Detecting Early Cell Injury Resulting From Asbestos Exposure

Determining when cell injury occurs as a result of asbestos exposure has been the subject of a myriad of tests.  One interesting study on point is called, "Interstitial accumulation of inhaled chrysotile asbestos fibers and consequent formation of microcalcifications." By A. R. Brody and L. H. Hill - Am J Pathol. 1982 October; 109(1): 107–114.  Here is an excerpt: "Previous studies have shown that inhaled chrysotile asbestos impacts initially at the bifurcations of alveolar ducts in the lungs of rats. Asbestos fibers are transported through alveolar epithelial cells at these bifurcation regions to the interstitium during the 24-hour period after a 1-hour exposure. To further these studies, white rats were exposed to an aerosol of chrysotile asbestos for 1 hour. Animals were sacrificed, and the lungs were fixed by vascular perfusion immediately after and 1 month after exposure. Blocks of tissue were prepared for light and electron microscopy. We report here, at 1 month after exposure, that numerous asbestos fibers had accumulated within the lung interstitium at alveolar duct bifurcations. Many of these interstitial fibers were found in te center of intracellular microcalcifications. The presence of calcifications was proven by X-ray energy spectrometric analysis of the inclusions in situ. Clear X-ray peaks for calcium and phosphorus were demonstrated. The authors propose that 1 month after a 1-hour exposure to chrysotile asbestos, fiber-induced membrane injury in cells of the lung interstitium leads to formation of microcalcifications. This may represent the presence of early cell injury in the initial pathogenetic sequence of asbestosis."

Another interesting study is called, "Pulmonary asbestos body counts and electron probe analysis of asbestos body cores in patients with mesothelioma. A study of 25 cases" by
Victor L. Roggli, MD, Malcolm H. McGavran, MD, James Subach, PhD, Harley D. Sybers, MD, PhD, Donald Greenberg, MD - Cancer Cytopathology - CA: A Cancer Journal for Clinicians Volume 50 Issue 11, Pages 2423 – 2432.  Here is an excerpt: "Abstract - Malignant mesotheliomas of the pleura and peritoneum are well-recognized risks of asbestos exposure. We determined the asbestos body content of the lungs from 24 cases of malignant mesothelioma (19 pleural, five peritoneal) and compared such to the content of lungs from 50 consecutive adult autopsies and four cases of overt asbestosis using a Clorox-digestion concentration technique.

The cores of 90 asbestos bodies were examined by energy dispersive x-ray analysis and compared with similar data from 120 standard asbestos fibers and 20 fiberglass fibers. The malignant mesothelioma patients had asbestos body counts intermediate between those of the general population and those of patients with asbestosis, although some of the mesothelioma cases overlapped with the general population. These latter cases often lacked an identifiable occupational exposure to asbestos. EDXA studies demonstrated an amphibole core in 88 of the 90 asbestos bodies (amosite or crocidolite in 80 of 88, anthophyllite or tremolite in eight of 88), and chrysotile in two instances."

A third study worth examining is called, "Exposure-response analysis of risk of respiratory disease associated with occupational exposure to chrysotile asbestos." By
L Stayner, R Smith, J Bailer, S Gilbert, K Steenland, J Dement, D Brown, and R Lemen - Occup Environ Med 1997;54:646-652.  Here is an excerpt: "Abstract - OBJECTIVES: To evaluate alternative models and estimate risk of mortality from lung cancer and asbestosis after occupational exposure to chrysotile asbestos. METHODS: Data were used from a recent update of a cohort mortality study of workers in a South Carolina textile factory. Alternative exposure-response models were evaluated with Poisson regression. A model designed to evaluate evidence of a threshold response was also fitted. Lifetime risks of lung cancer and asbestosis were estimated with an actuarial approach that accounts for competing causes of death. RESULTS: A highly significant exposure-response relation was found for both lung cancer and asbestosis. The exposure-response relation for lung cancer seemed to be linear on a multiplicative scale, which is consistent with previous analyses of lung cancer and exposure to asbestos. In contrast, the exposure-response relation for asbestosis seemed to be nonlinear on a multiplicative scale in this analysis. There was no significant evidence for a threshold in models of either the lung cancer or asbestosis. The excess lifetime risk for white men exposed for 45 years at the recently revised OSHA standard of 0.1 fibre/ml was predicted to be about 5/1000 for lung cancer, and 2/1000 for asbestosis. CONCLUSIONS: This study confirms the findings from previous investigations of a strong exposure-response relation between exposure to chrysotile asbestos and mortality from lung cancer, and asbestosis. The risk estimates for lung cancer derived from this analysis are higher than those derived from other populations exposed to chrysotile asbestos. Possible reasons for this discrepancy are discussed."

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