Abstract

To study the initial pleural cellular response to asbestos and to determine the relationship between this response and the development of pleural plaques, a model of asbestos pleurisy was developed in both normal and nitrogen-mustard-treated (neutropenic) New Zealand white rabbits. Animals were rendered neutropenic, as it has been shown that neutropenic rabbits do not develop a macrophage influx in the pleural space after the administration of either BCG or bacteria and that the pathology is different from that in normal rabbits treated in a similar fashion. Intrapleural asbestos induced an exudative effusion in normal animals within 4 h, and there was increased metabolic activity through 120 h, with a fall in pleural fluid pH and PO2 and a rise in pleural fluid PCO2. Neutropenic animals similarly developed an exudative pleural effusion but showed no change in metabolic activity of pleural fluid. Normal rabbits showed a marked cellular influx into the pleural space after asbestos treatment, with a peak total cell count of 27,208/microliters at 24 h; the majority of these cells were polymorphonuclear leukocytes. A macrophage influx occurred at 48 h and peaked at 72 h. By 120 h, lymphocytes were the predominant cell. Nitrogen-mustard-treated animals reached a peak of only 5,442 cells/microliters in the pleural space at 24 h, with a small percentage of polymorphonuclear leukocytes. A macrophage peak did not occur in these animals. There was a marked contrast between groups noted at autopsy. Normal animals developed pleural plaque formation, which was evident by 7 days and completely developed by 1 month.(ABSTRACT TRUNCATED AT 250 WORDS)