Asbestos Industry Regulation and Mortality Rates Among Workers

Most people are exposed to asbestos in the workplace, often due to lack of proper safety procedures and shortcuts.  Some occupations are considered more dangerous than others.  One interesting study is called, "A mortality study among workers in an English asbestos factory" By J Peto, R Doll, S V Howard, L J Kinlen, and H C Lewinsohn - Br J Ind Med 1977;34:169-173.  Here is an excerpt: "Abstract - The previous report on this cohort study of workers in an asbestos textile factory (Knox et al., 1968) showed little evidence of increased mortality among workers who had entered the factory after the implementation in 1932 of the first Asbestos Industry Regulation (1931) but observed that no firm conclusions could be drawn, as little carcinogenic effect would be expected for 20 years after first exposure. A further 8 1/2 years of follow-up has revealed some asbestos-related disease in this latter group, although very much less than for employees first exposed before 1933. Among the 963 workers first exposed in 1933 or later, mortality was increased for carcinoma of the bronchus (31 deaths; 19-3 expected for all lung cancers) and non-malignant respiratory disease (35 deaths, 25-0 expected), and a further 5 deaths were attributed to pleural mesothelioma."

Another interesting study is called, "Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation." By Sekhon H, Wright J, Churg A. -
Department of Pathology, University of British Columbia, Canada - Int J Exp Pathol. 1995 Dec;76(6):411-8.  Here is an excerpt: "Abstract - In order to determine whether exposure to both cigarette smoke and asbestos leads to enhanced cell proliferation, and whether pleura cell proliferation reflects the presence of fibres at or near the pleura, rats were exposed to air (control), daily cigarette smoke, a single intratracheal instillation of amosite asbestos, or a combination of smoke and asbestos. Dividing cells were labelled with bromodeoxyuridine (BrdU) and animals were sacrificed at 1, 2, 7 or 14 days. Both cigarette smoke and asbestos produced increases in the labelling index of small airway wall, epithelial cells and pulmonary artery cells. In the small airways there was a brief marked positive synergistic interaction between these two agents, but synergism was not seen in the vessels. Cigarette smoke did not increase the labelling of mesothelial or submesothelial cells, whereas asbestos caused a persisting increase in mesothelial cell labelling. There was no correlation between the number of BrdU labelled mesothelial or submesothelial cells and the number of fibres touching the pleura, or located within 180 microns of the pleura. We conclude that the combination of cigarette smoke and asbestos exposure produces a complex set of interactions and has the potential to markedly increase cell proliferation in the parenchyma, an effect that may be important in both fibrogenesis and carcinogenesis. In contrast to the diminishing effects over time of a single dose of asbestos on cell proliferation in the small airways and vessels, the same dose of asbestos leads to sustained mesothelial cell proliferation. However, the latter process does not correlate with local accumulation of asbestos fibres."

A third study is called, "Asbestos bodies, their formation, composition and character" by F. D. Pooley - Environmental Research - Volume 5, Issue 4, December 1972, Pages 363-379.  Here is an excerpt: "Abstract - Asbestos bodies extracted from human lungs have been examined under the electron microscope to determine their morphology and diffraction characteristics. The asbestos bodies were extracted from the lungs of persons exposed to the four types of commercial asbestos fiber, namely cocidolite, amosite, anthophyllite and chrysotile.

Asbestos bodies were rarely formed on fibers less than 10 μm in length and practically always on straight fibers. They were found to occur on all the four commercial varieties of asbestos but less frequently on chrysotile fibers. The characteristics of the individual fibers were found to play a large part in determining the range and frequency of body shapes observed. There appears to be no evidence to suggest stepwise formation of asbestos bodies.

Asbestos bodies were found to have a major crystalline component which is structurally similar to extracts of ferritin produced from animal and human organs. The material forming the asbestos body is definitely biological in origin and corresponded closely to the material defined in the medical literature as hemosiderin."

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