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Title: Pulmonary functional and morphological changes induced by a 4-week exposure to 0. 7 ppm ozone followed by a 9-week recovery period

Journal Article · · J. Toxicol. Environ. Health; (United States)

Male Fischer-344 rats were subjected to pulmonary-function testing procedures, then exposed to 0.7 ppm ozone for 28 d, 20 h/d. Another group of animals was similarly treated, but at each test point one-third were sacrificed for microscopic evaluation. When percent changes from preexposure values were compared to controls at each time point, the ozone exposure produced obstructive changes in the lung, including significant decreases in forced expiratory flows, lung volumes, and DL/sub CO/; and a significant increase in functional residual capacity. The total lung capacity was not significantly changed by the ozone. Microscopic examination revealed characteristic lesions in the region of terminal bronchioles and central acinar alveoli marked by peribronchiolar edema, bronchiolization of alveolar duct epithelium, and type II cell proliferation in involved alveoli with increased numbers of macrophages and a few leucocytes. Clearly discernable was a focal interalveolar-alveolar duct reaction made up of fibroblasts, a few inflammatory cells, and conspicuous mast cells, all embedded in a loose metachromatic matrix. After 4 wk of recovery, all measurements of lung volume and DL/sub CO/ had returned to the values of the control group; however, even after 9 wk some of the measurements of lung flow remained significantly although less depressed. Histologically, after 4 wk recovery, there remained only a slight unevenly distributed inflammatory reaction. In these foci there was often a residual, narrower, more condensed band of eosinophilic material, presumably colagen, that sometimes contained interspersed mast cells. After 9 wk, this collagen accumulation within the thickened wall of the alveolar duct could occasionally still be noted.

Research Organization:
General Motors Research Labs., Warren, MI
OSTI ID:
5766592
Journal Information:
J. Toxicol. Environ. Health; (United States), Vol. 17:1
Country of Publication:
United States
Language:
English