Pleural response to diesel exhaust particulates: A morphometric study

The effect of diesel exhaust particulates on the pleura were studied in Fischer 344 rats exposed to 0, or to 250 {dollar}mu{dollar}g/m{dollar}sp3{dollar} of diesel exhaust for 18 months, 21 months, and 24 months with no recovery period following termination of exposure, and rats exposed to 250 {dollar}mu{dollar}g/m{dollar}sp3{dollar} for 18 months of diesel exhaust followed by either a 3 or a 6 month recovery period, and rats exposed to 1500 {dollar}mu{dollar}g/m{dollar}sp3{dollar} for 18 months to diesel exhaust with no recovery period. Lung tissues were processed using conventional transmission electron microscopic techniques and the resulting micrographs were morphometrically analyzed (point and intersect counts using a Zeiss MOP 3) and statistically analyzed (ANOVA and Newman-Keuls test for comparison of means) for the duration of exposure effect, dosage effect, and recovery period effect.; Analysis of the dose response effect indicated that cells of inflammation, especially mast cells, were present in increasing numbers in the 1500 {dollar}mu{dollar}g/m{dollar}sp3{dollar} treatment group. Also there was an increase in fibroblasts but no increase in total collagen. Macrophages increased in numerical density but no increase in macrophage cell volume was detected although they were loaded with diesel carbon particulates. The duration response also indicated the presence of inflammatory cells in all treatment groups with the neutrophils and mast cells being the most frequently observed cells. Evidence of a possible mild fibrosis may have been seen. In the recovery treatment groups, no evidence of fibrosis was seen. There was no significant change in either the collagen volume density nor in the interstitial mean thickness. Macrophages were seen disrupting the integrity of the pleura by releasing hydrolytic enzymes causing localized dissolution of the pleura. Cells of inflammation were present with the neutrophils and mast cells being the most prevalent cell type.