The Importance Of Asbestos In Two-stage Carcinogenesis
The impetus for this article is to delve into the various studies concerning asbestos and cigarette smoke
. One interesting study is called, Cocarcinogenic and tumor promoting properties of asbestos and other minerals in tracheobronchial epithelium. By Mossman BT, Cameron GS, Yotti LP. - Carcinog Compr Surv. 1985;8:217-38. Here is an excerpt: Abstract - Epidemiologic and experimental studies document a synergistic effect of asbestos and smoking in the induction of bronchogenic carcinoma. Whereas the increased risk of these cancers in nonsmoking asbestos workers is 4-fold or less in comparison to nonsmokers in the general population, individuals who smoke and are exposed to asbestos occupationally have a 80-90 fold increased risk. The observations summarized above provide substantial insight into the interactions between asbestos and chemical carcinogens in cigarette smoke at the cellular level (Fig. 8). On the one hand, asbestos fibers and other particulates appear to act as condensation nuclei for PAH in the occupational setting or environment. They then facilitate the transfer of these chemical carcinogens into target cells, i.e., those destined to develop into tumor cells. As a result, the adduct formation of PAH to DNA is encouraged, an event linked intrinsically to initiation of transformation. Alternatively, asbestos appears to enhance and modulate the further development of initiated cells to neoplastic cells by a process resembling tumor promotion in mouse skin. In this regard, the most dramatic example illustrating the importance of asbestos in two-stage carcinogenesis is an experiment by Topping and Nettesheim. These investigators inserted the PAH, 7,12-dimethyl-benz(a)anthracene (DMBA) into the lumen of rat trachea which then were implanted on syngeneic animals. Subsequently, chrysotile asbestos was introduced, and grafts were removed for histology when palpable tumors occurred. At non-tumorigenic (i.e., initiating) amounts of DMBA, asbestos promoted the development of malignancies, although two neoplasms were observed with use of asbestos alone. Asbestos was not carcinogenic at these amounts, but a low incidence (5%) of squamous cell carcinoma was observed with use of chrysotile alone at much higher concentrations. These results suggest that asbestos is a weak carcinogen, but more importantly a promoter of carcinogenesis in the respiratory tract. Studies in this laboratory show striking effects of asbestos fibers on cell proliferation and differentiation although these responses appear to occur also after exposure of tracheobronchial cells to nonasbestos fibers including fiberglass.
Another interesting study is called, Endocrine cell proliferation in the rat lung following asbestos inhalation by N. F. Johnson, J. C. Wagner and H. A. Wills Here is an excerpt: Abstract - Endocrine cells occur rarely in the adult lung. When they do, they occur mainly in the tracheobronchial lining. These particular cells are thought to be implicated in the development of bronchial carcinoids and oat cell carcinomas. However, there are few reports of abnormal proliferations in animals. Endocrine cells have been found in SPF rats following either chrysotile or crocidolite inhalation for 6 months to 2 years. Attempts to differentiate these cells by conventional light microscopical techniques were unsuccessful. However, the cells were characterised at the ultrastructural level by the presence of dense cored vesicles typical of endocrine cells. The cells were found in several locations in the respiratory portion of the lung. The abundance and various locations of these cells was unexpected.
A third study is called, Clinical features to stage alveolitis in asbestos workers by R. Bgin MD, A. Cantin MD, Y. Berthiaume MD, R. Boileau MD, G. Bisson MD, G. Lamoureux MD, M. Rola-Pleszczynski MD, G. Drapeau MSc, S. Mass MD, M. Boctor MD, J. Breault MSc, S. Ploquin BS, D. Dalle PhD Here is an excerpt: Abstract - To analyze the clinical features of asbestos-induced alveolitis and stage its activity, we evaluated 217 asbestos workers by the usual clinical, radiological, and functional parameters and computerized gallium 67(Ga) lung scan; we obtained bronchoalveolar lavage (BAL) in 33 and lung biopsy in 6. In addition, we scored the profusion of lung rales and correlated it with other parameters of severity of asbestosis. In the 55 workers without asbestosis and normal 67Ga scan, BAL analyses were comparable to those of controls. Of the 56 without asbestosis but increased 67Ga lung uptake, BAL analyses in 8 documented a predominantly macrophagic alveolitis (confirmed on lung biopsy in 3), with the highest levels of BAL fibronectin. In the 106 workers with asbestosis, 67Ga lung uptake was increased in 75; BAL in 17 demonstrated a macrophagic and neutro-philic alveolitis with elevated fibronectin levels. Lung biopsy in 3 of the latter workers documented peribronchiolar fibrosing alveolitis. Rale scores in all workers or in those without asbestosis did not correlate with 67Ga scores; they correlated fairly well with profusion of parenchymal opacities (Rs = 0.42) and rigidity of the lung pressure-volume curve (Rs = 0.39). Thus, 67Ga lung uptake is an early indicator of chronic macrophagic alveolitis in asbestos workers, which usually progresses to asbestosis. In the disease, profusion of lung rales constitutes a simple clinical mode of assessment of disease severity that correlates better with radiological and functional parameters than with parameters of alveolitis.
Monty Wrobleski is the author of this article, for more information please click on the following links
by: Mont Wrobleski
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