Difference in Frequency of Known or Presumed Exposure to Asbestos Between the Pleural Plaque Cases
Investigating the investigation concerning asbestos exposure and illness development is essential. 1 intriguing study is referred to as, “Parietal pleural plaques, asbestos bodies, and neoplasia. A clinical, pathologic, and roentgenographic correlation of 25 consecutive circumstances.” 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 produced 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 (five.8 percent) had pleural plaques but no gross evidence of parenchymal fibrosis. Review of the posterior-anterior chest roentgenograms employing the International Labor Office criteria for classification of pneumoconiosis (1980) revealed that only seven of the 25 circumstances had detectable pleural thickening or calcification, which demonstrates the poor sensitivity of regular x-ray films. There was no detectable distinction in frequency of known or presumed exposure to asbestos between the pleural plaque cases and controls as determined by occupational details obtained from chart review. Asbestos bodies had been identified in lung tissue digests from all 25 instances with pleural plaques, and exceeded the regular range for our laboratory in 14 circumstances (56 percent). Of the 25 cases with pleural plaques, four also had bronchogenic and 3 had laryngeal carcinoma. The prevalence of bronchogenic carcinoma in patients with plaques was not diverse from those without having plaques (p greater than .50). However, the association between plaques and laryngeal carcinoma was extremely substantial (p = .004).”
Another interesting study is referred to as, “In vitro Impact 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 typical human peripheral blood polymorphonuclear leukocytes (PMN) resulted in a considerable stimulation of PMN metabolic activity and generation of toxic oxygen by-products as measured by chemiluminescence (CL). Although all asbestos fibers tested had been cytotoxic to PMN, cytotoxicity and CL varied disproportionately with fiber sort. 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 sorts examined. We postulate that asbestos-induced release of toxic oxygen by-goods from PMN which have infiltrated into the pulmonary alveoli may contribute to illness pathogenesis in asbestosis.”
An additional interesting study is referred to as, “Lengthy term radiological effects of short term exposure to amosite asbestos amongst factory workers.” By R Ehrlich, R Lilis, E Chan, W J Nicholson, I J Selikoff – Br J Ind Med 199249:268-275. Here is an excerpt: “Abstract – Chest radiographs had been read from a sub-cohort of 386 factory workers with short term exposure to amosite asbestos (median exposure six months) and lengthy follow up (median 25 years). Prevalence of abnormality was determined independently by two readers from the 1st film offered following 20 years from first employment. Serial films had been 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 comparable plants. With as small as one month or much 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) had been similarly found to have high rates of abnormality. Dose-response relations had been present in the information 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 initial employment was the variable most closely related to pleural abnormality. Progression (such as first attacks) 20 or far more years soon after ceasing employment occurred and was more widespread 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 generate 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.”
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