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PubMed1981

Serum protein concentrations and respiratory tract abnormalities following short-term exposure to amosite: a comparison between former asbestos workers and unexposed controls.

A group of 176 former asbestos workers and 76 unexposed controls of similar age were evaluated and compared for concentrations of serum immunoglobulins, alpha 1-antitrypsin, carcinoembryonic antigen (CEA), pulmonary function, radiographic appearance of the lungs, rales, cellular atypia and ferruginous bodies in sputum, and smoking habits. Test subjects were evaluated as a single group and also according to years of exposure to asbestos. Both test and control populations were independently subjects to parametric and nonparametric correlation analyses. Partial correlations were also determined for both groups after controlling for age, race, sex and smoking habits. Analysis of variance was used to compare test and control groups. Smoking, particularly heavy smoking, was an important variable influencing abnormalities of the respiratory tract and CEA in former asbestos workers but not in controls. Except for immunoglobulin A (IgA), serum proteins, CEA, and alpha 1-antitrypsin were not significantly different between test and control subjects. Analysis of variance revealed significant increases between test and control groups for cellular atypia, X-ray abnormalities, rales, and pulmonary restriction. Partial correlation analysis of the asbestos-exposed group revealed important correlations between ferruginous bodies in sputum, rales, and radiographic appearance of the lungs.

Adult↗

PubMed1983

Deposition of Crocidolite asbestos and glass microfibers inhaled by the Beagle dog.

The respiratory tract deposition of neutron activated Crocidolite asbestos and glass microfibers was determined in two groups of four Beagle dogs. The dogs were given 60-minute, nose-only inhalation exposures to an aerosol of either asbestos or glass fibers. The radioactivity in tissues and excreta four days after exposure was used to determine the fraction of inhaled fibers deposited in the upper respiratory tract and the deep lung. The activity median aerodynamic diameter (AMAD), count median diameter (CMD) and count median length (CML) were determined from fibers sampled during exposure. Crocidolite asbestos fibers (obtained from the Union Internationale Contre le Cancer) had an AMAD of 1.8 microns, a CMD of 0.25 micron and a CML less than 5 microns. The fraction of inhaled mass deposited in deep lung was 13-19 percent, while total deposition in the respiratory tract was 54-72 percent. Glass microfibers had an AMAD of 2.5 microns, a CMD of 0.15 microns and a CML of 5.4 microns. Five to 17 percent of the mass of glass fiber was deposited in the deep lung; total respiratory tract deposition was 45-64 percent. The deposition patterns were similar for these small asbestos and glass fibers inhaled by dogs and in good agreement with previous predictions made for man.

Aerosols↗

PubMed1983

In vitro and in vivo response after exposure to man-made mineral and asbestos insulation fibers.

The relative in vitro and in vivo toxicity of several types of manufactured fibrous glass insulation and crocidolite asbestos was investigated to aid in selection of a suitable glass fiber for subsequent use in inhalation exposures. The in vitro cytotoxicity to pulmonary alveolar macrophages of small glass fibers from microfiber insulation (count median diameter (CMD) approximately 0.1-0.2 micrometer) was greater than that of the larger fibers from household insulation (CMD approximately 2.4 micrometers). To screen for in vivo pulmonary toxicity, 2-21 mg of glass or asbestos fibers were administered in divided doses to male Syrian hamsters by intratracheal instillation. Animals were sacrificed at 1, 3.5 and 11 months following initial administration of material. One type of glass microfiber [count median diameter (CMD) approximately 0.1 micrometer] caused deaths from pulmonary edema at early times after instillation. High levels of asbestos, a second glass microfiber (CMD approximately 0.2 micrometer) and one type of household insulation fiber (CMD 2.3 micrometers) all resulted in increase in total collagen and mild pulmonary fibrosis at later times after instillation, although microfiber insulation produced a greater response than household insulation. Asbestos insulation produced the greatest response. A five-day inhalation exposure to a high level of glass microfibers deposited in lung less than 10 percent of the lowest instilled amount which elicited indications of lung injury. This amount did not produce significant biological changes at 1 to 12 months after exposure.

Animals↗

PubMed1991

Activation of protein kinase C by crocidolite asbestos in hamster tracheal epithelial cells.

To determine the mechanisms of cell signalling by asbestos in epithelial cells of the respiratory tract, the activity of protein kinase C (PKC) was examined in hamster tracheal epithelial (HTE) cells exposed to mitogenic concentrations of crocidolite asbestos. In the histone phosphorylation assay, asbestos significantly increased activity of PKC associated with the membrane fraction of HTE cells. However, in contrast to 12-O-tetradecanoylphorbol-13-acetate, which caused redistribution of almost all PKC activity from the cytosolic to the membrane fraction, the majority of the PKC activity was associated with the cytosolic fraction at all time periods examined. Asbestos did not inhibit binding of [3H]phorbol-12,13-dibutyrate to intact HTE cells, whereas binding was inhibited by the phorbol compounds phorbol dibutyrate and phorbol dibenzoate. Thus, crocidolite-induced activation of PKC does not appear to be mediated through the same mechanism as classical phorbol ester tumor promoters, compounds which activate PKC by structurally resembling diacylglycerol.

Animals↗

PubMed1996

Asbestos promotes morphological transformation and elevates expression of a gene family invariably induced by tumor promoters in C3H/10T1/2 cells.

The murine proliferin gene family, which has been shown to respond consistently to tumor promoters and other cellular pro-oxidant agents in C3H/10T1/2 cells, was used to monitor responses after treatment of these cell cultures with toxic, pro-oxidant asbestos fibres. Proliferin mRNA levels were increased by amosite, crocidolite or chrysotile asbestos fibres, especially in the presence of fresh serum and at low cell densities. Promotion of morphological transformation was confirmed in two-stage focus formation assays using crocidolite at a fibre density that induced proliferin expression. Asbestos-induced gene expression was inhibited by millimolar levels of N-acetylcysteine (NAC), supporting a linkage between: (i) induced oxidant stress that was sufficient to promote morphological transformation; (ii) induction of proliferin expression. Other anti-oxidant compounds (dithiothreitol and pyrrolidine dithiocarbamate) or enzymes (superoxide dismutase and catalase) did not inhibit induced expression. Non-fibrous powders (titanium dioxide, quartz or silica gel) were also effective inducers of proliferin mRNA accumulation. Latex beads and activated charcoal were effective at higher particle densities, implying that ubiquitous particle-induced surface membrane effects can lead to an NAC-reversible step necessary for proliferin induction. The results showed that asbestos resembled all other promoters of morphological transformation in C3H/10T1/2 cells in that an antioxidant-sensitive induction of the proliferin gene family occurred following treatment.

Animals↗

PubMed1986

Studies on the role of oxygen radicals in asbestos-induced cytopathology of cultured human lung mesothelial cells.

The possible role of oxygen radicals in mediating the cytopathologic effects of asbestos was studied using human mesothelial cells in culture. Electron paramagnetic resonance measurements of intact cells using the spin trap 5,5-dimethyl-1-pyrroline-1-oxide failed to detect any increase in oxygen radicals in mesothelial cells after exposure to amosite asbestos, although oxygen radicals were readily detected in cells exposed to menadione, an uncoupler of oxidation-reduction reactions. Cellular thiol levels were reduced after exposure to menadione, but were not affected by exposure to asbestos. Addition to the culture media of the free radical scavengers superoxide dismutase, reduced glutathione, N-acetylcysteine, or D-alpha-tocopherol had no affect on the dose-dependent cytotoxicity of amosite fibers. Furthermore, exposure of the mesothelial cells to amosite fibers resulted in no significant increase in the level of DNA single-strand breaks. These results all suggest that for cultured human mesothelial cells, oxygen free radicals are not important mediators of the cytopathic effect of asbestos.

Asbestos↗

PubMed1992

Metsovo-tremolite asbestos fibres: in vitro effects on mutation, chromosome aberration, cell transformation and intercellular communication.

Samples of Metsovo-tremolite asbestos, previously found to be the causative agent of endemic pleural calcification and an increased level of malignant pleural mesothelioma in a rural area of north-western Greece (Metsovo area), were tested in various in vitro toxicity test systems. It was found that asbestos fibres of this type were strong inducers of micronuclei and numerical chromosomal abnormalities while they induced low levels of chromosomal aberrations in mammalian cells in culture. Furthermore, this type of asbestos can induce a low level of in vitro transformation of Syrian hamster embryo cells. The fibres had no effect on gap-junctional cell-cell communication (followed by the dye-transfer method) and did not induce any mutations in the Salmonella typhimurium strain TA102 which is known to be sensitive to the action of various oxidative agents. These results support the hypothesis generated from studies on other types of asbestos that such fibres induce tumours by causing chromosomal mutations.

Aneuploidy↗

PubMed1990

Active oxygen species mediate asbestos fiber uptake by tracheal epithelial cells.

To examine the mechanism whereby asbestos fibers penetrate tracheal epithelial cells, we exposed rat tracheal explants to amosite asbestos alone, or with varying concentrations of substances that scavenge active oxygen species (catalase and superoxide dismutase) or prevent formation of active oxygen species (deferoxamine). All three agents decreased asbestos fiber uptake in a dose-response fashion, but no agent provided complete protection against fiber penetration. We conclude that uptake of amosite asbestos fibers is mediated in part by active oxygen species (most likely OH.), but that other mechanisms of fiber uptake must also exist.

Animals↗

PubMed1994

Asbestos-induced nitric oxide production: synergistic effect with interferon-gamma.

This study has shown, for the first time, that in vitro exposure of rat AMs to either crocidolite (amphibole) or chrysotile (serpentine) asbestos fibers induces the synthesis not only of the O2*- anion, but also of the nitrogen radical, NO*. Furthermore, this asbestos-related effect is enhanced in the presence of interferon-gamma. NO* has been implicated in several pathologic reactions, such as inflammation and immune complex-mediated cell injury. Additionally, NO* may interact with secondary amines to generate nitrosamines, which are potent carcinogens. Our findings could represent a novel type of asbestos-mediated injury, and we propose that the injurious effects of asbestos might be mediated via the interaction of NO* with O2*-, with the generation of ONOO- and other potent toxic free radicals.

Animals↗

PubMed1991

Desquamative interstitial pneumonia associated with chrysotile asbestos fibres.

The drywall construction trade has in the past been associated with exposure to airborne asbestos fibres. This paper reports a drywall construction worker with 32 years of dust exposure who developed dyspnoea and diminished diffusing capacity, and showed diffuse irregular opacities on chest radiography. He did not respond to treatment with corticosteroids. Open lung biopsy examination showed desquamative interstitial pneumonia. Only a single ferruginous body was seen on frozen section, but tissue examination by electron microscopy showed an extraordinary pulmonary burden of mineral dust with especially high concentrations of chrysotile asbestos fibres. This report emphasises the need to consider asbestos fibre as an agent in the aetiology of desquamative interstitial pneumonia. The coexistent slight interstitial fibrosis present in this case is also considered to have resulted from exposure to mineral dust, particularly ultramicroscopic asbestos fibres.

Asbestos↗

PubMed2002

Chrysotile and tremolite asbestos fibres in the lungs and parietal pleura of Corsican goats.

BACKGROUND AND AIMS: Environmental exposures to chrysotile and tremolite from the soil cause pleural plaques and mesothelioma in northeast Corsica. Goats grazing in the contaminated areas inhale asbestos fibres. We used this natural animal model to study whether these exposures actually result in increased fibre burdens in the lungs and parietal pleura. METHODS: Ten goats from areas with asbestos outcrops and two from other areas were slaughtered. Fibre content of lung and parietal pleural samples was determined by analytical transmission electron microscopy. RESULTS: Both chrysotile and tremolite fibres were detected. In the exposed goats, the geometric mean concentrations of asbestos fibres longer than 1 microm were 0.27 x 10(6) fibres/g dry lung tissue and 1.8 x 10(6) fibres/g dry pleural tissue. Asbestos fibres were not detected in the lungs of the two control goats. Chrysotile fibres shorter than 5 microm were predominant in the parietal pleura. Tremolite fibres accounted for 78% and 86% of the fibres longer than 5 microm in lung and parietal pleural samples, respectively. CONCLUSIONS: Environmental exposure in northeast Corsica results in detectable chrysotile and tremolite fibre loads in the lung and parietal pleura of adult goats. Tremolite fibres of dimensions with a high carcinogenic potency are detected in the parietal pleura.

Animals↗

PubMed1997

Role of extracellular signal-regulated protein kinases in apoptosis by asbestos and H2O2.

Stimulation of cell signaling cascades by oxidants may be important in the pathogenesis of pulmonary and pleural diseases. Here, we demonstrate in rat pleural mesothelial cells that apoptotic concentrations of crocidolite asbestos and H2O2 induce phosphorylation and activation of extracellular signal-regulated protein kinases (ERK). Activation of c-jun-NH2-terminal protein kinases (JNK)/stress-activated protein kinases was also observed in response to H2O2. In contrast, asbestos caused more protracted activation of ERK without JNK activation. Both H2O2- and asbestos-induced activation of ERK was abolished by catalase. Moreover, chelation of surface iron from crocidolite fibers or addition of N-acetyl-L-cysteine prevented ERK activation and apoptosis by crocidolite, indicating an oxidative mechanism of cell signaling. The MEK1 inhibitor PD-98059 abrogated asbestos-induced apoptosis, confirming a causal relationship between ERK activation and apoptosis. These results suggest that distinct cell-signaling cascades may be important in phenotypic responses elicited by oxidant stresses.

Acetylcysteine↗

PubMed1999

Asbestos exposure upregulates the adhesion of pleural leukocytes to pleural mesothelial cells via VCAM-1.

This study was designed to assess the effects of in vitro and in vivo asbestos exposure on the adhesion of rat pleural leukocytes (RPLs) labeled with the fluorochrome calcein AM to rat pleural mesothelial cells (RPMCs). Exposure of RPMCs for 24 h to either crocidolite or chrysotile fibers (1.25-10 microgram/cm(2)) increased the adhesion of RPLs to RPMCs in a dose-dependent fashion, an effect that was potentiated by interleukin-1beta. These findings were not observed with nonfibrogenic carbonyl iron particles. Crocidolite and chrysotile plus interleukin-1beta also upregulated vascular cell adhesion molecule-1 mRNA and protein expression in RPMCs, and the binding of RPL to asbestos-treated RPMCs was abrogated by anti-vascular cell adhesion molecule-1 antibody. PRLs exposed by intermittent inhalation to crocidolite for 2 wk manifested significantly greater binding to RPMCs than did RPLs from sham-exposed animals. The ability of asbestos fibers to upregulate RPL adhesion to RPMCs may play a role in the induction and/or potentiation of asbestos-induced pleural injury.

Administration, Inhalation↗

PubMed1981

Chrysotile asbestos inhalation in rats: deposition pattern and reaction of alveolar epithelium and pulmonary macrophages.

The initial deposition and subsequent translocation of chrysotile asbestos were studied in the lungs of rats exposed for 1 h in inhalation chambers. Using scanning and transmission electron microscopy of tissue fixed by vascular perfusion, we determined that the majority of fibers that pass through the conducting airways deposits at the bifurcations of alveolar ducts. The farther an alveolar duct bifurcation was from its terminal bronchiole, the less asbestos were observed. The amount of asbestos present on the alveolar duct surfaces was significantly decreased 5 h after cessation of the 1-h exposure. Some fibers were taken up by Type I epithelial cells during the first hour of dusting, and this process continued through the 8-day period in which the animals were studied. As early as 24 h after exposure, there was an accumulation of macrophages at the sites of initial asbestos deposition. This may be a significant cellular response in the early pathogenesis of asbestosis.

Animals↗

PubMed1984

Interstitial pulmonary fibrosis induced in hamsters by intratracheally administered chrysotile asbestos. Histology, lung mechanics, and inflammatory events.

The development of interstitial pulmonary fibrosis (IPF) is associated with persistent cellular infiltration and progressive connective tissue accumulation in the alveolar walls. To develop and characterize an animal model of IPF in which pulmonary fibrosis evolves slowly, as well as to develop an inexpensive, easily produced, model of asbestosis, Syrian golden hamsters received single intratracheal injections of either UICC chrysotile asbestos or saline. Animals were then examined at time points up to 180 days for pulmonary histologic and physiologic changes, cytologic characteristics of cells recovered by bronchoalveolar lavage, and spontaneous release of neutrophil chemoattractant activity by alveolar macrophages. Within days after asbestos treatment, hamsters developed a patchy bronchopneumonia centered around terminal airways, which progressed peripherally with time to involve the alveolar walls with persistent inflammation and the gradual development of interstitial and peribronchiolar fibrosis. These histologic changes were accompanied by physiologic findings of air-flow obstruction with air trapping. Bronchoalveolar lavage revealed a persistent neutrophilia that began within 24 h of asbestos treatment; this was associated with the spontaneous release of neutrophil chemotactic activity by cultured alveolar macrophages. In this animal model, pulmonary inflammation and fibrosis can be predictably produced by a single intratracheal instillation of chrysotile asbestos. It represents a useful tool for studying both asbestosis and pulmonary fibrosis in general.

Animals↗

PubMed1983

Asbestos in drinking water: a Canadian view.

For several years now, public health professionals have been faced with evaluating the potential hazards associated with the ingestion of asbestos in food and drinking water. In Canada, this is a subject of particular concern, because of the widespread occurrence of chrysotile asbestos in drinking water supplies. The results of available Canadian monitoring and epidemiologic studies of asbestos in drinking water are reviewed and discussed in light of other published work. It is concluded that the risk to health associated with the ingestion of asbestos, at the levels found in municipal drinking water supplies, is so small that it cannot be detected by currently available epidemiologic techniques.

Asbestos↗

PubMed1993

Malignant pleural mesothelioma caused by environmental exposure to asbestos or erionite in rural Turkey: CT findings in 84 patients.

OBJECTIVE: Malignant pleural mesothelioma in rural Turkey frequently results from environmental exposure to tremolite asbestos or fibrous zeolite (erionite). The aim of this study was to determine the CT features of malignant pleural mesothelioma in patients exposed to asbestos or erionite. MATERIALS AND METHODS: The CT scans of 84 patients with proved malignant pleural mesothelioma were retrospectively evaluated. Twenty patients (24%) had been exposed to erionite and 64 patients (76%) had been exposed to asbestos. The CT scans were interpreted by seven observers who did not know the clinical or pathologic findings. RESULTS: CT scans showed either unilateral pleural thickening or pleural nodules/masses in all patients. Pleural nodules were present in 25 patients (30%) and pleural masses in 44 patients (52%). Pleural effusion was found in 61 patients (73%), mediastinal pleural involvement in 78 (93%), pleural calcifications in 52 (62%), involvement of the interlobar fissures in 64 (76%), and volume contraction in 61 (73%). Reduced size of the hemithorax was significantly correlated with chest wall involvement. On the basis of CT findings, the preassigned staging was changed in 21 patients (25%), including 44% of the patients with disease that had been classified as stage I. CT findings were not significantly different between the patients exposed to erionite and those exposed to asbestos. CONCLUSION: The most common CT findings in cases of malignant pleural mesothelioma were unilateral pleural thickening or pleural nodules/masses with or without effusion. CT provided valuable information on the extent of the disease, which was important for staging. Although the CT features are not pathognomonic, they provide valuable clues to the diagnosis in patients who have been exposed to mineral fibers.

Adult↗

PubMed2001

Amphibole fibres in Chinese chrysotile asbestos.

Ten chrysotile bulk samples originating from six Chinese chrysotile mines were studied for amphibole fibres. Five of the mines operate on ultramafic rocks whereas one exploits a dolomite-hosted deposit. The asbestos fibre content in lung tissue was examined from seven deceased workers of the Shenyang asbestos plant using these raw materials. The bulk samples were pretreated with acid/alkali-digestion, and thereafter, scanning and transmission electron microscopy, X-ray microanalysis, selected area electron diffraction and X-ray powder diffractometry were used to identify the minerals. Sample preparation of lung tissue involved drying and low-temperature ashing. All of the bulk samples contained amphibole fibres as an impurity. The amphibole asbestos contents were between 0.002 and 0.310 w-%. Tremolite fibres were detected in every sample but anthophyllite fibres were present only in the sample originating from the dolomite-hosted deposit. In comparison, anthophyllite (71%), tremolite (9%) and chrysotile (10%) were the main fibre types in the lung tissue samples indicating faster pulmonary clearance of chrysotile fibres. The total levels ranged from 2.4 to 148.3 million fibres (over 1 microm in length) per gram of dry tissue, and they were consistent with heavy occupational exposure to asbestos.

Aged↗