Asbestos Exposure Cancer And Lymphoid Structures

Inhalation of asbestos fibers can lead to a deadly form of cancer called mesothelioma. Some theories stated 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.

The epidemiologic literature linking asbestos exposure with gastrointestinal malignancy is reviewed. The study is comparing problems to be discussed, find appropriate strategies for comparison are developed and result of the study are pooled using a model which accounts for both intrastudy and interstudy variability.

Asbestos exposure cancer and lymphoid structures

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 wntitled “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 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 brain which is suggesting 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 Hibert School of Medicine, Bethesda, Maryland 20814-4799- J Clin Invest. 1998 July 15; 102(2): 445+454.

Here is an excerpt:

To determine if 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. At 1 or 6 weeks after exposure, the rats were killed.  At 1 week, 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. The evident from chrysotile is strong immunoreactivity for nitrotyrosine, a marker of peroxynitrite formation. A crocidolite-exposed rats at 1 and 6 week.

Themost evident at alveolar duct bifurcations and within bronchiolar epithelium, alveolar macrophages, and the visceral and parietal pleural mesothelium was staining. 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 .

more information you can visit asbestoswatchtoowoomba.com.au

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