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PubMed1993

Characterization of asbestos fibers in lungs and mesotheliomatous tissues of baboons following long-term inhalation.

Changes in the dimensions of inhaled asbestos fibers in the lung and translocation of intrapulmonary asbestos fibers into mesothelial tissues were investigated in 17 baboons (5 exposed to amosite, 4 to chrysotile, 5 to crocidolite, and 3 unexposed). The animals received different cumulative doses of asbestos by inhalation, followed by varying recovery periods (0-69 months). All asbestos types induced pulmonary asbestosis with severity directly related to the cumulative dose. There were a larger number of asbestos bodies in the lung of the amphibole-exposed animals than in those exposed to chrysotile. A tissue burden study, using transmission electron microscopy on 25-microns paraffin sections, ashed in a low-temperature asher, was performed. Intrapulmonary amosite fibers were shorter in geometric mean length compared with a standard amosite sample (UICC) (3.3 microns). In explanation, it was considered that long fibers might not be able to reach the lower respiratory tract and/or long fibers might be fragmented into shorter fibers. Further, in the amosite-exposed group, the mean length of intrapulmonary fibers increased with the extension of recovery period, suggesting that shorter fibers had been cleared from the lung. The chrysotile standard sample (UICC) had a shorter geometric mean length (1.1 microns) than amosite. The mean length of intrapulmonary chrysotile did not noticeably change with the extension of inhalation and recovery periods; however, the mean width decreased with the extension of these periods. This finding strongly suggested that separation of thick chrysotile fibers had occurred in the lung. The crocidolite standard sample (Transvaal) had a shorter geometric mean length (1.4 microns) than amosite.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Intracellular protein binding to asbestos induces aneuploidy in human lung fibroblasts.

Exposure to the natural mineral fiber asbestos causes severe lung-damaging fibrosis and cancer, yet it continues to be used as an industrial insulating material throughout the world. When cultured human lung cells are exposed to asbestos, individual fibers are engulfed into the cytoplasm where they induce significant mitotic aberrations leading to chromosomal instability and aneuploidy. The mechanisms of how asbestosis ultimately leads to lung cancer remain unclear. However, our experiments indicate that intracellular asbestos fibers induce aneuploidy and chromosome instability by binding to a subset of proteins that include regulators of the cell cycle, cytoskeleton, and mitotic process. Moreover, precoating of fibers with protein complexes efficiently blocked asbestos-induced aneuploidy in human lung cells without affecting their uptake by cells. These results provide new evidence that asbestos fibers can contribute to significant spindle damage and chromosomal instability by binding to proteins needed for the assembly and regulation of the cytoskeleton or the cell cycle.

Aneuploidy↗

PubMed1995

Lung adenocarcinoma and indicators of asbestos exposure.

A case-control study was carried out on 145 male lung-cancer patients diagnosed at autopsy and 178 controls, in order to investigate the relationship between asbestos exposure and the cell type of pulmonary carcinoma. Adenocarcinomas (AD) were individually matched with other cell types and with controls. The relative risk (RR) of developing AD in relation with lung asbestos body (AB) content as the exposure indicator was calculated by using logistic-regression analysis for matched sets. Two cutoff levels, 1,000 and 10,000 asbestos bodies per gram dry weight (AB/gdw), were used in the analysis. In addition, AB counts were treated as a continuous variable (log AB+I). A significant association was found between AD and asbestos exposure, using levels and logarithmic transformation. However, an association of asbestos exposure with cell types other than AD could not be ruled out.

Adenocarcinoma↗

PubMed1993

Respiratory findings among millwright and machinery erectors: identification of health hazards from asbestos in place at work.

Asbestos-associated diseases are prevalent in the construction trades primarily because of the previously widespread use of asbestos-containing insulation materials. Workers in metal-related trades, employed at construction sites and power facilities, but who do not routinely handle such materials as part of their work, may also be at risk for significant asbestos exposure. In order to evaluate such risk, a clinical field survey was conducted of 110 millwright and machinery erectors from the New York metropolitan area. A high prevalence of chest roentgenologic abnormalities was found. Forty-nine (44.5%) of the examined workers had pleural abnormalities consistent with asbestos-induced effects. Eighteen workers showed evidence of unilateral pleural thickening. Duration from onset of employment was significantly longer for those with pleural abnormalities (mean 32.3 years) as compared to those with normal chest radiographs (mean 18.5 years). Thirteen workers (11.8%) had radiographic signs of interstitial lung disease. The workers with pleural abnormalities had lower mean values of restrictive and obstructive lung function parameters than those with normal pleura. Multivariate and logistic regression analyses demonstrated association between duration of employment in the millwright trade and pleural abnormalities which was independent of smoking status. These findings suggest that millwright and machinery erectors employed in work environments where there is potential for primarily indirect exposure to airborne asbestos-containing dust are at risk for adverse effects from such exposure.

Adult↗

PubMed2002

Chemiluminescent detection of induced reactive oxygen metabolite production of human polymorphonuclear leucocytes by anthophyllite asbestos.

Incidences of lung cancer and pleural plaque have been reported in relation to exposure to anthophyllite asbestos. To investigate the pathogenic mechanisms of anthophyllite, chemiluminescence (CL) detection of reactive oxygen metabolite (ROM) generation of human polymorphonuclear leucocytes (PMN) stimulated by anthophyllite asbestos was determined and compared with that of other asbestos and mineral fiber samples. When anthophyllite fiber sample was mixed with the luminol-primed PMN, high levels of CL which exhibited a specific time course characterized by two separate peaks were induced. The CL induced by anthophyllite sample was greater than that induced by chrysotile, crocidolite, and amosite asbestos. We further investigated the two peaks of CL using specific inhibitors of signal transduction mechanisms. The two peaks of CL by anthophyllite sample were different in sensitivity to cytochalasin B and genistein; the former relates to the cytoskeleton-dependent mechanism and the latter has been shown to inhibit tyrosine kinase, which resides in the pathway to cause PMN activation. The strong ROM reaction of PMN by anthophyllite suggests that the surface characteristics of the fiber may participate in the pathogenic mechanisms of anthophyllite asbestos.

Androstadienes↗

PubMed1994

Asbestos in New York City public school buildings--public policy: is there a scientific basis?

The most recent of New York City's asbestos emergencies occurred in the late summer of 1993. It prevented schools from opening that fall, precipitated much media excitement, and caused a flurry of widespread abatement activities. This resulted in large measure from the U.S. Environmental Protection Agency's subjective school building inspection policy concerning identification of asbestos hazards in buildings and the subsequent Asbestos Hazard Emergency Response Act mandate for inspection. Data on concentrations of asbestos in the air, important for the calculation of risk to building occupants, were not required and therefore not obtained, as part of the abatement strategy or priority setting. Based on fiber-in-air measurements obtained elsewhere, the calculated risk to NYC school children, using the most pessimistic models, was less than six excess cancer deaths per million lifetimes equivalent to smoking less than a dozen cigarettes in a lifetime. The NYC administration responded to pressure from parent groups concerned with perceived asbestos risks to their children by closing the schools. The hysteria occurred because much of EPA's policy lacked a scientific basis for risk evaluation and assessment.

Air Pollution, Indoor↗

PubMed1988

Substantiating hazardous exposure to asbestos by examination of pulmonary dust.

Substantiation of relevant asbestos risks by microscopic examination sets a lower detection limit at fibres longer than 5 to 10 micron and thicker than 0.5 micron. Such microscopically detectable fibres are, of course, in respect to "total quantity" the insignificant part of the overall dust burden, but apparently a necessary part of the whole fraction when assessing the relevance of exposure. Until now, no epidemiologically conclusive asbestos risks resulting from occupational exposure have been made known solely with fibre fraction below the microscopic detection limit. Demands for supplementary electromicroscopic examination on the basis of case reports of lung parenchyma damage by fibres of a lower calibre than the microscopic detection limit are, therefore, presently without foundation. The subject examinations reveal that substantiation of asbestos risks with light-optical means, using different methods, provides comparable results. Initially, of course, it is surprising to obtain fluctuations in results of 100,000 to 600,000 asbestos particles for the same case. However, one must realize that calculations based on intermediate results are responsible for this range of fluctuation, due to the varying degree of asbestos fibre dispersion in the different sections of the lung and, depending on the method of detection used. Interest on the part of everyday occupational medicine and expert opinion is determined by the need to categorize individual cases into different basic classes of risk by referring to relevant morphological facts, such as substantiation of asbestosis or drawing a borderline between persons with occupational risk and those with a non-occupational risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗

PubMed1993

Pleural thickening: a comparison of oblique chest radiographs and high-resolution computed tomography in subjects exposed to low levels of asbestos pollution.

The present study was conducted to investigate the value of oblique chest radiographs, compared with high-resolution computed tomography (HRCT), in the assessment of pleural asbestosis in a group of subjects exposed to low levels of asbestos pollution. The study population consisted of 23 people derived from a previously reported cohort of subjects working in university buildings insulated with asbestos-containing material. Subjects were selected on a voluntary basis from among patients whose initial oblique chest X-rays showed pleural thickening. Sixteen patients were maintenance workers occupationally exposed to asbestos; the remaining seven were environmentally exposed to asbestos. For each subject, two standard chest radiographs [posteroanterior (PA) and right anterior oblique (RAO) views] were taken and HRCT was performed. Films were interpreted after agreement by three chest physicians and a radiologist. Pleural thickening was considered present in all 23 patients on RAO films and in six patients on PA films. HRCT revealed unequivocal pleural plaques in three maintenance workers and doubtful pleural abnormalities in three other maintenance workers. Considering HRCT as the "gold standard," the positive predictive value of RAO film was only 13%-26%. Most of the 17 false-positive diagnoses of pleural fibrosis were due to significant subpleural fat. These results suggest that the routine use of oblique radiographs as a screening test in cohorts of subjects exposed to low levels of pollution by asbestos should be reevaluated.

Air Pollutants, Occupational↗

PubMed1989

Health hazards from fine asbestos dusts. An analysis of 70,656 occupational preventive medical investigations from 1973 to the end of 1986.

For the period from 1973 to the end of 1986, 70,656 data sets on occupational preventive medical examinations in employees exposed occupationally to asbestos dust (G 1.2) were made available to us by the Central Registry for Employees Exposed to Asbestos Dust (ZAS). On the basis of this data, an analysis of asbestosis risk was to be made in relation to specific areas of work, taking into consideration the beginning and duration of exposure. Proceedings for declaratory appraisal in accordance with occupational disease no. 4103 were instituted in 1760 cases in the report period. In accordance with the character of the available data, the X-ray findings in the lungs were available from the persons investigated as parameters of possible asbestosis risk on the basis of coding consistent with the International Pneumoconiosis Classification (ILO U/C 1971 and/or ILO 1980 West Germany). The major result of the statistical analyses on the mainframe macrocomputer of the University of Erlangen-Nuremberg was that the relatively highest risk of asbestosis was present in persons whose exposure began before 1955. On the other hand, with increasing duration of exposure, an unequivocal rise of the asbestosis risk could not be detected on the basis of the overall population. In relation to the individual fields of work, the relatively highest risk of asbestosis was shown to be in the asbestos textile and paper industry, as well as in the asbestos cement industry. No detectable risk of asbestosis was present in the fields of mining, traffic and health service and for women in the industrial sectors of building material, gas and water, catering trade, building, commerce as well as banking and insurance. Accordingly, it can be assumed that certain fields of work are or were exposed to such a small extent or not at all that a risk of asbestosis which is relevant in terms of occupational medicine is no longer to be assumed or was not to be assumed. This applies above all to certain work in the frictional coating (brake lining) and asbestos paper industry. Furthermore, the analysis of the data material did not provide any unequivocal indications that inhalative smoking habits have a negative effect on the risk of asbestosis. In principle, it can be stated that the occupational preventive medical investigations according to G 1.2 are effective.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1986

Pathogenesis of pulmonary fibrosis induced by chrysotile asbestos. Longitudinal light and electron microscopic studies on the rat model.

A single instillation of 1 mg chrysotile B with a fiber length between 0.05 and 0.2 micron in 0.1 ml tricaprylin was made via a polyvinyl catheter into the lower lobe of the right lung of 120 six-week-old Wistar rats under anesthesia. The animals were killed at intervals between five minutes and two years. The lower lobes of the right lung were investigated by light and electron microscopy. The process of pulmonary fibrosis induced by asbestos can be subdivided into four phases: these are the phase of phagocytosis (five to 15 min), the phase of granuloma formation (between one and two weeks), the phase of septal fibrosis (between two and six months) and finally the scar stage (after one year). After instillation of small asbestos fibers into the alveoli, a major proportion of these fibers is phagocytosed by alveolar macrophages after five minutes and leaves the lungs via the airways. A proportion of the fibers penetrates through the alveolar wall (mostly conveyed by type I pneumocytes) and reaches the interstitium of the lungs. There, the fibers are taken up by pulmonary tissue macrophages and giant cells. Within the phagolysosomes, the fibers are broken down into fragments less than 0.01 micron in length. Type II pneumocytes produce surfactant in excess. These cells become necrotic, tubular myelin and lamellar bodies pass into the alveoli and into the interstitium. Surfactant is phagocytosed by resident macrophages. These macrophages can break down. Besides asbestos and surfactant, mediators of fibrillogenesis are released. Macrophages following up from blood monocytes ingest surfactant and asbestos. This process is perpetuated up to complete scarring. After two years, small asbestos fibers less than 0.01 micron long are present in fibroblasts and pleural mesothelia.

Animals↗

PubMed1985

Does asbestos exposure cause gastrointestinal cancer?

The relationship between asbestos exposure and gastrointestinal malignancies is unlike the well-established correlation between occupational asbestos exposure and the subsequent development of pleuropulmonary neoplasms and mesotheliomas. Cohort studies on occupationally exposed workers suggest an association between asbestos and gastrointestinal cancer, but evaluation of dose-response, tissue analysis, animal experiment, and cell culture data yield inconsistent conclusions. No simplistic cause-effect relationship can be ascribed to asbestos at the present time, and the answer to the question, "Does asbestos exposure cause cancer?" must await the results of additional studies.

Adult↗

PubMed1996

Exposure to asbestos fibres during gasket removal.

In the chemical industry, asbestos gaskets have been used extensively to prevent leakage between solid surfaces. The purpose of this study was to assess the potential personal exposure to asbestos fibres during gasket removal and thus to determine what is reasonably required in terms of protective regime and work method. Two groups were studied: group A, who only removed gaskets if they could be removed easily and without breaking; and group B, who removed gaskets which were left by the first group. For both groups, the gasket was first made wet before removal. The samples were analysed using phase-contrast microscopy and transmission electron microscopy. The average exposure to fibres for group A, averaged over the work period, was 0.04-0.242 fibres ml-1 as determined by phase-contrast microscopy. On further analysis with transmission electron microscopy it was found that only four of the 11 samples contained asbestos in very low concentrations and that most of the fibres, which were identified using phase-contrast microscopy, probably originated from the glass fibre lagging around the pipes. For group B the average fibre concentration, averaged over the work period, as determined by phase-contrast microscopy, ranged between below the detection limit and 0.02 fibres ml-1. The subsequent transmission electron microscopy analysis shows that the exposure to asbestos fibres ranged between below the limit of detection to 0.004 fibres ml-1. This study shows that the exposure to asbestos fibres during gasket removal activities was well within the 8-h average exposure limit of 0.3 fibres ml-1.

Asbestos↗

PubMed1983

Asbestos bodies in a bile duct cancer after occupational exposure.

A case of asbestosis after 5 years of occupational asbestos exposure is presented. At the postmortem examination, cholelithiasis and a cancer developing from the cystic duct were found and identified histologically as a squamous cell carcinoma. After digesting the tumor tissue, short asbestos bodies and fragments could be identified having a similar shape as those observed in the lung. The possible role of asbestos in the carcinogenesis of the observed bile duct cancer is proposed. The digestive examination of all malignant tumors of any origin after an asbestos exposure is suggested for the identification of the possible presence of ingested asbestos fibers, and to obtain further comprehensive human pathological data.

Adult↗

PubMed1985

Airborne asbestos in Colorado public schools.

Levels of airborne asbestos for six Colorado public school facilities with sprayed-on asbestos materials were documented using three analytical techniques. Phase contrast microscopy showed levels up to the thousandths of a fiber per cubic centimeter (f/cc), scanning electron microscopy (SEM) up to the hundredths of a f/cc, and transmission electron microscopy coupled to selected area electron diffraction and energy dispersive X-ray analysis (TEM-SAED-EDXA) up to the tenths of an asbestos f/cc. Phase contrast microscopy was found to be an inadequate analytical technique for documenting the levels of airborne asbestos fibers in the schools: only large fibers which were not embedded in the filter were counted, and asbestos fibers were not distinguished from nonasbestos.

Air Pollutants↗

PubMed1985

Circulating immune complexes in asbestos workers.

Circulating immune complexes, rheumatoid factor, and antinuclear antibodies were evaluated in 25 asbestos insulation workers and 32 brick mason controls. There were 10 asbestos workers with radiographic parenchymal or pleural changes, consistent with their asbestos exposure. There were no differences in antinuclear antibodies or rheumatoid factor between asbestos workers and controls. The asbestos workers had significantly increased levels of IgG and IgA circulating immune complexes. There was a significant correlation between IgA circulating immune complexes and radiographic changes.

Adult↗

PubMed1980

Fibrous ceramic aluminum silicate as an alternative to asbestos liners.

The actual risk to those exposed to asbestos fibers in the dental laboratory is presently unknown. The ADA Council on Dental Materials and Devices and ADA Council on Dental Therapeutics have received encouragement from the National Institute for Occupational Safety and Health to conduct further studies, including monitoring airborne asbestos in dental laboratories. It has been suggested that no really safe threshold limit exists for airborne asbestos fibers. Low level asbestos exposure has been implicated in numerous serious diseases. Exposures as brief as 1 month have produced disease many years later. Numerous researchers have advocated the use of a safer material. Casting ring liners compound of currently available fibrous ceramic aluminum silicate are technically adequate substitutes for asbestos.

Aluminum Silicates↗

PubMed1976

Possible asbestos hazards in clinical allergy.

The potential hazards of biological products contaminated by asbestos fibers are quite properly being reviewed by the food and pharmaceutical industries. We have demonstrated that glycerinated saline solutions can be contaminated with asbestos fibers under certain conditions of simulated clinical use of asbestos-packed syringes. Because the fibrogenic and carcinogenic effects of asbestos are subtle and may not be manifest for a long latent period, the future use of asbestos containing materials in allergy practice might be more harmful than now realized.

Asbestos↗

PubMed1979

Binding of immunoglobulin and activation of complement by asbestos fibers.

Asbestos fibers adsorbed IgG from whole human serum in amounts comparable to that taken up by crystals of calcium pyrophosphate or hydroxyapatite, but less than that adsorbed by crystals of monosodium urate monohydrate. Chrysotile asbestos was much more active in binding IgG than was amphibole asbestos. The electrophoretic mobility of adsorbed IgG was a function of the surface charge of the crystal studied. Negatively charged fibers adsorbed cationic IgG, and positively charged fibers adsorbed anionic IgG. Complement activation by asbestos, as judged by electrophoretic conversion of C3, was similar for all fiber types tested. Properdin factor B was also activated in the presence of asbestos. Activation of both properdin factor B and C3 was only partially inhibited by ethylene glycol tetraacetic acid, demonstrating that activation was occurring through both the classical and alternative pathways.

Adsorption↗