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PubMed1990

Asbestos fibers induce release of collagenase by human polymorphonuclear leukocytes.

The asbestos fibers chrysotile and crocidolite cause a dose-dependent release of specific granule collagenase by human polymorphonuclear leukocytes (PMNL). Release of azurophil granule elastase was induced by the asbestos fibers at higher concentrations, suggesting that asbestos fibers primarily cause the release of specific granule contents of human PMNL. Wollastonite, a fibrous silicate mineral, causes a weaker collagenase release and no elastase release. The collagenase was released in inactive, latent form. Carboxymethyl cellulose (CMC), an agent known to blunt chrysotile-induced hemolysis and production of reactive oxygen metabolites by human PMNL, specifically inhibits chrysotile-induced release of collagenase. Chrysotile asbestos was found to bind the PMNL serine proteinase cathepsin G. A role of collagenase release, production of reactive oxygen metabolites and cathepsin G binding by chrysotile for the perpetuation of the asbestos-induced alveolitis is suggested.

Asbestos↗

PubMed1996

A study of the synergistic interaction of asbestos fibers with cigarette tar extracts for the generation of hydroxyl radicals in aqueous buffer solution.

Several models attempt to explain the synergistic increase in lung cancer among workers exposed to asbestos fibers, who were smokers at the same time. It is known that reactive oxygen species (ROS) are important mediators in asbestos-induced diseases, especially cancer. We studied quantitatively the formation of ROS (by spin trapping with DMPO) in aqueous buffer suspensions containing crocidolite (UICC), chrysotile (UICC and commercial, long fibers) alone, and in combination with aqueous cigarette tar extracts. It was observed that asbestos and cigarette tar act in a cooperative or synergistic way in the generation of hydroxyl radical spin adducts. Grinding of asbestos fibers and addition of EDTA (iron chelator) enhanced the intensity of the ESR signal. This enhancement progressed with time, probably due to the reaction of the extracted iron with the slow released hydrogen peroxide from tar extracts. It was observed a fivefold increase in the ESR signal (for crocidolite and aqueous tar extracts) in the formation of hydroxyl radicals via an iron-catalyzed Fenton reaction. These experimental results are suggest to be strong evidence to the fact that lung cancer has been found in asbestos workers exposed to high concentrations of fibers in the working environment who were smokers, and only rarely in nonsmokers.

Asbestos↗

PubMed2003

Diallylsulfide attenuates asbestos-induced genotoxicity.

It is well known that asbestos fibers induced genotoxicity is mediated by reactive oxygen species (ROS) and insufficient endogenous antioxidant protection. Asbestos exposure can result in ROS generation in two different ways: (a) by catalyzation of Fe(2+), which is present in asbestos fibers, and (b) via oxidative bursts during phagocytosis of the fibers. On the other hand, it has been discussed that the physical presence of the fibres may mechanically influence the normal segregation of chromosomes during mitosis resulting in the induction of micronuclei in late ana/telophase, and aneuploidy. Glutathione and the glutathione redox system protect cells from the oxidative damage after exposure to xenobiotics. Glutathione depletion occurs during oxidative stress conditions and it is observed that supplementation of a precursor of glutathione and other sulphur containing compounds results in reduced toxicity. In the present study, diallyl sulfide (DAS), a lipid soluble allyl sulphur compound present in fresh extracts of garlic was evaluated for its protective effects. The micronucleus (MN) assay was performed in human mesothelial cells (HMC) exposed to 1 microg/cm(2) of crocidolite and chrysotile. Simultaneously, the cells were treated with 5 and 10 microM DAS, incubated for 48 and 66 h. Asbestos fibers induced significant genetic damage in HMC. The assay revealed a significant reduction in MN induction after treatment of cells with 5 microM but not with 10 microM DAS in mesothelial cells. The study revealed that at appropriate concentrations DAS protects mesothlelial cells against asbestos induced genotoxicity.

Allyl Compounds↗

PubMedDate not supplied

Lung mineral fibers of former miners and millers from Thetford-Mines and asbestos regions: a comparative study of fiber concentration and dimension.

Fiber dimension and concentration may vary substantially between two necropsy populations of former chrysotile miners and millers of Thetford-Mines and Asbestos regions. This possibility could explain, at least in part, the higher incidence of respiratory diseases among workers from Thetford-Mines than among workers from the Asbestos region. The authors used a transmission electron microscope, equipped with an x-ray energy-dispersive spectrometer, to analyze lung mineral fibers of 86 subjects from the two mining regions and to classify fiber sizes into three categories. The most consistent difference was the higher concentration of tremolite in lung tissues of workers from Thetford-Mines, compared with workers from the Asbestos region. Amosite and crocidolite were also detected in lung tissues of several workers from the Asbestos region. No consistent and biologically important difference was found for fiber dimension; therefore, fiber dimension does not seem to be a factor that accounts for the difference in incidence of respiratory diseases between the two groups. The greater incidence of respiratory diseases among workers of Thetford-Mines can be explained by the fact that they had greater exposure to fibers than did workers at the Asbestos region. Among the mineral fibers studied, retention of tremolite fibers was most apparent.

Aged↗

PubMed1992

Comparison of the pulmonary responses to chrysotile and amosite asbestos administered intratracheally. I) Early phase of cellular reactions.

To clarify whether serpentine and amphibole asbestos have different effects on the lung, UICC chrysotile and amosite asbestos were injected intratracheally into hamster lung, and the lungs were examined at 30 min, 1, 4, 8, and 24 h, and 2 and 4 days after asbestos application by light and scanning electron microscopy. A leukocyte and macrophage reaction appeared at 4 h and increased up to 2 days, and the cell reaction was stronger and more prolonged after application of chrysotile than after application of amosite asbestos. Furthermore, chrysotile induced more prominent cell (leukocytes or/and macrophages) necrosis and alveolar wall thickening. These findings indicate that chrysotile asbestos induces more stronger cell reactions in the alveolar wall, and is more noxious than amosite.

Animals↗

PubMed1990

Asbestos: scientific developments and implications for public policy.

Asbestos is a commercial term for a group of fibrous minerals often associated with the development of pulmonary interstitial fibrosis (asbestosis), lung cancer, and malignant mesothelioma in occupationally exposed individuals. The pathogenicity of different forms of asbestos varies--long, thin amphibole fibers are most pathogenic, particularly in the induction of mesothelioma. Available data do not support the concept that low-level exposure to asbestos is a health hazard in buildings and schools. The concentration of asbestos fibers in air, type of asbestos, and size of fibers must be considered in evaluation of potential health risks.

Animals↗

PubMed1996

Black spots concentrate oncogenic asbestos fibers in the parietal pleura. Thoracoscopic and mineralogic study.

Epidemiologic and pathologic data demonstrate that malignant mesothelioma occurs preferentially after exposure to long amphibole asbestos fibers. However, mineralogic studies have rarely detected such fibers in the parietal pleura. We hypothesized that the distribution of asbestos fibers in the pleura was heterogeneous and that they might concentrate in certain areas, as does coal dust in patients showing anthracotic "black spots" of the parietal pleura during thoracoscopy. We collected thoracoscopic biopsy samples from these black spots and from normal areas of the parietal pleura and lung from 14 subjects (eight with and six without asbestos exposure). Asbestos content was determined by transmission electron microscopy. In exposed subjects, mean fiber concentrations were 12.4 +/- 9.8 x 10(6) fibers/g of dry tissue in lung, 4.1 +/- 1.9 in black spots, and 0.5 +/- 0.2 in normal pleura. In unexposed patients, concentrations were 0, 0.3 +/- 0.1, and 0, respectively. Amphiboles outnumbered chrysotile in all samples. A total of 22.5% of fibers were > or = 5 microns in length in black spots. A histologic similarity of these black spots with milky spots is suggested by conventional and electron microscopy. We conclude that the distribution of asbestos fibers is heterogeneous in the parietal pleura. Indeed, the fibers concentrate in black spots, where they can reach high concentrations. These findings could explain why the parietal pleura is the target organ for mesothelioma and plaques.

Adenocarcinoma↗

PubMed1984

Lung asbestos content in chrysotile workers with mesothelioma.

The role of chrysotile asbestos in the genesis of mesotheliomas in humans is disputed. We analyzed the asbestos content of the lung in 6 long-term chrysotile miners and millers who had pleural mesotheliomas. In five patients, only chrysotile ore components (chrysotile and tremolite/actinolite/anthophyllite types of amphibole asbestos) were found, while the sixth patient presented both chrysotile ore components and amosite, a type of asbestos that is not derived from the mining process. The mean number of fibers/g dry lung for the 5 patients with mesothelioma containing only chrysotile ore components was higher (chrysotile 64 X 10(6) and tremolite group 540 X 10(6] than in a group of long-term chrysotile miner control subjects who had no asbestos-related disease (chrysotile 23 X 10(6), tremolite group 58 X 10(6], but some patients with mesothelioma had fiber burdens near the mean of the control range. Fiber sizes and aspect ratios in the mesothelioma group were approximately the same as those in the control subjects, and analysis of fiber distribution failed to show any preferential localization in the periphery of the lung. However, the concentration ratio of tremolite in the lungs of the mesothelioma cases compared to the control cases was 9.3, while the ratio of chrysotile was only 2.8. Our findings provide strong evidence that chrysotile mine dust (chrysotile and amphibole components) can produce mesotheliomas in humans; the greater relative amounts of tremolite group amphiboles present in the patients with mesothelioma raise the possibility that these fibers may be important in the pathogenesis of the tumors.

Aged↗

PubMed1990

Brief inhalation of asbestos compromises superoxide production in cells from bronchoalveolar lavage.

Production of superoxide (O-.2) was measured in alveolar macrophages (AM) exposed to asbestos in vitro and in cells obtained from bronchoalveolar lavage (BAL) of rats inhaling asbestos. Steady state levels of O-.2 released by AM in vitro were dose and time dependent in response to crocidolite, chrysotile, and opsonized zymosan, a particulate used to trigger O-.2 generation. In contrast, an inhalation exposure for 1 h to crocidolite or for 6 days to either crocidolite or chrysotile asbestos resulted in a decreased production of O-.2 by BAL cells. Likewise, BAL cells from rats inhaling chrysotile for 1 h or crocidolite for 9 days exhibited a diminished capacity to secrete O-.2 when challenged with the particulate opsonized zymosan. Diminished generation of O-.2 by asbestos occurred in BAL cell populations containing either significantly increased numbers of polymorphonuclear leukocytes and lymphocytes (6- and 9-day exposures) or 99% AM (1-h exposure). Thus, these novel observations suggest that short-term inhalation of asbestos compromises the ability of BAL cells to produce O-.2 in the presence or absence of an additional phagocytic stimulus.

Administration, Inhalation↗

PubMed1983

Chronic effects of dietary exposure to amosite asbestos and tremolite in F344 rats.

Carcinogenesis bioassays of blocky (nonfibrous) tremolite and amosite asbestos alone or in combination with the intestinal carcinogen 1,2-dimethylhydrazine dihydrochloride (DMH) were conducted with male and female Fischer 344 rats. The minerals were administered at a concentration of 1% in pelleted diet for the entire lifetime of the rats starting with the dams of the test animals. One group of amosite rats also received chrysotile asbestos via gavage during lactation. Group sizes varied from 100 to 250 animals. The offspring from mothers exposed to tremolite or amosite asbestos were smaller at weaning than those from untreated mothers and remained smaller throughout their life. The administration of dimethylhydrazine (DMH) did not affect body weight gain, either in amosite-exposed or nonexposed animals. Survival was comparable in the tremolite and control groups. The amosite-exposed rats showed enhanced survival compared to the untreated controls. DMH exposure reduced survival by approximately one year, although the amosite plus DMH groups survived slightly better than the DMH alone groups. No toxicity or increase in neoplasia was observed in the tremolite-exposed rats compared to the controls. Significant increases (p less than 0.05) in the rates of C-cell carcinomas of the thyroid and monocytic (mononuclear cell) leukemia in male rats were observed in amosite-exposed groups. However, the biological significance of the C-cell carcinomas in relation to amosite asbestos exposure is discounted because of a lack of significance when C-cell adenomas and carcinomas were combined and the positive effect was not observed in the amosite plus preweaning gavage group. The biological significance of an increased incidence of mononuclear cell leukemia is questionable, because of a lack of statistical significance in the amosite group when evaluated using life table analysis, lack of significance when compared to the tremolite control group, and the fact that no toxic or neoplastic lesions were observed in the target organs, i.e., gastrointestinal tract and mesothelium. DMH caused a high rate of (62-74%) of intestinal neoplasia in amosite and nonamosite-exposed groups. Neither an enhanced carcinogenic nor protective effect was demonstrated by exposure to amosite asbestos.

1,2-Dimethylhydrazine↗

PubMed1993

Enhanced release of an alveolar macrophage-derived chemoattractant for fibroblasts in rats after asbestos inhalation.

Our studies indicate the effects of in vivo asbestos exposure on the ability of alveolar macrophages (AM) to elaborate a chemoattractant for fibroblast using a rat model of asbestos inhalation. Two groups of rats were exposed by intermittent inhalation (6 hr/day for 5 days/week over a total period of 4 weeks) to either amphibole (crocidolite) or serpentine (chrysotile) asbestos. A group of control rats were sham-exposed to clean air only. The animals were sacrificed 2-5 months after the cessation of exposure. The AM were obtained from the 3 exposure groups in 2 different rat strains by the bronchoalveolar lavage and the cultured in RPMI-1640 medium for 24-96 hr at 37 degrees C. The supernatants from cultured AM were tested for chemotactic activity towards fetal rat skin fibroblasts in a chemotactic assay using 8 microns pore-size filters. The culture supernatants of AM obtained from crocidolite-exposed rats exhibited a significantly greater chemotactic activity towards rat fibroblasts than similar culture supernatants from sham-exposed control animals (p < 0.01) in both rat strains. Significant chemotactic activity was observed after chrysotile exposure (p < 0.05) in ACI rats but not in Fischer-344 rats. Maximal chemoattractant release from AM was noted after 48 hr in culture. Preliminary characterization of the chemoattractant has shown that it is a thermolabile and trypsin sensitive factor whose activity was partially reduced after dialysis. Since AM accumulate at sites of intrapulmonary asbestos deposition, these findings may have relevance to the pathologic accumulation of interstitial lung fibroblasts which occurs during asbestos-mediated lung injury.

Administration, Inhalation↗

PubMedDate not supplied

[Atmospheric asbestos pollution in the urban environment: Milan, Casale Monferrato, Brescia, Ancona, Bologna and Florence].

The atmospheric concentrations of asbestos fibres were measured in 6 towns by long term sampling of air (3 weeks) and by counting at TEM both long and short fibres. Chrisotile and amphiboles were separately counted. For each town high traffic, low traffic and no traffic zones were considered as well as industrial areas and areas with possible and probable sources of asbestos pollution. For Milano the seasonal variations in atmospheric concentrations of asbestos fibres were also recorded in a central square. The maximum concentrations of total fibres was found in Milano (251.7 fibres/liter) and the minimum in Bologna (0.3 fibres/liter). Chrisotile and ultrashort fibres are the most frequent component of the atmospheric pollution. The fibre counts to which people is exposed are far below the levels at which it has been possible to detect risks in industry: however the possibility of a synergism between asbestos and other pollutants with consequent increase of the total carcinogenic potential of the polluted atmosphere cannot be ruled out. The control of the most active sources of asbestos dispersion must be considered in a correct balance between costs and social benefits.

Air Pollutants↗

PubMed1991

[Maximum permissible levels of asbestos and other natural minerals with fibrous structure--necessity of verification].

MACs of asbestos are from 2 to 20 times higher in Poland than in other Western Europe countries. The analysis of occupational diseases reported between 1983 and 1988 among workers of asbestos-cement plants has showed that Polish MAC values do not protect people from work-related asbestosis. Asbestosis was frequently diagnosed in workers employed at mining and processing of nickel ore containing admixtures of fibrous antigorite. The risk of asbestosis in workers of a nickel++ metallurgical plant was 8 times higher that in those employed at an asbestos-cement plant. In an animal study, fibrogenic, carcinogenic and mutagenic activity of antigorite was similar to the biological aggressiveness of crocidolite. Based on own studies and literature data, the following MACs for asbestos and other natural fibrous minerals were established: a) for dusts containing asbestos and other fibrous minerals except crocidolite and fibrous antigorite, total dust concentration equals 1 mg/m3 and concentration of fibres longer than 5 microns = 0.5 fibre/cm3 b) for dusts containing crocidolite and fibrous antigorite total dust concentration = 0.5 mg/m3 and concentration of fibres longer than 5 microns = 0.2 fibre/cm3.

Air Pollutants, Occupational↗

PubMedDate not supplied

Environmental and occupational exposures to chrysotile asbestos: a comparative microanalytic study.

Previous light microscopic analysis of lung tissue from persons living close to a large open-pit asbestos mine demonstrated asbestos body counts intermediate between those of referents and those of miners and millers. In this study, we examined via electron microscopy and x-ray energy dispersive spectrometry autopsy lung specimens from individuals ascertained to be environmentally or occupationally exposed and from a referent group. Environmental group concentrations of chrysotile fibers longer than 5 microns were significantly higher than those of referents, and 50% lower than those observed in the occupational group. Tremolite was markedly increased in the occupational group, but only marginally greater in the environmentally exposed. Electron-microscopy-derived concentrations of amphibole fibers longer than 5 microns correlated well with light microscopic asbestos body counts in the occupational group but not in the environmental or referent groups. Chrysotile concentration was not related to asbestos body concentration in any group. Crocidolite fiber, a commercial amphibole not native to the region, was nonetheless identified in lung tissue from 15 of 23 chrysotile miners and millers. Environmental exposure to asbestos fiber as a result of residence within 40 km of the mines results in increased lung chrysotile content.

Aged↗

PubMed1984

Intrapulmonary distribution of inhaled chrysotile and crocidolite asbestos: ultrastructural features.

Although all commercial types of asbestos can cause pulmonary fibrosis, little is known about ultrastructural differences in the evolution of pulmonary lesions induced by amphiboles and serpentines. The present study was designed to compare the histological and ultrastructural effects produced by chronic inhalation of either crocidolite (amphibole) or chrysotile (serpentine) asbestos in the rat. Animals, exposed by intermittent inhalation for 3 months, were killed after 2 to 16 months. When inhaled, both types of asbestos caused thickened alveolar duct bifurcations associated with macrophage aggregates. Crocidolite inhalation also produced subpleural collections of alveolar macrophages and lymphocytes. Electron microscopy revealed some similarities, but also distinct differences, in the pulmonary distribution of inhaled chrysotile and crocidolite. Whereas both asbestos varieties were identified within the pulmonary interstitium, only crocidolite was detected inside alveolar macrophages. Chrysotile fibres were seen infrequently within the vascular compartment. Microcalcifications were noted after chrysotile inhalation, but were never observed following crocidolite exposure. Both asbestos types induced slight pulmonary fibrosis. These findings indicate that crocidolite and chrysotile produce different pathogenetic features, although both are fibrogenic.

Animals↗

PubMed1984

Correlation of asbestos-induced cytogenetic effects with cell transformation of Syrian hamster embryo cells in culture.

The cytogenetic effects of chrysotile asbestos on Syrian hamster embryo cells in vitro were investigated at doses which induced morphological and neoplastic transformation but which failed to induce measurable gene mutations in the cells at two genetic loci. Chrysotile asbestos treatment of the cells significantly induced chromosome changes in a dose-dependent manner. Up to 50% of the cells had chromosome abnormalities in number or structure following treatment with asbestos (2.0 micrograms/sq cm) for 48 hr. Numerical chromosome changes were the most pronounced abnormalities although significant increases in metaphases with other chromosome aberrations (breaks, fragments, exchanges, and/or dicentrics) and cells with binuclei or micronuclei were also observed. A linear relationship was observed between the incidences of cells with tetraploid metaphases and binucleated cells, suggesting that binucleation and tetraploidy are related. Cytogenetic effects of other mineral dusts were also tested 48 hr following treatment at a concentration of 2.0 micrograms/sq cm. Crocidolite asbestos was less potent than chrysotile asbestos in its ability to induce cell transformation and cytogenetic damage. Treatment of the cells with thin glass fibers (Code 100) was also able to induce cell transformation and cytogenetic effects, but thick glass fibers (Code 110) were much less potent for both endpoints. Milling of the thin glass fibers decreased the length of the fibers and abolished their ability to induce cell transformation and cytogenetic effects. Nonfibrous alpha-quartz induced neither cell transformation nor cytogenetic effects at the dose of 2.0 micrograms/sq cm. The results indicate that the physical characteristics of the fibers determine their ability to induce cell transformation and their ability to induce chromosome mutations, suggesting a possible mechanistic relationship.

Animals↗

PubMed1997

Lobe of origin and histologic type of lung cancer associated with asbestos exposure in the Carotene and Retinol Efficacy Trial (CARET).

Lower lobe origin and histologic diagnosis of adenocarcinoma have been described as useful parameters for attributing lung cancer to prior asbestos exposure. To assess whether these characteristics differed between asbestos-exposed individuals and smokers, we evaluated lobe of origin and histologic type of tumors in 78 asbestos-exposed and 214 nonexposed heavy smokers developing lung cancer during the Carotene and Retinol Efficacy Trial (CARET), a prospective cancer chemoprevention trial. Most tumors in both cohorts, regardless of radiographic fibrosis at baseline, originated in upper lobes, representing 67% in asbestos-exposed and 80% in smokers, respectively (adjusted OR for lower lobe = 1.41; 95% CI = 0.69-2.91). Adenocarcinoma represented 32% of lung tumors in the asbestos cohort, and 30% in the smoking cohort (adjusted OR = 0.78; 95% CI = 0.40-1.55), and was inversely associated with radiographic fibrosis (adjusted OR = 0.19; 95% CI = 0.06-0.62). We conclude that neither anatomic site nor histologic cell type of tumors distinguishes effectively between smoking and asbestos as causal factors in development of lung cancer.

Adenocarcinoma↗

PubMed1991

Asbestos-related disease in public school custodians.

A cross-sectional prevalence study of 120 public school custodians was carried out. The purposes were 1) to investigate the prevalence of asbestos-related disease in a group of custodians at risk for asbestos exposure in public schools and 2) to determine the proportion with disease attributable to exposures in school buildings. Medical and occupational histories, flow-volume loops, and posterior-anterior, lateral, and anterior oblique (AO) chest radiographs were obtained. Single breath DLCO was measured and chest auscultation performed. Mean age of subjects was 57 years and mean duration of work as a custodian, 27 years. Fifty-seven (47.5%) had no known or likely exposure to asbestos outside of their work as a school custodian (NOE). Pleural plaques (PP) occurred in 40 (33%) of the total group and 12 (21%) of the group with NOE. Pulmonary restriction (FVC less than 80% predicted, FEV1/FVC% greater than or equal to 70) occurred in 22 (18%) of the total group and 10 (17%) of those with NOE. DLCO was lower in the group with restriction. Multivariate analysis revealed significant associations (p less than 0.05) between both PP and restriction and duration of asbestos exposure. AO radiographs increased PP detection by a factor of 1.9. Our results reveal PP prevalence in excess of background and pulmonary restriction in the study population, and indicate that PP are attributable to asbestos in schools. Findings with regard to pulmonary restriction need further investigation. Prudent management of asbestos in buildings is indicated for the prevention of related disease.

Adult↗