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PubMed1991

The reproducibility of the self-report of occupational exposure to asbestos and dust.

The reproducibility of self-reported exposure to asbestos and dust was examined in 116 male veterans who completed an initial mail survey and subsequent occupational clinic questionnaire a mean of 213 +/- 68 days later. For the 114 subjects who answered the asbestos question of the mail survey, 68 (60%) gave concordant replies, while 46 (40%) gave discordant answers later in the clinic. Of 51 subjects who answered yes to asbestos exposure in the clinic, 11 (22%) had answered no and 13 (26%) had answered not sure. Failure to note asbestos exposure could not be blamed exclusively on past, relatively low-level of exposure because many of the respondents had significant exposure histories. For dust exposure, 31 (29%) had discordant replies and 77 (71%) had concordant answers. Self-reported history of occupational exposure to asbestos and dust were not as reproducible as the smoking history and may be underreported when mail survey methods alone are used.

Adult↗

PubMed1991

[Familial clustering of asbestos-related diseases].

This article describes the case histories of four individuals in the same family, all of whom developed asbestos-related disease. Special emphasis is placed upon the case of a woman, who after seemingly minimal exposure to asbestos, in the form of cleaning her husband's working clothes, developed a malignant mesothelioma. The incidence of asbestos-related disease has increased steadily over the past ten years. This probably reflects the extensive use of asbestos in Norway since World War II, and the long latency period of the disease. The authors recommend obtaining an in-depth history of exposure when asbestos-related disease is suspected.

Aged↗

PubMed1990

[A case of simultaneous double cancer (lung and stomach cancer) related to asbestos exposure].

A 76 year-old male with simultaneous double cancer (lung and stomach cancer) was reported. The patient was followed up for pleural plaque on chest X-ray from 1986. The diagnosis of stomach cancer was decided by biopsy and lung cancer by operation at the same time in 1989. The histology of these two tumors were different (stomach: well differentiated tubular adenocarcinoma, lung: moderately differentiated papillary adenocarcinoma) and the stomach cancer was early stage and lung cancer was stage IIIa. He had a definite history of asbestos exposure in Japanese naval shipyard. Pleural plaque with calcification was found on chest X-ray and numerous asbestos bodies were detected in the resected lung tissue. Almost all asbestos fibers examined by an X-ray analyzer with scanning microscopy were chrysotile or tremolite. Furthermore, he was a heavy smoker (B.I., 1650). These tumors developed after 59 years of the first asbestos exposure. Asbestos exposure and smoking are considered to be important pathogenesis factors related to these two tumors.

Adenocarcinoma↗

PubMed1990

[Clinical study on asbestos pleurisy and review of literature].

Seven asbestos workers with asbestos pleurisy were investigated in terms of clinical symptoms, findings of pleural biopsies and course of chest roentgenograms. All cases were male and smokers. Duration of asbestos exposure ranged from 3 to 33 years (mean: 20.6 years). Duration between initial exposure and onset of the pleurisy ranged from 22 to 34 years (mean: 28.7 years). Five pleural effusions were aseptic and exudative, and one had sanguineus and eosinophilic effusion. According to the findings of pleural biopsies, our cases were classified into 2 groups. Group A (4 cases) had "basket-weaving formation" on the parietal side and inflammatory changes on the visceral side. No circulating autoantibodies were found in group A. Group B (3 cases) had no "basket-weaving formation" but only intensive inflammatory changes. These 3 cases were respectively complicated with anti-GBM antibody mediated glomerulonephritis, with acute interstitial pneumonia, and with rheumatoid arthritis and acute interstitial pneumonia. They all had circulating autoantibodies. In the course of chest roentgenograms, 6 of the 7 cases finally showed diffuse pleural thickenings which involved obliterations of costo-phrenic angles. Among them, one case developed into progressive pleural fibrosis. It was concluded that asbestos pleurisy can be classified into 2 groups according to the mechanism of occurrence, and immunological changes should be recognized as one of the mechanisms of asbestos pleurisy.

Adult↗

PubMed1990

[Evaluation of double cancers in relation to previous asbestos exposure].

Ten cases of double cancers (a lung cancer and a stomach cancer) were evaluated in relation to previous asbestos exposure. Ten cases involved male more than 69 years old. Five cases had developed their two cancers simultaneously and other 5 cases had developed their lung cancer after stomach cancer surgery. The lung cancer was their main disease. Four cases had early stage stomach cancers and 5 cases with a stomach cancer had no relapse after surgery. Eight cases had occupational histories of asbestos exposure. Significantly high numbers of asbestos bodies were detected in the autopsied lung in almost all cases. According to the X-ray analysis, almost all asbestos fibers detected in the lung were chrysotile. Additionally, the Brinkman Index (B.I.) of these 10 cases ranged between 700 and 2,000. The combination of asbestos exposure and smoking is thought to be an important factor in the development of such double cancers.

Adenocarcinoma↗

PubMed1990

Malignant mesothelioma in a clerk working in an asbestos factory.

Mesothelioma is a rare cancer which is associated with asbestos exposure. Generally most medical professionals are aware of this. However, not many of them may realise that individuals could develop asbestos related mesothelioma as a result of 'bystander' exposure. We report here a case of asbestos related pleural mesothelioma in a clerk who was not directly exposed to asbestos. The patient presented with signs and symptoms of a massive right pleural effusion. The diagnosis of a malignant diffuse pleural mesothelioma was made only after the pleural tissue (obtained during the thoracotomy) was sent for histology. Patient was started on chemotherapy but he succumbed to the disease and died ten months after the onset of the first symptoms. The risk of developing mesothelioma among individuals who are not directly working with asbestos is discussed in this report.

Air Pollutants, Occupational↗

PubMed1989

[Epidemiological problems of non-occupational exposure to asbestos dust].

We have presently a sufficient amount of evidence based on epidemiological and experimental investigations to regard asbestos as a carcinogen in human environment. The use of asbestos-containing products and asbestos pollution of the natural environment of man are the risk factors for neoplasms in the general population. The sources of pollution and the values of asbestos dust concentration in community environment and the estimation of the risk related to asbestos dust are presented in the light of epidemiological and ecological studies.

Air Pollutants↗

PubMed1989

[Asbestos-induced bronchopulmonary diseases].

Asbestos is a collective term for fibrous crystalline silicate minerals, which can be used to produce technically useful fibers. The various types of asbestos, such as chrysotile, crocidolite and amosite, may induce not only fibrotic changes in the pleura and lungs, but also carcinomas and mesotheliomas. The increasing industrial use of asbestos has led to a marked increase in bronchopulmonary diseases, which can be shown to be caused by occupational exposure to fine asbestos dust. In this overview, the pathological anatomy, differential diagnosis and occupational-medical assessment of the various conditions induced by asbestos are discussed.

Asbestos↗

PubMed1989

[Evaluation of primary multiple cancer manifesting exposure to asbestos].

Twenty five cases (71%) of 35 primary multiple cancer, confirmed by autopsy, were proved to have been exposed to asbestos. Of these cases, lung and stomach cancers, which were related to the asbestos exposure, were main component of the multiple cancers. Thirteen of these cases had definite occupational histories of asbestos exposure and the number of asbestos bodies in five grams of autopsied wet lung tissue amounted to more than 1000. This result suggests that asbestos exposure might possibly induce a high incidence of multiple cancers.

Aged↗

PubMed1988

Asbestos-induced activation of the respiratory burst in rabbit neutrophils.

Small particles of chrysotile asbestos cause an activation of the respiratory burst in rabbit neutrophils measured as an increase of NBT reduction. The increase of NBT reduction, which is mainly due to superoxide release, is inhibited by the polyanion poly-D-glutamic acid and by negatively charged proteins. This indicates that positive charges on asbestos play a crucial role in the interaction. Activation of the respiratory burst by asbestos is strongly dependent on high Ca2+ concentrations, and is inhibited by pertussis toxin. The stable GTP analogue guanosine-5'-O-(3-thio)-triphosphate (GTP gamma S) and asbestos have a synergistic effect on activation of the respiratory burst. The results suggest that a G-protein is involved in activation of the respiratory burst by asbestos.

Animals↗

PubMed1989

Incorporation of tritiated thymidine by epithelial and interstitial cells in bronchiolar-alveolar regions of asbestos-exposed rats.

Inhaled asbestos causes progressive interstitial lung disease. The authors have performed a series of studies to elucidate early pathogenetic events at sites of fiber deposition in asbestos-exposed rats. This study reports that a single 5-hour exposure to chrysotile asbestos induces significant increases in incorporation of tritiated thymidine (3HTdR) into nuclei of epithelial and interstitial cells of bronchiolar-alveolar regions. No cell populations in air-exposed or carbonyl iron-exposed control animals exhibited more than 1% labeling at any point in time. Immediately after the 5-hour asbestos exposure, incorporation was normal. By 19 hours after exposure there was a significant increase in incorporation of 3HTdR, particularly by Type II epithelial cells of the first alveolar duct bifurcations. The greatest increase in degree of incorporation (up to 18-fold) was observed 24 hours after exposure, and increased percentages of 3HTdR-labeled cells were maintained through the 48 hours postexposure period. Normal labeling was present by 8 days after exposure, and this level remained through the 1-month period studied. This apparent mitogenic response correlates with increased numbers of bronchiolar-alveolar epithelial and interstitial cells demonstrated by ultrastructural morphometry in correlative studies. The authors speculate that the incorporation of 3HTdR could be induced by the direct effects of inhaled fibers or by mitogenic factors released from macrophages attracted to the inhaled asbestos.

Animals↗

PubMed1988

Electron microscopic analysis of asbestos body cores from the Belgian urban population.

Typical ferruginous bodies considered as asbestos bodies (AB) were collected from the lungs of 19 asbestos-exposed and 25 non-exposed urban subjects. Of the 319 body cores analysed by energy dispersive spectrometry (EDS), 315 were asbestos. The non-asbestos cores were talc and crystalline silica. 89.2% of the asbestos cores were commercial amphiboles (amosite/crocidolite), 7% were chrysotile and 3.8% were non-commercial amphiboles (anthophyllite/tremolite). The commercial amphibole bodies were found in exposed and non-exposed subjects and chrysotile bodies mostly in exposed subjects. The non-commercial amphibole bodies were detected in non-exposed patients with low lung AB levels; this background contamination would be more difficult to detect in lungs containing large amounts of bodies due to occupational exposure. Chrysotile bodies and tremolite/anthophyllite bodies were not observed together. We suggest that in Belgium the source of non-commercial amphiboles exposure is not contamination by chrysotile.

Aged↗

PubMed1986

Identification of asbestos fibers within single cells.

Identification of asbestos fibers and other mineral particles in tissues is important for the diagnosis of interstitial lung disease. Conventional procedures to identify mineral particles are applicable to tissue digests, homogenates, or thin sections prepared for transmission electron microscopy. Positive identification of mineral particles in these samples is achieved by energy dispersive x-ray analysis or crystalline diffraction patterns. These analytical techniques are difficult to use for identification of long, thin asbestos fibers within cells collected from effusions or by saline lavage. A new preparative procedure is presented which allows intracellular visualization of fibers in these samples. Mice were injected intraperitoneally with 100 micrograms of crocidolite asbestos. After 1 to 30 days, the free peritoneal cell population was collected by saline lavage and allowed to attach to Formvar/carbon coated grids in vitro. Cell spreading was induced by exposure to phorbol-12-myristate-13-acetate for an additional 4 hours. The flattened cells were fixed, dehydrated and air-dried before examination by transmission electron microscopy. This procedure allows direct visualization of intracellular fibers. The characteristic Fe and Si peaks of crocidolite asbestos were confirmed by energy dispersive x-ray analysis. This technique was used to study the kinetics of clearance of asbestos fibers from the free peritoneal macrophage population of mice.

Animals↗

PubMedDate not supplied

Effects of chrysotile asbestos on DNA synthesis and growth of human embryonic lung fibroblasts.

The in vitro effects of asbestos fibers on thymidine (TdR3H) incorporation and growth of lung fibroblasts have been studied. Incubation of human embryonic lung fibroblasts with UICC Chrysotile B asbestos for 48 hr caused a 3 to 5-fold increase of TdR3H incorporation as compared with control cultures. This increase was dose-dependent with optimal effect obtained with doses as low as 10 micrograms/ml and with cell density of 5 X 10(4) fibroblasts per culture. However, enhanced TdR3H incorporation in treated cells was not correlated with an overall increase of the fibroblast population compared with control cultures as evidenced by cell counts and microscopic examination. Fibroblasts exposed to relatively low concentrations of UICC chrysotile (5-10 micrograms/ml) displayed an initial decrease in cell number compared to controls during the first 24 hr of incubation. At 48 hr however, enhanced TdR3H incorporation occurred with a concomittant increase in cell number. Moreover, continuous exposure of fibroblast cultures to chrysotile (10 micrograms/ml) for a longer period of time led to sustained increase of TdR3H incorporation and resumption of cell proliferation. It is suggested that increased thymidine incorporation is directly related to the effectiveness of asbestos in inhibiting the growth of lung fibroblasts and that measurement of TdR3H incorporation may represent a sensitive means of assessing rapidly the biological activity of asbestos. The possible relevance of this activity to asbestos-induced fibrogenesis and tumorigenesis is also discussed.

Asbestos↗

PubMed1985

Bronchoalveolar lavage and clearance of 99m-Tc-DTPA in asbestos workers without evidence of asbestosis.

We performed BAL and measured the clearance of 99m-Tc-DTPA in 20 non-smoking subjects (mean age 50, range 36-68 years) occupationally exposed to asbestos (mean duration 14, range 3-30 years). All had normal lung function and none had clinical or radiological evidence of asbestosis. The mean BAL results were: total cells per ml 737 X 10(3) (360-1210), percentage macrophages 79 (49-96), percentage lymphocytes 13 (1-42), percentage neutrophils 8 (1-40), percentage eosinophils 0 (0-3), asbestos bodies per ml 83 (0-550). Eight subjects showed increased percentage of lymphocytes and four others showed increased percentages of neutrophils when compared with normal ranges in our laboratory. Higher percentages of neutrophils correlated with longer duration of exposure to asbestos (r = 0.54, P less than 0.025), and shorter time since last exposure to asbestos (r = -0.54, P less than 0.025). Four subjects showed faster clearance of 99m-Tc-DTPA than was observed in 31 normal non-smoking control subjects. There was a tendency for faster solute clearance to be associated with greater numbers of BAL macrophages (r = -0.39, P less than 0.10) but there were no significant relationships between solute clearance and other BAL variables. BAL profiles in asbestos workers may be abnormal in the absence of clinical or radiological evidence of asbestosis.

Adult↗

PubMed1986

Alveolar macrophage stimulation of lung fibroblast growth in asbestos-induced pulmonary fibrosis.

Asbestotic lesions are characterized by macrophagic accumulation, fibroblast proliferation, and collagen deposition. To evaluate the potential involvement of alveolar macrophages in the subsequent fibrogenic reaction, the authors studied the effects of macrophages from normal and asbestos-treated rats upon lung fibroblast proliferation in vitro. Culture supernatants from bronchoalveolar (BAL) cells (99% macrophages) of normal rats stimulated lung fibroblast DNA synthesis and growth in a dose-dependent manner. Fibroblast growth factor (FGF) release by alveolar macrophages (AMs) was rapid (within 1 hour of incubation) and dependent on the number of AMs in culture. Moreover, culture supernatants from BAL cells of animals exposed to asbestos (single intratracheal injection) stimulated fibroblast proliferation to a greater degree than culture supernatants from BAL cells of control animals. Enhanced FGF production occurred 1 week after asbestos instillation and persisted up to 24 weeks. This change was accompanied in the early stages (1-4 weeks) by an increase in the total number of BAL cells which returned to control values by 12 weeks. Differential analysis of BAL cell populations showed a transient infiltration of neutrophils in the bronchoalveolar compartment followed by a significant accumulation of macrophages which persisted up to 1 month. Furthermore, lungs of asbestos-treated animals showed evidence of pathologic alterations characterized by fibroblast proliferation and collagen deposition. This study demonstrates that increased production of fibroblast growth factor by alveolar macrophages in vitro coincides with the development of asbestos-induced fibrosis. Prolonged stimulation of FGF release may contribute to excessive fibroblast proliferation and fibrosis.

Animals↗

PubMed1979

[Occupational risk in asbestos textile manufacture].

Detailed investigations of the environment in asbestostextile industry ("Asbestos produce" plant in the town of Sevlievo) were carried out. The parameters determined were: overall dusting, amount of asbestos in aerosol, its mineral and disperse composition. Data on the degree of dusting in the plant for the period 1960--1976 were analyzed and summarized. Professiograms were elaborated, with chronometry and appraisal of the burden of the work operations. All workers were tested clinically and roentgenologically. The data obtained on the degree of dusting in the different departments were re-calculated as amount of inhaled asbestos, depending on how hard the work is, resp. the pulmonary ventilation. The actual risk of asbestos injury was highest in the carding department, followed by the preparatory and the spinning departments. A distinct correlation exists between the degree of professional risk, determined by the asbestos contaminations, and the clinical and laboratory findings.

Air Pollutants, Occupational↗

PubMed1979

[Air concentration of asbestos fibers at work sites].

The paper presents a method for measuring the concentration of asbestos fibres at workplaces. This method consists in sampling the dusted air onto membrane filters, making the filters transparent and counting asbestos fibres under an optical microscope with a positive phase contrast. Errors in counting asbestos fibres, sampling and precision of the method were discussed (total error of the method). Measurements of the concentration of asbestos fibres in the air at workplaces were made at plants producing asbestos textile products, seal plates, packings and frictional goods. 0.1 fibre/cm3 was the lowest concentration (sensitiveness of the method).

Air Pollutants↗