Radiologic Changes And Malignant Mesothelioma Disease

One interesting study is called, Malignant and non-malignant asbestos-related pleural and lung disease: 10-yearfollow-up study. By Slavica Cvitanovi, Ljubo Znaor, Toni Konsa, Zeljko Ivancevi, Irena Peri, Marijan Erceg, Mirjana Vujovi, Jonatan Vukovi, Zlata Beg-Zec - Croat Med J 2003; 44(5):618-625. Here is an excerpt: AIM: To examine the presence of radiologically visible lung and pleuralchanges in patients who were exposed to the asbestos dust, and to correlate the progression of thesechanges with the duration and intensity of exposure and smoking. We also evaluated possible correlationbetween non-malignant asbestos-related pleural abnormalities and the occurrence of malignant pleuralmesothelioma. METHODS: Among 7,300 patients who visited our department between 1991 and 2000 due to non-specificrespiratory symptoms, we selected 2,420 with chest X-rays indicating the possible existence of non-malignantasbestos-related diseases. The selected group was followed-up for progression of radiological changesand the development of malignant pleural mesothelioma, and the changes were correlated with the intensityand duration of exposure to asbestos dust and smoking. RESULTS: Radiological changes characteristic fo rnon-malignant asbestos-related pleural disease or lung asbestosis were identified in 340 (14%) out of2,420 examined patients, of whom 77 (22.6%) developed malignant pleural mesothelioma, as compared with 13 patients out of 2,080 (0.6%) without radiological signs of asbestosis or pleural changes. Twenty-three(29.9%) patients who presented with a progression of pleural disease and lung asbestosis had a very significantincidence of malignant pleural Mesothelioma.

Another interesting study is called, Cytokine regulation of lung fibroblast proliferation. Pulmonary and systemic changes in asbestos-induced pulmonary fibrosis. By Lemaire, I Beaudoin, H Dubois, C - American Journal of Respiratory and Critical Care Medicine [AM. REV. RESPIR. DIS.]. Vol. 134, no. 4, pp. 653-658. 1986. Here is an excerpt: A complex series of interactions between immunocompetent cells and fibroblasts exists. Because pulmonary fibrosis may result from an increased number of collagen-producing fibroblasts, the authors studied the production of fibroblast growth factors derived from alveolar macrophages (AM) and peripheral blood mononuclear leukocytes (PBML) during the development of asbestos-induced fibrosis. One month after asbestos exposure, when fibrotic lesions were apparent, AM production of fibroblast growth factor was significantly enhanced, and such increase persisted for as long as 6 months.

Another study is called, Sister chromatid exchange frequency in asbestos workers.Rom WN, Livingston GK, Casey KR, Wood SD, Egger MJ, Chiu GL, Jerominski L - J Natl Cancer Inst. 1983 Jan;70(1):45-8. Here is an excerpt: Abstract - In vitro cytogenetic studies of amosite, chrysotile, and crocidolite asbestos have shown that these fibers may induce chromosome abnormalities and an elevated sister chromatid exchange (SCE) rate in mammalian cells. Twenty-five asbestos insulators (6 with radiographic asbestosis) were compared to 14 controls frequency matched for age and were found to have a marginally increased SCE rate in circulating lymphocytes with increasing years of exposure (P= 0.057). There was a significant association between SCE rate and smoking (P=0.002) after controlling for years of asbestos exposure and age. Smoking asbestos insulators had the highest SCE rate. Sister chromatid exchanges in chromosomes of group A, i.e., the group with the longest chromosomes, were significantly associated with asbestos exposure and cigarette smoking, with an interaction between the two.

Another study is called, Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure. By D. Filipenko, J. L. Wright, and A. Churg - Am J Pathol. 1985 May; 119(2): 273278. Here is an excerpt: Abstract - To determine whether asbestos dust produces pathologic changes in the small airways, and to determine where the anatomic lesions of asbestosis commence, the authors examined lungs from guinea pigs exposed to 10 or 30 mg of amosite asbestos by intratracheal instillation and sacrificed 6 months later. Measurement of airway wall thickness revealed that membranous and respiratory bronchioles of all sizes in exposed animals were significantly thicker than those of controls. Amosite fibers were found embedded in the walls of bronchi and in membranous and respiratory bronchioles; where these fibers penetrated the airway walls, an interstitial inflammatory and fibrotic reaction (asbestosis) occurred. It is concluded that 1) amosite asbestos produces diffuse abnormalities throughout the noncartilagenous airways and possibly the cartilagenous airways as well; 2) this effect is independent of interstitial fibrosis of the parenchyma (classical asbestosis); 3) asbestosis, at least that induced by amosite, commences at any site in the parenchyma to which the asbestos fibers can gain access, either by deposition in alveoli and alveolar ducts or by direct passage of fibers through the walls of all types and sizes of small airways.

If you found any of these excerpts interesting, please read the studies in their entirety. We all owe a debt of gratitude to these fine researchers.

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