Clinical utility of asbestos bodies in BAL fluid.
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Biomedical subjects
Publications and source records attributed to P Dumortier.
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Asbestos body (AB) concentrations in bronchoalveolar lavage samples of 15 brake lining (BL) workers exposed only to chrysotile have been determined and compared with those from 44 asbestos cement (AC) workers extensively exposed to amphiboles. The mean AB concentrations (263 +/- 802 and 842 +/- 2086 AB/ml respectively) for those groups did not differ significantly but were much higher than those found in control groups. Analytical electron microscopy of asbestos body cores showed that in the BL group 95.6% were chrysotile fibres whereas in the AC group amphiboles accounted for 93.1%. The size characteristics of the central fibres differed for chrysotile and amphibole AB, the former being shorter and thinner. Examination of repeated bronchoalveolar lavage samples showed that the mechanisms of clearance of chrysotile fibres do not affect AB concentration for at least 10 months after cessation of exposure. It thus appears that routine counting of ABs in BAL allows the assessment of current or recent occupational exposures to asbestos. Exposures to chrysotile lead to AB concentrations comparable with those encountered in exposures to amphiboles.
A 63 year old woman developed progressive shortness of breath, pulmonary hypertension, and respiratory failure and died from pulmonary fibrosis 45 years after thoracic fistulography with Thorotrast. Bouts of acute respiratory failure occurred with features of noncardiogenic pulmonary oedema. Lung tissue obtained by biopsy and at necropsy showed abundant radioactive particles of thorium dioxide in the lungs. The particles were congregated in the walls of blood vessels and in perivascular fibrous zones, consistent with a causal role of Thorotrast in the development of lung fibrosis. It is suggested that the fibrosis was due to the combined effects of alpha radiation on the interstitial perivascular zones and of recurrent pulmonary oedema due to endothelial damage.
Bronchoalveolar lavage (BAL) is a simple and non-invasive sampling technique of the deep lung. Analytical electron microscopy was used for the identification and quantification of non-fibrous inorganic particles recovered in BAL fluid samples from 51 subjects with various occupational exposures (silica, silicates, metals and alloys, metallic oxides, precious and hard metals, abrasives). Around 4750 particles were analysed. More than sixty different compounds were identified, among which silica, kaolinite, illite, mica, Fe oxides and hydroxides, appeared to be ubiquitous. Feldspar, talc, chlorite, Al oxide, Ti oxide, tungsten carbide, stainless steel, carbonaceous compounds and flyash were also frequently encountered. From 1 to 21 compounds were identified in each sample. Repeated BAL samples obtained for 2 subjects did not show significant differences. Particles characteristic of the occupational exposure were found in BAL up to 21 years after cessation. BAL content can also reflect mixed occupational exposures. Absolute particle concentrations measured in twelve samples ranged between 0.1 and 9.9 x 10(6) particles/ml BAL fluid and mean particle diameter ranged between 0.5 and 1.2 microns. Mineralogical analysis of non-fibrous particles in BAL can be a useful tool to investigate occupational exposures. It allows, in most cases, a better characterization of the exposure than medical questioning. It may be helpful in identifying pathogenic particles, however it must be kept in mind that a positive result is only a proof of exposure and never a proof of disease. The main limitations of this technique are difficulties in sampling severely diseased subjects and inaccuracy in detecting easily soluble compounds and particles with a high rate of alveolar clearance.
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The analytical techniques routinely used for the mineralogical analysis of small particles, ranging from light microscopy (LM) to electron microscopy (EM) coupled with energy dispersive X-ray spectrometry (EDS), can be applied to evaluate the content of broncho-alveolar lavage (BAL) in various inorganic particles. The evaluation of the concentration of asbestos bodies (AB's) in BAL samples allows in some cases to assess an asbestos exposure not revealed through a detailed occupational inquiry, and consequently can have important medico-legal implications. However it must be kept in mind that even a very positive BAL is an indicator of exposure, but can never be considered as a proof of disease. The interest of these studies is not limited to asbestos related pathologies, but they have also contributed to a better diagnosis and understanding of the pathogenesis of unusual pneumoconiosis like aluminium induced interstitial lung disease and dental technicians pneumoconiosis.
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.
Asbestos body (AB) countings on both bronchoalveolar lavage (BAL) fluids and digested lung tissue samples were performed in one hundred consecutive subjects submitted to a thoracotomy procedure, mostly for lung carcinoma. A good correlation (r = 0.73) was found between the two groups of values for the total group of subjects. When restrictive selection criteria were taken into account, such as lavage homolateral to the analysed lung, performed by the same trained physician, this correlation improved (r = 0.82). Absence of AB's or low AB counts (less than 1 AB/ml) in BAL corresponded in about 70% of cases to concentrations of less than 1,000 AB/gm and in 100% of cases to concentrations less than 10,000 AB/gm. In subjects with BAL containing more than 1 AB/ml, the lung tissues of 85% contained more than 1,000 AB/gm and the tissues of 44% contained more than 10,000 AB/gm. Above 10 AB/ml BAL, all lung tissues contained more than 10,000 AB/gm. Since lung tissue is not readily available in patients undergoing assessment of their asbestos exposure, BAL fluid analysis seems to be a useful tool to evaluate lung AB concentrations. This technique cannot be performed, however, in patients with severe lung impairment which does not allow sufficient recovery of BAL fluid.
Asbestos bodies (AB) were counted by light microscopy in bronchoalveolar lavage (BAL) fluid obtained from 563 subjects. The presence of AB was found to reflect occupational exposure to asbestos and was rarely found in unexposed control subjects at concentrations above 1/ml of fluid (6.9% of white collar workers and 17.8% of blue collar workers). The overlap of results observed between subjects with definite exposure and those without underlines the difficulty in assessing exposure by questioning alone, which leads to underestimations or even overestimations of the risk. The highest counts (log mean, 120.5 AB/ml; range, 0 to 42,600) were found in patients with radiologic evidence of asbestosis, most likely reflecting the known association of this disease with retention of large amounts of long amphiboles, rather than in patients with pleural disease. A considerable overlap of results was also observed between groups with different diseases or without any apparent disease. Apart from uncertainties in the radiologic diagnosis, this may be explained by differences in latency since first exposure, in individual response to asbestos inhalation, or in pathogenic properties of different asbestos types. Because the presence of AB in BAL fluid appears to be a marker of exposure and not of disease, AB are more likely to be detected in patients presenting with asbestos-related diseases but in whom exposure is not confirmed by the occupational history (65 of 78 cases).
Interstitial lung disease developed in a 32-yr-old chemist after working 8 yr in a dusty atmosphere containing aluminum powders. Bronchoalveolar lavage disclosed a helper T-lymphocyte alveolitis, and transbronchial lung biopsies showed sarcoidlike epithelioid granulomas. These granulomas contained dust identified by mineralogic analyses as consisting mainly of aluminum particles. Nasal and liver biopsies and a Kveim test did not reveal extrapulmonary granulomatous infiltration. An extensive immunologic work-up showed none of the abnormalities classically seen in sarcoidosis, but peripheral blood lymphocytes exhibited blastic transformation in the presence of soluble aluminum compounds. About 1 yr after cessation of exposure, a chest radiograph and lung function tests remained essentially unchanged, but signs of alveolitis disappeared. This observation suggests that aluminum may cause granulomatous lung disease accompanied by a helper T-lymphocyte alveolitis, similar to that of berylliosis and sarcoidosis. Further observations would be necessary to show if this constitutes an early stage of aluminum-induced fibrosis (aluminum lung).
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Bronchoalveolar lavage (BAL) fluid obtained from six talc workers with pneumoconiosis was studied by optical and electron microscopy for its mineral content. Two of these workers were mainly exposed to American and Australian talc, and the other four were exposed to French talc (Luzenac). In all lavage fluids, talc particles and talc bodies were abundant, sometimes many years after the end of exposure. A qualitative difference was the presence of tremolite asbestos fibres in the two patients exposed to American and Australian talc and its absence in the four French talc workers. The presence of tremolite in lavage is attributed to a geological association of this mineral with the inhaled talc. On the other hand, chlorite was abundant in BAL of the French talc workers. Hence, we suggest that bronchoalveolar lavage can confirm exposure to talc and provide information about the heterogeneity of inhaled dust.
Diagnosis of pneumoconiosis was made in 2 dental technicians presenting with interstitial lung disease. The occupational origin of inhaled dust was confirmed by mineralogic analyses, which disclosed mainly large amounts of chromium-cobalt-molybdenum particles originating from Vitallium prostheses, but also showed abrasives (silica and silicon carbide) and asbestos in 1 patient. The presence of Vitallium and its chemical stability in bronchoalveolar lavage and lung several years after cessation of exposure confirm the resistance of this alloy to corrosion by body fluids. This contrasts with the high solubility of cobalt described in cobalt or hard metal disease. We suggest that dental technician's pneumoconiosis is a complex pneumoconiosis distinct from silicosis, asbestosis, or hard metal disease and that Cr-Co-Mo alloys play a role in its pathogenesis.
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An aluminium polisher developed severe lung fibrosis complicated by bronchial carcinoma. Although he was not submitted to the exposure risks usually described in aluminium lung (bauxite smelting, use of aluminium powders, aluminium welding), he worked in a high concentration of aluminium dust. This was demonstrated by mineralogical analyses which revealed large amounts of small metallic aluminium particles (0.5 micron - 5 micron) in bronchoalveolar lavage, lung tissue and lymph nodes 5 years after the end of exposure. Aluminium polishing seems to be a potential cause of aluminium lung.
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