asbestos--amosite and Pneumoconiosis

The different pulmonary macrophage (airway macrophages, alveolar macrophages, interstitial macrophages, intravascular macrophages, pleural macrophages) are an important part of the lungs' defences against non-fibrous and fibrous particles deposited by inhalation. The first line of defence is airway macrophages and alveolar macrophages (AM) which initially interact with deposited chrysotile fibres and subsequently release a number of mediators including growth regulatory and chemotactic proteins, arachidonic acid metabolites, proteases, NO and active oxygen species, all of which can affect--also adversely--specific target cells in the lung. Mechanical clearance via the mucociliary escalator and dissolution of phagocytized fibres in the acidic milieu of the phagolysosome in pulmonary macrophages are further important functions of AM. Chrysotile appears to be more toxic or at least has the same toxicity to AM as amphibole fibres when doses of a similar mass are administered. However, on a fibre number basis chrysotile appears to be less toxic to AM. The importance of the appropriate dose parameter--i.e. fibre mass, number or surface area--needs to be considered in in vitro as well as in in vivo studies. Short chrysotile fibres are cleared from rat lungs very rapidly whereas longer ones are cleared at a much slower rate. This is due to efficient phagocytosis of short fibres by AM accompanied by dissolution in the acidic milieu of the phagolysosome. Prediction of chrysotile clearance in primate lung based on results from rat studies result in an overall retention half-time of approximately 105 days, based on which no long-term accumulation of chrysotile in the primate lung is to be expected. Long-term inhalation studies in baboons exposed to chrysotile confirm the very fast build up of a low steady-state lung burden, consistent with a pulmonary retention half-time for chrysotile of approximately 90 days. Despite the fast clearance and low pulmonary accumulation of chrysotile, the resulting effects, such as asbestosis, were found to be of the same severity in rats as those induced by amphibole exposure. In the amphibole-exposed rats, the fibre lung burden continued to increase with exposure time. The potential contamination of chrysotile with tremolite cannot explain these results since there was no increased pulmonary accumulation of fibres in the chrysotile-exposed rats. Effects due to lung particle overload are not to be expected in long-term chrysotile inha

Topics: Animals; Asbestos, Amosite; Asbestos, Crocidolite; Asbestos, Serpentine; Asbestosis; Coal Mining; Cytokines; Dogs; Dust; Humans; Lung; Lymph; Macrophages, Alveolar; Papio; Pneumoconiosis; Quartz; Rats; Silicosis; Time Factors

The effects of mixed dust exposure on pulmonary clearance during chronic exposure has been investigated using rats exposed to combinations of toxic and relatively nontoxic dusts: quartz (at respirable dust concentrations of 1 and 10 mg/m3) plus titanium dioxide (at 30 and 20 mg/m3, respectively), and amosite asbestos (2.5 mg/m3) plus titanium dioxide (15 mg/m3). The rats were exposed for 5 days per week, and for up to 16 weeks (for quartz) or up to 32 weeks (for asbestos). The lung burdens were compared with previously published results for exposure to single dusts under the same exposure regimens. The main feature of all these comparisons was the absence of significant differences between the lung burdens (at 3, 10, and 38 days postexposure) for single-dust and mixed-dust exposures. There was, however, some reduction in the postexposure clearance (as shown by the lung burdens at 94, 150, and 260 days postexposure) of titanium dioxide which appeared to be due to the presence of quartz in the lung. For the quartz plus titanium dioxide experiments, the lymph nodes were dissected and analyzed separately. These results showed that transfer to lymph nodes accounted for most of the postexposure clearance for titanium dioxide, and almost all for the quartz.

Topics: Animals; Asbestos; Asbestos, Amosite; Atmosphere Exposure Chambers; Chronic Disease; Dose-Response Relationship, Drug; Drug Interactions; Lung; Male; Minerals; Pneumoconiosis; Quartz; Rats; Rats, Inbred Strains; Specific Pathogen-Free Organisms; Time Factors; Titanium

The effects of Candida albicans, of amosite dust, and of the 2 agents combined, on some biochemical parameters of the lung in male guinea pigs were determined. Adult guinea pigs were intratracheally injected with 50 mg of amosite dust and 0.3 mg of viable suspension of mycelia of Candida albicans. The other groups received either dust or organism or none. Biochemical measurements done at 30, 60 and 90 days after infection showed that the superimposed state produced more rapid and drastic changes in pulmonary contents of collagen, mucopolysaccharides and phospholipids and activities of lactic dehydrogenase and succinate dehydrogenase. The levels of lactic acid and pyruvic acid were also more profoundly changed after amosite + Candida. These results indicate that Candida albicans which is commonly found in upper respiratory tract could aggrevate the lesions caused by exposure to asbestos.

Topics: Animals; Asbestos; Asbestos, Amosite; Candida albicans; Candidiasis; Collagen; Glycosaminoglycans; Guinea Pigs; L-Lactate Dehydrogenase; Lung Diseases, Fungal; Male; Organ Size; Phospholipids; Pneumoconiosis; Proteins; Succinate Dehydrogenase