Cumulative Asbestos Exposure and Railroad Workers

Mortality and death rates increase as cumulative exposure to asbestos increases.  One group of employees that have been closely studied are those in the railroad industry.

One interesting study is called, "Mortality among asbestos-exposed workers in a railroad workshop." By Ohlson CG, Klaesson B, and Hogstedt C. - Scand J Work Environ Health. 1984 Oct;10(5):283-91.  Here is an excerpt: "Abstract - The mortality experience of a cohort of 3 297 railroad maintenance shopworkers exposed to asbestos was investigated. The study period was 1951-1980, and the vital status was assessed for 99.6% of the men. Individual estimates of cumulative asbestos exposure were based on detailed records on work tasks and divisions. Dust measurements were scanty in earlier decades, and estimates of average fiber levels were therefore based on information on the amount and kind of asbestos used, job descriptions, and interviews with older workers. The overall mortality was lower than expected from the national death rates (standardized mortality ratio = 82). The mortality from lung cancer increased as cumulative exposure increased in consistent dose-response relationships. Employment times of less than 30 years in workplaces with moderate levels of mainly chrysotile asbestos was not associated with any apparent increase in the risk of lung cancer. A subgroup exposed for more than 30 years in workplaces repairing steam engines, where amphiboles were used as well, had a standardized mortality ratio of 192 for lung cancer. This figure may be an underestimation due to healthy worker selection and fewer smokers than normal. The "true" standardized mortality ratio was estimated to be about 300. Five cases of mesothelioma were observed."

A second study that is interesting is called, "Cellular ingestion, toxic effects, and lesions observed in human bronchial epithelial tissue and cells cultured with asbestos and glass fibers" by Aage Haugen, Paul W. Schafer, John F. Lechner, Gary D. Stoner, Benjamin F. Trump, Curtis C. Harris - Radiation Oncology Investigations - Volume 30 Issue 3, Pages 265 – 272.  Here is an excerpt: "Abstract - Although exposure to asbestos has been shown in previous epidemiological studies to synergistically increase the risk of bronchogenic carcinoma for cigarette smokers, the pathobiological mechanism(s) responsible for the cocarcinogenic action of asbestos is not known. Therefore, the effects of asbestos fibers on normal human tracheobronchial epithelium are of interest. Asbestos fibers, i.e., amosite, crocidolite and chrysotile (UICC samples) and glass fibers were initially assayed for their cytotoxcity. Bronchial epithelial cells exposed to either asbestos or glass fibers displayed inhibition of cell growth as a function of fiber concentration. When compared to glass fibers, asbestos fibers caused a statistically significant (p<0.05) decrease in cell population doubling rate. Chrysotile was approximately 10 times more cytotoxic than either amosite or crocidolite and more than 100 times more cytotoxic than the glass fibers. Epithelial cells were 10 to 15 times more sensitive to the cytotoxic effects of asbestos fibers than bronchial fibroblasts from the same donor. Using electron microscopy, asbestos fibers were seen to be ingested by epithelial cells. After exposure for 2 h short fibers (<12m) were found both in the cytoplasm and within phagosomes. High-voltage electron microscopy combined with stereo-microscopy revealed asbestos fibers in the cytoplasmic matrix.

A single exposure to amosite asbestos (100-1000 g/ml) was found to induce focal hyperplasia and epidermoid metaplasia with cellular atypia in human tracheobronchial explants. Surface fine structure observations revealed asbestos fibers protruding from these lesions. Intra-cytoplasmic and intranuclear fibers of amosite were identified in these focal lesions using X-ray microanalysis in combination with transmission electron microscopy. With increasing time, fibers were also seen deposited within the submucosa of the explants. The preferential cytotoxicity of asbestos for epithelial cells and the metaplastic response of bronchial epithelium may be important in the cocarcinogenic action of asbestos. "

A third study is called, "Pleural calcification associated with exposure to chrysotile asbestos in southeast Turkey." By Yazicioglu S. - Chest. 1976 Jul;70(1):43-7.  Here is an excerpt: "Abstract - In this study, pleural calcifications prevailing in the inhabitants of some villages and towns around Diyarbakir, a city in southeast Turkey, have been found to be caused by the inhalation of chrysotile asbestos, the mineral commonly used indiscriminately to paint the walls and floors of houses. There were no industrial establishments in the area, except some local mining, and asbestos deposits were even not included on the mining map of the country. Chest roentgenograms from the Chest Hospital and the tuberculosis dispensaries were screened: and, additionally, 15,239 photofluorograms were obtained during a survey. Of all these, 511 patients were found to have pleural calcifications, some with pericardial and diaphragmatic involvement. Forty-four percent (28) of the 64 patients who had examinations of samples of their sputa had asbestos bodies, and asbestosis was also induced in rabbits by administration of the raw material."