subject: Difference In Frequency Of Known Or Presumed Exposure To Asbestos Between The Pleural Plaque Cases [print this page] Investigating the research concerning asbestos exposure and disease development is important.One interesting study is called, Parietal pleural plaques, asbestos bodies, and neoplasia. A clinical, pathologic, and roentgenographic correlation of 25 consecutive cases. By S L Wain, V L Roggli, and W L Foster, Jr - CHEST November 1984 vol. 86 no. 5 707-713.Here is an excerpt: Abstract - An investigation was made to correlate autopsy and roentgenographic findings of pleural plaques with occupational exposure to asbestos and occurrence of respiratory tract tumors. Of the 434 autopsies performed over a 2 1/2 year period, 25 (5.8 percent) had pleural plaques but no gross evidence of parenchymal fibrosis. Review of the posterior-anterior chest roentgenograms using the International Labor Office criteria for classification of pneumoconiosis (1980) revealed that only seven of the 25 cases had detectable pleural thickening or calcification, which demonstrates the poor sensitivity of standard x-ray films. There was no detectable difference in frequency of known or presumed exposure to asbestos between the pleural plaque cases and controls as determined by occupational information obtained from chart review. Asbestos bodies were identified in lung tissue digests from all 25 cases with pleural plaques, and exceeded the normal range for our laboratory in 14 cases (56 percent). Of the 25 cases with pleural plaques, four also had bronchogenic and three had laryngeal carcinoma. The prevalence of bronchogenic carcinoma in patients with plaques was not different from those without plaques (p greater than 0.50). However, the association between plaques and laryngeal carcinoma was highly significant (p = 0.004).
Another interesting study is called, In vitro Effect of Asbestos Fibers on Polymorphonuclear Leukocyte Function by James Doll, Richard P. Stankus, Susan Goldbach, John E. Salvaggio - International Archives of Allergy and Immunology Vol. 68, No. 1, 1982.Here is an excerpt: Abstract - Incubation of chrysotile and amphibole asbestos fibers with normal human peripheral blood polymorphonuclear leukocytes (PMN) resulted in a significant stimulation of PMN metabolic activity and generation of toxic oxygen by-products as measured by chemiluminescence (CL). Although all asbestos fibers tested were cytotoxic to PMN, cytotoxicity and CL varied disproportionately with fiber type. Anthophyllite asbestos produced the greatest PMN cytotoxicity. It also depressed PMN phagocytosis of latex beads the most and induced the greatest PMN CL response of the fiber types examined. We postulate that asbestos-induced release of toxic oxygen by-products from PMN which have infiltrated into the pulmonary alveoli may contribute to disease pathogenesis in asbestosis.
Another interesting study is called, Long term radiological effects of short term exposure to amosite asbestos among factory workers. By R Ehrlich, R Lilis, E Chan, W J Nicholson, I J Selikoff - Br J Ind Med 1992;49:268-275.Here is an excerpt: Abstract - Chest radiographs were read from a sub-cohort of 386 factory workers with short term exposure to amosite asbestos (median exposure six months) and long follow up (median 25 years). Prevalence of abnormality was determined independently by two readers from the first film available after 20 years from first employment. Serial films were obtainable for 238 men (median interval from first to last film: nine years). Progression was classified with a direct progression scoring scale. Individual dust exposure estimates were derived from dust counts from two similar plants. With as little as one month or less of employment, about 20% of the films showed parenchymal abnormality and about a third showed pleural abnormality. Those in the lowest cumulative exposure stratum (less than 5 fibre-years/ml) were similarly found to have high rates of abnormality. Dose-response relations were present in the data of both readers. Smokers had higher rates of parenchymal abnormality. On multivariate analysis, cumulative exposure was the exposure variable most closely related to parenchymal abnormality, and time from first employment was the variable most closely related to pleural abnormality. Progression (including first attacks) 20 or more years after ceasing employment occurred and was more common for pleural than for parenchymal abnormality. It is concluded that with exposure to high concentrations to amosite such as existed in this factory and with follow up for at least 20 years, (1) exposure for as little as a month was sufficient to produce radiological signs of parenchymal and pleural fibrosis, (2) no cumulative exposure threshold for parenchymal and pleural fibrosis was detectable, and (3) parenchymal and pleural progression were still detectable >/= 20 years after the end of exposure.
We all owe a debt of gratitude to these fine researchers for their important work.If you found any of these excerpts helpful, please read the studies in their entirety.
