Epidemiologic and pathologic data demonstrate that malignant mesothelioma occurs preferentially after exposure to long amphibole asbestos fibers. However, mineralogic studies have rarely detected such fibers in the parietal pleura. We hypothesized that the distribution of asbestos fibers in the pleura was heterogeneous and that they might concentrate in certain areas, as does coal dust in patients showing anthracotic "black spots" of the parietal pleura during thoracoscopy. We collected thoracoscopic biopsy samples from these black spots and from normal areas of the parietal pleura and lung from 14 subjects (eight with and six without asbestos exposure). Asbestos content was determined by transmission electron microscopy. In exposed subjects, mean fiber concentrations were 12.4 +/- 9.8 x 10(6) fibers/g of dry tissue in lung, 4.1 +/- 1.9 in black spots, and 0.5 +/- 0.2 in normal pleura. In unexposed patients, concentrations were 0, 0.3 +/- 0.1, and 0, respectively. Amphiboles outnumbered chrysotile in all samples. A total of 22.5% of fibers were > or = 5 microns in length in black spots. A histologic similarity of these black spots with milky spots is suggested by conventional and electron microscopy. We conclude that the distribution of asbestos fibers is heterogeneous in the parietal pleura. Indeed, the fibers concentrate in black spots, where they can reach high concentrations. These findings could explain why the parietal pleura is the target organ for mesothelioma and plaques.
aaAsbestos comprises a group of six hydrated silicate minerals capable of forming very thin fibres: chrysotile, crocidolite, amosite, anthophyllite, tremolite and actinolite [1]. Chrysotile belongs to the serpentine group and the other five to the amphibole group of minerals. Chrysotile fibre bundles split easily and magnesium can be leached under weak acid conditions. These factors may contribute to the lower biopersistence of chrysotile in the lungs.
The fibrogenicity and carcinogenicity of asbestos fibers are dependent on several fiber parameters including fiber dimensions. Based on the WHO (World Health Organization) definition, the current regulations focalise on long asbestos fibers (LAF) (Length: L ≥ 5 μm, Diameter: D < 3 μm and L/D ratio > 3). However air samples contain short asbestos fibers (SAF) (L < 5 μm). In a recent study we found that several air samples collected in buildings with asbestos containing materials (ACM) were composed only of SAF, sometimes in a concentration of ≥10 fibers.L−1. This exhaustive review focuses on available information from peer-review publications on the size-dependent pathogenetic effects of asbestos fibers reported in experimental in vivo and in vitro studies. In the literature, the findings that SAF are less pathogenic than LAF are based on experiments where a cut-off of 5 μm was generally made to differentiate short from long asbestos fibers. Nevertheless, the value of 5 μm as the limit for length is not based on scientific evidence, but is a limit for comparative analyses. From this review, it is clear that the pathogenicity of SAF cannot be completely ruled out, especially in high exposure situations. Therefore, the presence of SAF in air samples appears as an indicator of the degradation of ACM and inclusion of their systematic search should be considered in the regulation. Measurement of these fibers in air samples will then make it possible to identify pollution and anticipate health risk.
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).
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