotile asbestos.

Chrysotile asbestos has been implicated with lung disorders, notably fibrotic lesions and cancer. In vitro, chrysotile fibers are cytotoxic to lung macrophages and stimulate the release of inflammatory mediators. Reports to the effect that chemical modifications of asbestos fibers reduce their cytotoxic and inflammatory potential initiated the present study of three fiber modifications. The cytotoxic and inflammatory effects of magnesium-leached chrysotile, POCL3-treated chrysotile, and CaO-treated chrysotile were studied in a perifused rat alveolar macrophage culture system, relative to untreated fibers. Natural Canadian chrysotile (UICC "B") caused dose-dependent cell mortality and clumping. The release of beta-glucuronidase (beta-Glu), a lysosomal enzyme, was also dose dependent. Rhodesian chrysotile (UICC "A") caused similar cytotoxic and inflammatory effects. However, magnesium-leached chrysotile was less cytotoxic (39% less) and had a lesser clumping capacity (31% less) than untreated chrysotile. Total secretion of beta-Glu elicited by magnesium-leached chrysotile was reduced by 43% from the untreated sample, but kinetic monitoring indicates that this reduction in inflammatory potential is only significant during the first 12 h of an 18-h culture period. POCl3 treatment of chrysotile fibers produced differing effects depending on the length of the fibers under study. Treating fibers with a mean length of 8 micron produced a secretion pattern similar to that produced by acid leaching. The total output for the treated sample was 44% lower than with untreated chrysotile; the difference was only significant during the first 12 h of perifusion. Cell mortality and aggregation were not reduced in any important way with POCl3 treatment of these longer fibers. When ultra-short fibers (mean length = 0.8 micron) were treated with POCl3, the total decrease in beta-Glu output was equal to 41%, and the release of enzyme was significantly lower during the whole 18-h experiment. Cell aggregation was not appreciably affected, but cell mortality was significantly lower than for untreated fibers. CaO treatment did not alter the cytotoxic (cell death and aggregation) or inflammatory (beta-Glu release) effects of chrysotile asbestos. These results suggest that chemical modifications affecting the integrity of the surface magnesium and/or the polarity of the surface charge of chrysotile can reduce to some extent the cytotoxic and inflammatory properties of this type of asbestos.

Animals↗

PubMed1991

Pulmonary hypertension induced by amosite asbestos: a physiological and morphologic study in the guinea pig.

Although there is increasing evidence that mineral dust exposure will produce obstructive lung disease, there is little information on the effects of mineral dust on the pulmonary vascular system. To examine whether exposure to amosite asbestos would affect the pulmonary vasculature and produce pulmonary hypertension, we instilled 5 mg amosite asbestor intratracheally into guinea pigs. After periods of 3 and 6 months, we examined their pulmonary and pulmonary vascular function, and compared these data to those obtained from groups of control animals. We found that, at both time periods, there was pulmonary arterial hypertension, with alteration of the vascular pressure-flow relationships. This was accompanied by abnormalities in the structure of the small pulmonary arterioles. The animals also showed airflow obstruction, with air trapping and an upward shift of the pressure-volume curve. There was evidence of emphysema, and the animals were moderately hypoxic. We found no consistent increase in inflammatory cells either in lavage or peripheral blood, and the histamine dose-response curves were similar in control and asbestos-exposed animals at 6 months. We conclude that intratracheal instillation of asbestos in the guinea pig produces pulmonary hypertension associated with modest hypoxia, emphysema, and airflow obstruction. Whether pulmonary hypertension reflects emphysema-induced hypoxia and loss of vascular bed, or is related to the brief but intense inflammatory infiltrate induced by asbestos, is unclear.

Animals↗

PubMed2006

Involvement of IL-10 and Bcl-2 in resistance against an asbestos-induced apoptosis of T cells.

To analyze the possibility that immunological alteration in asbestos-related diseases (ARDs) such as asbestosis (ASB) and malignant mesothelioma (MM) may affect the progression of cancers, a human adult T cell leukemia virus-immortalized T cell line (MT-2Org) was continuously exposed to 10 mug/ml of chrysotile-B (CB), an asbestos. After at least 8 months of exposure, the rate of apoptosis in the cells became very low and the resultant subline was designated MT-2Rst. The MT-2Rst cells were characterized by (i) enhanced expression of bcl-2, with regain of apoptosis-sensitivity by reduction of bcl-2 by siRNA, (ii) excess IL-10 secretion and expression, and (iii) activation of STAT3 that was inhibited by PP2, a specific inhibitor of Src family kinases. These results suggested that the contact between cells and asbestos may affect the human immune system and trigger a cascade of biological events such as activation of Src family kinases, enhancement of IL-10 expression, STAT3 activation and Bcl-2 overexpression. This speculation was partially confirmed by the detection of elevated bcl-2 expression levels in CD4 + peripheral blood T cells from patients with MM compared with those from patients with ASB or healthy donors. Further studies will be required to verify the role of T cells with enhanced bcl-2 expression in tumor progression induced by asbestos exposure.

Apoptosis↗

PubMed1983

The hemolytic activity of chrysotile asbestos fibers: a freeze-fracture study.

Short asbestos fibers isolated by a sedimentation procedure have a strong hemolytic activity. In the presence of ferritin particles, hemolysis by chrysotile fibers is inhibited at least during the first 10 min. Freeze-fracture studies show that after 20 sec or 2 min of contact between the fibers and the RBC membrane, the intramembranous particles remain randomly distributed over the whole surface of the P-face. On the E-face of the asbestos-treated red blood cell membranes, the number of intramembranous particles is significantly reduced. With the transmission electron microscopy, it is not possible to resolve the trilaminar structure of the ghost membrane around the deeply buried asbestos fibers. It is postulated that the membrane defects brought about by asbestos are caused by the adsorption of one membrane constituent, possibly phospholipids, on the chrysotile fibers.

Animals↗

PubMedDate not supplied

Interactions of asbestos fibers with hepatocytes in vitro: an ultrastructural study.

Cultures of rat hepatocytes have been used to study the interaction of chrysotile asbestos fibers with epithelial cells. The hepatocytes were incubated for 20 h with chrysotile asbestos (UICC B and a preparation of short fibers: 90% less than 2 micron) at concentrations of 1 or 10 micrograms/ml. Morphologic studies were then performed by means of transmission electron microscopy. Fibers were incorporated into plasma membrane invaginations, cytoplasmic vacuoles and phagolysosomes. These observations demonstrate that rat hepatocytes can engage in phagocytosis of chrysotile fibers. The results are compared to those previously obtained with mesothelial cells and tracheobronchial epithelium, exposed to asbestos in vitro. The advantages of the hepatocyte model to investigate the effects on cells of the association of asbestos fibers with genotoxic agents in relation to carcinogenesis are discussed.

Animals↗

PubMed2004

Benzo[a]pyrene-enhanced mutagenesis by asbestos in the lung of lambda-lacI transgenic rats.

To study the suspected mechanism of the interaction between tobacco smoking and asbestos exposure in the modulation of cancer risk, the mutagenic potential of asbestos in combination with the tobacco smoke carcinogen benzo[a]pyrene (B[a]P) was examined in vivo in the rat lung. B[a]P was administered intratracheally in one set of experiments, or by two daily intraperitoneal injections in another set of experiments, to lambdalacI transgenic rats, together with 1, 2 or 4 x 2 mg amosite in one experiment. In the first experiment, the combined action of amosite and B[a]P caused a synergistic (superadditive) increase of mutation frequency in the lung, as compared to groups treated only with asbestos or B[a]P. In the second experiment, i.p. treatment with B[a]P did not significantly alter the mutation frequency induced by amosite, neither after 4 nor after 16 weeks of exposure. The B[a]P-DNA adduct levels were unaffected by amosite co-treatment in both experiments. We assume that the synergistic increase of mutation frequency after intratracheal treatment was due to the mitogenic activities of B[a]P and of amosite. In conclusion, our findings indicate that a weak and delayed mutagenic effect of amosite in rat lung observed in another study was strongly enhanced by the concomitant action of B[a]P. The striking enhancement effect of B[a]P may provide a basis for understanding the suspected synergism of smoking on asbestos carcinogenesis.

Animals↗

PubMed1992

Occupational exposure to asbestos and urinary bladder cancer.

By the use of transmission electron microscopy (TEM) and energy dispersion spectrometry the amount (mean value mean = 191 +/- 94 fibers/mg of tissue) and the type (chrysotile and tremolite) of asbestos fibers have been determined in tissue samples of four bladder cancer patients affected by pulmonary asbestosis, working in the same plant producing asbestos-cement pipes and boards. Similar measurements were carried out on samples of bladder cancers of eight control patients not professionally exposed to asbestos. Only five of them also revealed chrysotile fibers (mean = 151 +/- 196 fibers/mg of tissue). The paucity of the study and control cases and the small quantitative difference between them regarding the presence of infraneoplastic asbestos fibers does not consent us to hypothesize a causal relationship between tumor and occupational exposure.

Aged↗

PubMed1987

Clearance and dimensional changes of crocidolite asbestos fibers isolated from lungs of rats following short-term exposure.

Previous studies in this laboratory have demonstrated fiber clearance and dimensional changes in chrysotile asbestos using a rat inhalational model of short-term exposure. The purpose of the present study was to determine whether or not similar changes occurred in crocidolite asbestos fibers isolated from the lungs of rats at various intervals after termination of exposure. Fibers were recovered on a membrane filter using a sodium hypochlorite digestion-concentration technique, and the numbers and dimensions of the fibers assessed using scanning electron microscopy. The mass of crocidolite asbestos retained in the lung was then calculated. Of the respirable fraction, 19% was deposited in the lungs, and 25% of this amount was still present 1 month after exposure. These values are similar to the 23% deposition and 19% retention rates for chrysotile determined in our previous study. There was a progressive increase in mean fiber length with time postexposure (P less than 0.05), but no significant changes in the diameter of the population of crocidolite fibers retained in the lung. Thus it appears that the tendency for longer fibers to be retained within lung tissue is a characteristic shared by serpentine and amphibole asbestos fibers, whereas longitudinal splitting with progressive decrease in mean fiber diameter in vivo occurs primarily with the serpentine fibers.

Aerosols↗

PubMed1987

A predictive model for determining asbestos concentrations for fibers less than five micrometers in length.

The controversy of whether small asbestos fibers are biologically significant has not been resolved. The present standard method for evaluating asbestos fiber concentrations in workroom air excludes fibers less than 5 micron long even though it has been shown that small fiber concentrations dominate in a dust cloud. This research project was conducted to develop a mathematical model whereby one could predict small (less than 5 micron length) asbestos fiber concentration based on the fiber count concentration determined by phase contrast microscope analysis. Dry chrysotile asbestos was aerosolized into a chamber and sampled by membrane filtration. Segments from each filter were analyzed by both the NIOSH technique using phase contrast microscopy (PCM) and scanning electron microscopy (SEM) at 2000 X for fiber concentrations. A linear relationship was found to exist between the natural logarithm of the SEM-determined concentration and the natural logarithm of the PCM-determined concentration (r = 0.852). Using these data, a mathematical model was developed to predict SEM concentrations based on PCM counts. This model may have application in retrospective epidemiological studies for estimating small fiber exposure levels to determine if small fibers play a role in disease production. The greatest utility would be in those retrospective studies where the only exposure information available is based on PCM counts.

Air Pollutants↗

PubMed2006

Soil fungi reduce the iron content and the DNA damaging effects of asbestos fibers.

Some soil fungi growing on asbestos fibers release chelators and antioxidants. The bioweathering potential of fungi has thus been envisaged as a possible route for bioremediation of asbestos rich soils, where no inactivation procedures have been established so far. The present study reports fungal-mediated modification of the surface reactivity of the fibers and of their potential to damage DNA in vitro. Verticillium sp. and Paecilomyces sp. were selected among the fungi isolated from fragments of chrysotile bearing rocks, as the most potent in iron extraction, and studied in parallel with F. oxysporum, previously reported to modify the surface reactivity of asbestos fibers. One sample of chrysotile from the Western Alps and a sample of UICC (Union Internationale Contre le Cancer) crocidolite were incubated with or without fungi. All fungi extracted iron from both fibers (7.3% from crocidolite and 33.6% from chrysotile by Verticillium sp.), releasing it into the medium. F. oxysporum and Paecilomyces sp. suppressed the potential of the fibers to release hydroxyl radical, while Verticillium sp. suppressed it on crocidolite but enhanced it on chrysotile, a hallmark of ongoing mobilization of reactive iron. Fibers incubated in the growth medium, but in the absence of fungi, exhibited a remarkable potential to damage DNA in vitro, measured by the generation of 8-oxo-7,8-dihydro-2'-deoxyguanosine, while all the fungi reduced such effect. Fungi may thus be regarded as appropriate candidates for bioremediation of asbestos rich soils whereby the reactive iron ions responsible for DNA damage are progressively removed from the fibers.

Asbestos, Crocidolite↗

PubMed2005

The biopersistence of Canadian chrysotile asbestos following inhalation: final results through 1 year after cessation of exposure.

Chrysotile asbestos, a serpentine mineral, has been shown to be notably different from amphibole asbestos such as amosite, crocidolite, and tremolite in that chrysotile once inhaled is rapidly removed from the lung while the amphiboles persist. This has been demonstrated for three different chrysotile samples from Canada, the United States, and Brazil. The initial results of the inhalation biopersistence study on the Canadian chrysotile were reported earlier. This article presents the full results through 365 days after cessation of exposure. In order to fully understand the dynamics of the clearance of chrysotile from the lung, the study included a standardised inhalation biopersistence study following the recommendations of the European Commission (EC) Interim Protocol for the Inhalation Biopersistence of synthetic mineral fibers (Bernstein & Riego-Sintes, 1999) in which the lungs were digested to evaluate fiber content remaining. In addition, confocal microscopy was used to examine lungs in three dimensions to determine where and what size the remaining fibers were in the lung tissue. The results showed that Canadian chrysotile is cleared from the lung with a clearance half-time of 11.4 days for the fibers longer than 20 microm. Canadian chrysotile clears in a range similar to that of glass and stone wools. It remains less biopersistent than ceramic and special purpose glasses and considerably less biopersistent than amphibole asbestos. At 1 yr after cessation of exposure, no long (L>20 microm) chrysotile fibers remained in the lung. In contrast, with amosite asbestos there were 4 x 10 (5) long fibers (L>20 microm) remaining in the lungs at one year after cessation of exposure (Hesterberg et al., 1998). These results fully support the differentiation of chrysotile from amphiboles reported in recent evaluations of available epidemiological studies (Hodgson & Darnton, 2000; Berman & Crump, 2004).

Animals↗