Asbestos Exposure Cancer And Lymphoid Structures
Inhalation of asbestos fibers can lead to a deadly form of cancer called mesothelioma
. Some theories posit that asbestos can actually travel through the blood stream and enter organs like the kidney, or even the brain. One interesting study is called, Asbestos Exposure and Gastrointestinal Malignancy Review and Meta-Analysis by Howard Frumkin, MD, Jesse Berlin - American Journal of Industrial Medicine - Volume 14 Issue 1, Pages 79 95 Jan 2007. Here is an excerpt: Abstract - The epidemiologic literature linking asbestos exposure with gastrointestinal malignancy is reviewed. Problems in comparing studies are discussed, appropriate strategies for comparison are developed, and study results are pooled using a model which accounts for both intrastudy and interstudy variability. Stratification of cohorts by dose reveals that significant asbestos exposure, as indicated by a lung cancer standardized mortality ratio (SMR) of at least 200, is associated with an elevated gastrointestinal cancer SMR for five or six end points examined.
Another interesting study is called, Migration of Asbestos Fibres from Subcutaneous Injection Sites in Mice by K. Kanazawa, M. S. C. Birbeck, R. L. Carter, and F. J. C. Roe - Br J Cancer. 1970 March; 24(1): 96106. Here is an excerpt: Crocidolite asbestos fibres, suspended in physiological saline, were injected subcutaneously into one or both flanks of 95 CBA/Lac female mice; 75 control mice received injections of saline only. Most animals were killed at chosen intervals of between 2 and 42 days after injection but some were left for longer periods of up to 623 days. At autopsy, many lymphoid and non-lymphoid structures were removed and examined for the presence of asbestos by the following techniques: haematoxylin and eosin staining followed by conventional and polarized light microscopy; Perl's stain; microincineration followed by phase-contrast microscopy; maceration with KOH followed by phase-contrast microscopy; and electron microscopy.A combination of haematoxylin and eosin staining and microincineration was found to be the most convenient and reliable method for demonstrating asbestos fibres in the tissues. Electron microscopy was essential for detecting very small fibres and for locating them to specific intracellular structures. The morphological findings indicate that some migration of asbestos fibres away from the initial site of injection takes place. Dissemination is usually along lymphatic pathways and fibres tend to accumulate in the lymphoid tissues, particularly in the regional (axillary) lymph nodes; smaller amounts were found in inguinal, mediastinal and lumbar nodes. The fibres were usually intracellular, lying inside the phagosomes of macrophages, but larger fibres were sometimes encountered lying free. Small numbers of fibres were seen in the spleen and also in non-lymphoid organs such as the liver, kidneys and brainsuggesting that some asbestos may enter the blood stream. There was no evidence of massive or selective spread to subserosal tissues in the thorax or abdomen, though trapping of asbestos fibres was observed in pleural milky spots in long-term survivors. The possible role of milky spots in the development of pleural plaques and mesotheliomata is discussed.
A third article worth looking at is called, Asbestos inhalation induces reactive nitrogen species and nitrotyrosine formation in the lungs and pleura of the rat. By S Tanaka, N Choe, D R Hemenway, S Zhu, S Matalon, and E Kagan - Department of Pathology, Uniformed Services University of the Health Sciences, F. Edward Hbert School of Medicine, Bethesda, Maryland 20814-4799- J Clin Invest. 1998 July 15; 102(2): 445454.
Here is an excerpt: To determine whether asbestos inhalation induces the formation of reactive nitrogen species, three groups of rats were exposed intermittently over 2 wk to either filtered room air (sham-exposed) or to chrysotile or crocidolite asbestos fibers. The rats were killed at 1 or 6 wk after exposure. At 1 wk, significantly greater numbers of alveolar and pleural macrophages from asbestos-exposed rats than from sham-exposed rats demonstrated inducible nitric oxide synthase protein immunoreactivity. Alveolar macrophages from asbestos-exposed rats also generated significantly greater nitrite formation than did macrophages from sham-exposed rats. Strong immunoreactivity for nitrotyrosine, a marker of peroxynitrite formation, was evident in lungs from chrysotile- and crocidolite-exposed rats at 1 and 6 wk. Staining was most evident at alveolar duct bifurcations and within bronchiolar epithelium, alveolar macrophages, and the visceral and parietal pleural mesothelium. Lungs from sham-exposed rats demonstrated minimal immunoreactivity for nitrotyrosine. Significantly greater quantities of nitrotyrosine were detected by ELISA in lung extracts from asbestos-exposed rats than from sham-exposed rats. These findings suggest that asbestos inhalation can induce inducible nitric oxide synthase activation and peroxynitrite formation in vivo, and provide evidence of a possible alternative mechanism of asbestos-induced injury to that thought to be induced by Fenton reactions.
If you found any of these studies interesting, please read them in their entirety. We all owe a debt of gratitude to these fine researchers.
by: Mont Wrobleski
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