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PubMed1989

Statistical analysis of data on airborne asbestos levels collected in an EPA survey of public buildings.

Data from a recent EPA study of airborne asbestos levels in 49 buildings occupied by the General Services Administration (GSA) are statistically analyzed. The study focuses on differences between indoor and outdoor levels, and on differences among buildings with no asbestos-containing material (ACM) (6 buildings), buildings with ACM generally in good condition (6 buildings), and buildings containing damaged ACM (37 buildings). Seven indoor samples and a single outdoor sample were collected from most buildings and analyzed by TEM (transmission electron microscopy) using a direct preparation method. No statistically significant differences were detected in asbestos levels between indoors and outdoors or among the three categories of buildings. The average indoor concentration of asbestos was 0.00073 fibers/cc (f/cc) for all fibers and 0.00007 f/cc for fibers 5 microns or longer. The current OSHA occupational standard is 0.2 f/cc for fibers 5 microns or longer as measured by phase-contrast microscopy.

Air Pollutants, Occupational↗

PubMed1980

Asbestos body phagocytosis by human free alveolar macrophages.

Phagocytosis of asbestos bodies by human free alveolar macrophages (FAMs) was documented employing light microscopy. This process was more carefully studied utilizing scanning electron microscopy (SEM) which demonstrated morphological and surface membrane changes in FAMs following phagocytosis of asbestos bodies. FAM viability was also evaluated following 24--72-h incubation of cells with asbestos bodies at a final concentration of 250 micrograms/ml. Slight, but significant, cytotoxicity was observed following the initial 24-h culture period (P = 0.032, paired, 2-tailed t-test). No further cytotoxicity was observed, however, when cells were further incubated for 48-h and 72-h intervals (P greater than 0.05 in all instances). These studies demonstrate asbestos bodies are readily phagocytized by cultured FAMs, and are only slightly cytotoxic to these human lung cells.

Adult↗

PubMed1996

In vivo studies on genotoxicity and cogenotoxicity of ingested UICC anthophyllite asbestos.

Early cytogenetic action of oral exposure to UICC anthophyllite, an amphibole type of asbestos, was studied in Fischer-344 rats. The animals were gavaged with a suspension of untreated fibres (50 mg/kg) and fibres which had been allowed to adsorb benzo[alpha]pyrene molecules from aqueous solutions of 0.25-2.5 micrograms/ml. HPLC measurements indicated effective adsorption of the benzo[alpha]pyrene molecules on the fibres. The authors consider this system a suitable model for the drinking of water containing asbestos fibres and organic micropollutants. The formation of micronuclei and sister chromatid exchanges was studied in bone marrow samples taken from animals 24 h after oral administration of suspensions. Whereas anthophyllite fibres failed to induce cytogenetic alterations, fibres pretreated with the polycyclic aromatic solutions caused dose-dependent increase in the sister chromatid exchange frequencies. The observed cytogenetic impact can be explained by a local action of carcinogen molecules accumulated and subsequently transported. The results support the hypothesis that epidemiological evidence of carcinogenicity of asbestos in potable water may rather be explained by cogenotoxic action of the asbestos fibres and biologically active organic micropollutants adsorbed on their surface.

Administration, Oral↗

PubMed2005

Increased sensitivity to asbestos-induced lung injury in mice lacking extracellular superoxide dismutase.

Asbestosis is a chronic form of interstitial lung disease characterized by inflammation and fibrosis that results from the inhalation of asbestos fibers. Although the pathogenesis of asbestosis is poorly understood, reactive oxygen species may mediate the progression of this disease. The antioxidant enzyme extracellular superoxide dismutase (EC-SOD) can protect the lung against a variety of insults; however, its role in asbestosis is unknown. To determine if EC-SOD plays a direct role in protecting the lung from asbestos-induced injury, intratracheal injections of crocidolite were given to wild-type and ec-sod-null mice. Bronchoalveolar lavage fluid (BALF) from asbestos-treated ec-sod-null mice at 24 h, 14 days, or 28 days posttreatment showed increased inflammation and total BALF protein content compared to that of wild-type mice. In addition, lungs from ec-sod-null mice showed increased hydroxyproline content compared to those of wild-type mice, indicating a greater fibrotic response. Finally, lungs from ec-sod-null mice showed greater oxidative damage, as assessed by nitrotyrosine content compared to those of their wild-type counterparts. These results indicate that depletion of EC-SOD from the lung increases oxidative stress and injury in response to asbestos.

Animals↗

PubMed2006

Polymorphisms in DNA repair genes as risk factors for asbestos-related malignant mesothelioma in a general population study.

Differences in response to carcinogenic agents are due to the allelic variants of the genes that control it. Key genes are those involved in the repair of the DNA damage caused by such agents. This paper describes the results of a case-control epidemiological study designed to determine the genotypes of four of these genes in persons exposed to a single genotoxic factor, i.e. asbestos, who had or had not developed malignant mesothelioma (MM). Our working hypothesis was that an imperfect DNA repair, as revealed by subtle polymorphic variants, could reduce protection against the chronic DNA insult provoked by asbestos and eventually result in mutagenesis and cancer. Seven variants (i.e. XRCC1-R399Q-NCBI SNP, XRCC1-R194W, XRCC3-T241M, XRCC3-IVS6-14, XPD-K751Q, XPD-D312N, OGG1-S326C) were investigated in 81 patients and 110 age and sex-matched controls, all residents at Casale Monferrato, a Piedmontese town highly exposed to asbestos pollution. Unconditional multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). When considered as a categorical variable, XRCC1-399Q showed an increased OR both in heterozygotes (OR=2.08; 95% CI=1.00-4.33) and homozygotes (2.38; 95% CI=0.82-6.94), although individual ORs were not significant. When it was considered as a continuous variable OR was significant (OR=1.68; 95% CI: 1.02-2.75). When genotypes were divided into "non-risk" and "risk" genotypes, i.e. those thought to be associated with increased risk in the light of the functional significance of the variants, XRCC1-399Q (Q homozygotes+Q/R heterozygotes versus R homozygotes) had an OR=2.147 (95% CI: 1.08-4.28), whereas that of XRCC3-241T (T homozygotes+M/T heterozygotes versus M homozygotes) was 4.09 (95% CI: 1.26-13.21) and that of OGG1-326C was increased, though not significantly. None of the haplotypes showed a significantly different frequency between patients and controls. This is the first report of an association between polymorphisms in DNA repair genes and asbestos-associated MM. Our data indicate that genetic factors are involved in MM development.

Aged↗

PubMed2005

Evaluation of cellular toxicity of TAFMAG, a natural substitute for asbestos from China.

Asbestos is a very important material for industrial use. However, the need for a substitute for asbestos fiber is currently on the rise due to its high disease causing potential. This study evaluated the potential bio-hazardous effects of TAFMAG, a natural fibrous silicate produced in China, in comparison with chrysotile, a typical toxic asbestos. The physicochemical properties of TAFMAG were very similar to those of chrysotile when it was examined by a scanning electron microscope (SEM) and X-ray diffraction (XRD) analyses. Both of TAFMAG and chrysotile showed high content of magnetite and Fenton activity when compared with wollastonite, a non-asbestos fiber with a known low toxicity. When their cellular toxicity was assessed, TAFMAG showed no or less comparable to that of chrysotile in the hemolysis and lipid peroxidation of erythrocytes, and also on a MTT assay in RLE-6TN, a rat alveolar epithelial cell line. Pre-treatment of fibers with desferrioxamine, an iron chelator, showed that iron content of TAFMAG and chrysotile might be important in their cellular toxicity. These results suggest that TAFMAG is potentially toxic when inhaled into the lung and appropriate laws and regulations should be established for its use.

Animals↗

PubMed2000

Increased phosphorylated extracellular signal-regulated kinase immunoreactivity associated with proliferative and morphologic lung alterations after chrysotile asbestos inhalation in mice.

Activation of extracellular signal-regulated kinases (ERK) has been associated with the advent of asbestos-associated apoptosis and proliferation in mesothelial and alveolar epithelial cells and may be linked to the development of pulmonary fibrosis. The objective of studies here was to characterize the development of inflammation, cellular proliferation, and fibrosis in asbestos-exposed C57Bl/6 mice in relationship to patterns of ERK phosphorylation. Inflammation occurred after 10 and 20 days of asbestos exposure as evidenced by increases in total protein and neutrophils in bronchoalveolar lavage fluid. Increases in cell proliferation were observed at 30 days in bronchiolar epithelia and at 4, 14, and 30 days in the alveolar compartment of the lung. Trichrome-positive focal lesions of pulmonary fibrosis developed at 30 days in the absence of elevations in lung hydroxyproline or procollagen mRNA levels. Striking increases in ERK phosphorylation were observed within pulmonary epithelial cells at sites of developing fibrotic lesions after 14 and 30 days of inhalation. In addition to characterizing a murine inhalation model of asbestosis, we provide the first evidence showing activation of ERK signaling within lung epithelium in vivo, following inhalation of asbestos fibers.

Administration, Inhalation↗

PubMed1998

A comparison of historic asbestos measurements using a thermal precipitator with the membrane filter-phase contrast microscopy method.

The published results and analytical methods used in a 1938 survey of the spinning area in a UK crocidolite asbestos factory have been described and re-interpreted, by comparing the method used with the current membrane filter-phase contrast microscopy (MF-PCM) method for asbestos. By good fortune, most of the original microscope, and thermal precipitator sampling heads similar to those used for sampling were available, as well as guidance from the factory inspector who collected and analysed the original samples. A textile grade crocidolite asbestos was used to generate a fibrous dust cloud whose size distribution was characterised by scanning and transmission electron microscopy and found to give a close approximation to the fibre size distributions monitored in 1938. Samples taken over the same sampling time, but at lower concentrations than originally sampled, showed that the thermal precipitator-oil immersion microscopy (TP-OI) method used at x 2000 magnification, gave higher > 5 microns long fibre counts by a factor of between 3 and 4, than the current MF-PCM method. The differences in performance could be explained by the superior resolving power of the TP-OI method for fine crocidolite fibres. Exposures of airborne asbestos fibres in the spinning area were found to be equivalent to about 20 f ml-1 for personal samples and 10 f ml-1 for area samples, but due to the high levels of ventilation on the day the samples were collected, the average levels throughout the year may have been somewhat higher.

Air Pollutants, Occupational↗

PubMed1985

Thoracic surgical problems in asbestos-related disorders.

Among 1,577 persons with asbestos exposure followed up from 3 to 30 years, 113 had thoracic surgical procedures for asbestos-related disorders. Twenty-six individuals suspected of having asbestosis with atypical features underwent open-lung biopsy; a different disease was revealed in 14. Most of the 29 patients with mesothelioma had a small thoracotomy for diagnosis only; chemotherapy in half of them proved entirely ineffective. Experience with 23 patients with bronchogenic carcinoma did not differ from that in persons not exposed to asbestos. Problems of causal relationship are discussed. Most of the 68 individuals with benign asbestos pleural effusion had no symptoms, but because of recurrence, 15 were operated on for decortication or for possible mesothelioma. Hyaline plaques often were mistaken for lung, rib, or diaphragmatic tumors, and sometimes mesothelioma was suspected. Operative intervention in the 24 patients with plaques could have been avoided by obtaining a more detailed occupational history and reviewing previous chest roentgenograms, which invariably showed identical or smaller plaques from 2 to 17 years earlier.

Adult↗

PubMed1991

Regulation of in-place asbestos-containing material.

Approximately two-thirds of New York City's 800,000 buildings contain asbestos. Most of this material is damaged or deteriorating. Legislation pending in the New York City Council (Bill number 453) would require virtually all building owners to inspect for asbestos, to develop management and maintenance plans to prevent disturbance of intact material, and to provide notice of the presence of asbestos to building occupants. This paper reviews the legislation and discusses its features that have been questioned. It concludes that regulation of in-place asbestos is necessary and appropriate.

Animals↗

PubMed1986

Outcome of asbestos exposure (lung fibrosis and antinuclear antibodies) with respect to skin reactivity: an 8-year longitudinal study.

Two hundred seventy asbestos workers were examined during an 8-year period. During this time five consecutive surveys were completed. Skin tests with streptokinase-streptodornase (SK-SD), tuberculin (PPD), and phytohemagglutinin (PHA) were performed in the middle of this period. The results of these tests were related to X-ray chest film results and the appearance of antinuclear antibodies (ANA). In all surveys, except the first, X-ray films with small irregular opacities with a profusion greater than or equal to 1/1 belonged more frequently to asbestos workers who did not respond to SK-SD or PHA. Thirty-one cases of asbestosis were diagnosed at that time, 23 of them became asbestotic after the skin tests were performed. Asbestotic cases contributed more frequently to the group with anergy as compared to asbestos workers lacking asbestosis. Furthermore, asbestosis was correlated with lack of response to second strength of SK-SD in males and PHA in both sexes. Lack of response to these activators was predictive of asbestosis. Asbestos workers with ANA frequently displayed a lack of response to the first strength of SK-SD, PPD, and PHA. This was partly due to the presence of asbestotic cases in the group. However, low responders to all these activators were found more frequently in the group with ANA independent of the presence of asbestosis.

Adult↗

PubMed1989

Bronchoalveolar lavage analysis, gallium-67 lung scanning and soluble interleukin-2 receptor levels in asbestos exposure.

This study examined different markers of lung immunologic and inflammatory responses to previous asbestos exposure. We performed bronchoalveolar lavage (BAL) and gallium-67 (67Ga) lung scans and measured serum and BAL soluble interleukin-2 receptor (IL-2R) and angiotensin-converting enzyme (SACE) levels in 32 subjects with a history of significant asbestos exposure, 14 without (EXP) and 18 with (ASB) radiographic evidence of asbestosis. BAL analysis revealed increases in neutrophils in both ASB and EXP when compared to controls (P less than 0.01), which persisted after adjustment for smoking category. Although significant abnormalities of macrophage and total lymphocyte profiles were not found in the study population, lymphocyte subpopulation analysis revealed elevation of BAL T4/T8 ratios in the entire study group (ASB + EXP) when compared to controls (P less than 0.05), independent of smoking category. 67Ga lung scan activity was increased in 56% of ASB and in 36% of EXP: no correlations between positive scans and different radiological and functional parameters could be found. There was no significant elevation of mean SACE, serum, or BAL IL-2R levels in any of the study categories. These data suggest that asbestos exposure may be associated with parenchymal inflammation, even in the absence of clinical criteria for asbestosis. Abnormalities of gallium uptake and of BAL analysis reflect the clinically inapparent inflammation. The increased BAL T4/T8 ratios observed suggest that abnormal local pulmonary immunoregulation may play a role in the pathogenesis of asbestos-related lung diseases.

Adult↗

PubMed1989

Plasma lipid peroxides among workers exposed to silica or asbestos dusts.

Plasma malondialdehyde (MDA) (an indicator of lipid peroxidation) was determined in random samples of workers (age range 25-60 years) exposed to silica dust (n = 31, mean exposure duration 21.3 +/- 8.3 years) or asbestos dust (n = 59, mean exposure duration 15.6 +/- 4.5 years) and in 52 age-matched healthy male controls. MDA levels of both exposed groups were significantly higher than that of the controls and were significantly higher among workers exposed to asbestos than among those exposed to silica dusts. Neither age nor smoking was related to MDA levels among both controls and exposed workers; among the latter group MDA was not significantly correlated with duration of exposure. Mean MDA levels of exposed workers with radiographic signs of lung fibrosis or pleural thickening and of those without such signs were not significantly different, except in the case of asbestos-exposed workers where it was significantly less than that of those without such signs. Differences between mean durations of dust exposure of workers with radiographic signs of lung fibrosis and those without such signs were statistically insignificant. The results suggest the possible involvement of lipid peroxidation on exposure to silica or asbestos dusts in humans and possible development of antioxidant mechanism(s) on prolonged dust exposure and support the opinion that development of pneumoconiosis depends on susceptibility factor(s).

Air Pollutants, Occupational↗

PubMed1997

Induction of micronuclei, hyperdiploidy and chromosomal breakage affecting the centric/pericentric regions of chromosomes 1 and 9 in human amniotic fluid cells after treatment with asbestos and ceramic fibers.

This article describes the induction of micronuclei, hyperdiploidy and chromosome breakage in human amniotic cells in vitro by amosite, chrysotile and crocidolite asbestos, and ceramic fibers. The response of human (amniotic fluid cells) and rodent (Syrian hamster embryo fibroblasts, SHE) cells to fiber treatment was compared using the micronucleus assay. The data of the rodent studies were taken from a previous investigation (Dopp, E. et al. (1995) Environ. Health Perspect., 103, 268-271). All types of mineral fibers caused a significant increase of micronucleated cells. The kinetochore analysis revealed that all three types of asbestos and ceramic fibers yielded similar effects. Approximately 50% of the induced micronuclei were kinetochore-negative indicating formation through clastogenic events. Human amniotic cells were much less susceptible than SHE cells to the induction of micronuclei by mineral fibers. This again demonstrates that SHE cells are more susceptible to chromosomal changes than human amniotic fluid cells. The application of fluorescence in situ hybridization (FISH) with tandem DNA probes yielded more detailed information about specific structural chromosome aberrations in the 1 (cen-q12) and 9 (cen-q12) regions and about abnormal numbers of chromosomes in interphase human amniotic fluid cells. Using this FISH approach we found a statistically significant increase of chromosomal breakage in the pericentric heterochromatin regions of chromosomes 1 and 9 in interphase human amniotic cells after exposure to asbestos and ceramic fibers compared to control cells. The number of hyperdiploid cells was also significantly increased. Our results show that asbestos fibers as well as ceramic fibers are inducers of structural and numerical chromosomal aberrations in human amniotic fluid cells.

Amniotic Fluid↗

PubMed2003

Oxalate deposition on asbestos bodies.

We report on a deposition of oxalate crystals on ferruginous bodies after occupational exposure to asbestos demonstrated in 3 patients. We investigated the mechanism and possible significance of this deposition by testing the hypothesis that oxalate generated through nonenzymatic oxidation of ascorbate by asbestos-associated iron accounts for the deposition of the crystal on a ferruginous body. Crocidolite asbestos (1000 microg/mL) was incubated with 500 micromol H(2)O(2) and 500 micromol ascorbate for 24 hours at 22 degrees C. The dependence of oxalate generation on iron-catalyzed oxidant production was tested with the both the metal chelator deferoxamine and the radical scavenger dimethylthiourea. Incubation of crocidolite, H(2)O(2), and ascorbate in vitro generated approximately 42 nmol of oxalate in 24 hours. Oxalate generation was diminished significantly by the inclusion of either deferoxamine or dimethylthiourea in the reaction mixture. Incubation of asbestos bodies and uncoated fibers isolated from human lung with 500 micromol H(2)O(2) and 500 micromol ascorbate for 24 hours at 22 degrees C resulted in the generation of numerous oxalate crystals. We conclude that iron-catalyzed production of oxalate from ascorbate can account for the deposition of this crystal on ferruginous bodies.

Asbestos, Crocidolite↗

PubMed1999

On the mechanism of cogenotoxic action between ingested amphibole asbestos fibres and benzo[a]pyrene: II. Tissue specificity studies using comet assay.

Epidemiological data seem to be equivocal on the probable increase in cancer incidence in populations exposed to asbestos-fibre contaminated drinking water. Although animal experiments failed to demonstrate carcinogenicity of oral asbestos exposure, the large surface area of the fibres, however, creates the possibility of cogenotoxic action with adsorbed water-borne organics. In our animal model, rats were gavaged with untreated UICC crocidolite and anthophyllite fibres and fibres that had been allowed to adsorb benzo[a]pyrene molecules from aqueous solutions. Peritoneal macrophages and intestine, parietal peritoneum and omentum samples were obtained from the animals after 24 h. The alkaline single-cell microgel electrophoresis assay (comet assay) was performed on cells isolated from the solid tissues. Tail moment was applied as a basis of evaluation following image analysis. Our results indicate high levels of DNA strand breaks in the cells prepared from the omentum and intestine. We could also demonstrate a significant potentiating effect of the adsorbed carcinogen on the induction of DNA damage in the omentum. The parietal peritoneum and macrophages were not involved in the early genotoxic alterations under study. Our results support the molecular model of asbestos cocarcinogenesis, including both asbestos-induced deletions and mutations caused by a mutagen carried by the same fibres.

Animals↗

PubMed2002

Dual role of inducible nitric oxide synthase in acute asbestos-induced lung injury.

Reactive oxygen and nitrogen species have been implicated in the pathogenesis of asbestos fibers-associated pulmonary diseases. By comparing the responses of inducible nitric oxide synthase (iNOS) knockout and wild-type mice we investigated the consequences of iNOS expression for the development of the inflammatory response and tissue injury upon intratracheal instillation of asbestos fibers. Exposure to asbestos fibers resulted in an increased iNOS mRNA and protein expression in the lungs from wild-type mice. Moreover, iNOS knockout mice exhibited an exceeded pulmonary expression and production of TNF-alpha as well as a higher influx of neutrophils into the alveolar space than wild-type mice. In contrast, iNOS knockout animals displayed an attenuated oxidant-related tissue injury reflected in a decrease in protein leakage and LDH release into the alveolar space as well as weaker nitrotyrosine staining of lung tissue compared to wild-type mice. Data presented here indicate that iNOS-derived NO exerts a dichotomous role in acute asbestos-induced lung injury in that iNOS deficiency resulted in an exacerbated inflammatory response but improved oxidant-promoted lung tissue damage.

Acute Disease↗

PubMed1998

In vivo evidence of free radical formation after asbestos instillation: an ESR spin trapping investigation.

It has been postulated that the in vivo toxicity of asbestos results from its catalysis of free radical generation. We examined in vivo radical production using electron spin resonance (ESR) coupled with the spin trap alpha-(4-pyridyl-1-oxide)-N-t-butylnitrone (4-POBN); 180 day-old rats were intratracheally instilled with either 500 microg crocidolite or saline. Twenty-four hours later, histologic examination revealed a neutrophilic inflammatory response. ESR spectroscopy of the chloroform extract from lungs exposed to asbestos gave a spectrum consistent with a carbon-centered radical adduct, while those spectra from lungs instilled with saline revealed a much weaker signal. This same radical formation persisted and, even one month after instillation, could be detected in the lungs of rats exposed to asbestos. The 4-POBN adducts detected by ESR are very similar to, if not identical with, ethyl and pentyl radical adducts, providing evidence of in vivo lipid peroxidation resulting from asbestos exposure. We conclude that, after instillation of crocidolite in the rat, ESR analysis of lung tissue demonstrates in vivo free radical production.

Animals↗