Asbestos Dust and DNA Damage

While studying the impact that asbestos dust has on workers, it is important to examine multiple factors such as data regarding smoking habits, age and other clinical and radiologic data.  One interesting study is called, "The role of catalytic iron in asbestos induced lipid peroxidation and DNA-strand breakage in C3H10T1/2 cells." By C. J. Turver and R. C. Brown - Br J Cancer. 1987 August; 56(2): 133–136.  Here is an excerpt: "Abstract - The involvement of catalytic iron in the vitro activities of crocidolite asbestos has been investigated. Exposure of C3H10T1/2 cells to either the UICC crocidolite standard reference sample or a non fibrous (milled) derivative resulted in an increase of thiobarbituric acid reactive substances. This catalytic activity was inhibited by pretreatment with the iron chelator desferrioxamine. The effect of this activity on cellular DNA was measured in an assay based on the production of DNA-strand breaks. Increased levels of DNA-strand breaks were detected in cultures treated with both the milled and UICC crocidolite. Inclusion of desferrioxamine with the asbestos inhibited DNA-strand breakage. It is concluded the catalytic iron present on the dust is capable of damaging both lipid and DNA and that this could be an important mechanism in asbestos pathogenicity."

Another interesting study is called, "Radiographic abnormalities in asbestos insulators: Effects of duration from onset of exposure and smoking. Relationships of dyspnea with parenchymal and pleural fibrosis" by R. Lilis, MD, A. Miller, MD, J. Godbold, PhD, E. Chan, MS, I. J. Selikoff, MD - American Journal of Industrial Medicine - Volume 20 Issue 1, Pages 1 – 15.  Here is an excerpt: "Abstract - Chest radiographs and spirometry were evaluated in 2,907 active and retired asbestos insulators; most (86.8%) had  30 years from onset of asbestos exposure. Testing was performed in 19 cities in the United States during 1981-1983. Complete demographic, smoking, clinical, and radiologic data were obtained for 2,790 workers. This is the largest single group of insulators that has been studied. Five hundred forty-eight (19.7%) had never smoked cigarettes, 942 (33.9%) were current cigarette smokers, and 1,300 (46.6%) were ex-smokers. Only 439 (15.7%) workers had no radiographic evidence of asbestos-related disease (normal chest X-ray); 668 (23.9%) had pleural fibrosis only, 325 (11.6%) had parenchymal fibrosis alone, and 1,358 (48.7%) had both parenchymal and pleural fibrosis.

The prevalence of radiographic parenchymal changes increased significantly (p < .001) from 38.6% (DURONSET < 30 years) to 70% (40 years). For pleural changes the comparative prevalences were 55% and 82%. Those with no history of cigarette smoking were more likely to have normal filMS than those with a history of smoking (19.2% versus 14.4% for current smokers and 15.2% among ex-smokers), and were less likely to have parenchymal fibrosis (44.5% versus 69.7% for current smokers and 60.2% of ex-smokers). Dyspnea, MRC grade 3 and higher, was more prevalent when pleural fibrosis was associated with interstitial pulmonary fibrosis (at all profusion levels of small opacities) than when pleural fibrosis was absent. Logistic regression analysis of factors contributing to such dyspnea showed that the presence of combined parenchymal and pleural abnormalities was a significant explanatory variable, in addition to age, smoking, and body mass (Quetelet index); the presence of parenchymal changes only or of pleural changes only, as factors contributing to dyspnea, did not reach the level of statistical significance in the regression analysis. The results of these examinations show that pleural fibrosis is a frequent finding in asbestos-exposed groups with long-term follow-up and that its functional significance is not negligible. The contribution of cigarette smoking to prevalence and severity of interstitial fibrosis is an additional reason for smoking cessation among asbestos-exposed individuals."

A third study is called, "A comparison of the ferruginous body and uncoated fiber content in the lungs of former asbestos workers." By Dodson RF, Williams MG Jr, O'Sullivan MF, Corn CJ, Greenberg SD, Hurst GA. - Am Rev Respir Dis. 1985 Jul;132(1):143-7.  Here is an excerpt: "Abstract - Tissue samples from 12 former asbestos workers were digested and analyzed for ferruginous body and uncoated fiber populations. It was noted that there were large numbers of nonasbestos fibers in each of the samples. In some samples, these fibers constituted over 80% of the total uncoated fibers, and they could greatly influence the data as to asbestos content of the tissue unless differentiated by light and electron microscopic techniques, such as X-ray energy-dispersive analysis. There were great variations in the numbers of uncoated fibers per ferruginous body between the individual workers. The digested samples from lungs of 2 workers yielded no ferruginous bodies by light microscopy, even though these samples by electron microscopy contained respective loads of 780,000 and 1.2 million uncoated amphibole fibers per gram. Light microscopy examination of adjacent tissues confirmed mild fibrosis in both workers. Ferruginous bodies serve as a general marker for asbestos exposure. However, our data suggest that their absence in tissue with interstitial fibrosis from a worker with previous occupational exposure may not be sufficiently conclusive to rule out asbestos-induced disease. Rather, as shown by our data, individual exceptions may require correlated analysis by analytical electron microscopy in order to define particulate load and support the diagnosis of the disease."

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