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Alterations in the Lung Following the Administration of Ozone
Gary L. Huber, MD;
Robert J. Mason, MD;
Marc LaForce, MD;
Nancy J. Spencer, MS;
Donald E. Gardner, MS;
David L. Coffin, DVM
Arch Intern Med. 1971;128(1):81-87.
Abstract
Inhalation of ozone (5 ppm for three hours) by rabbits resulted in morphologic alterations in the pulmonary alveolar macrophages recovered from the lungs of exposed animals. These structural alterations were characteristic of cellular injury or cell death and included intracellular vacuolization, dilatation of the endoplasmic reticulum and perinuclear envelope, swelling of mitochondria, cell lysis, and formation of myelin figures and autophagic vacuoles. Exposure to ozone had no significant effect on pulmonary surface activity, phosphatide composition, or fatty acid composition of phospholipids recovered from extracts of whole lung or by bronchioalveolar lavage from exposed animals. A dose-related functional impairment in alveolar macrophage intrapulmonary antibacterial defense mechanisms resulted from exposure to lower levels of ozone. Similar dose-related impairments in macrophage function were induced with prolonged oxygen administration.
Author Affiliations
Boston; Bethesda, Md; Boston; Cincinnati
From the Channing Laboratory and Thorndike Memorial Laboratory, Harvard Medical Unit, Boston City Hospital; the Department of Medicine, Harvard Medical School; and the Department of Physiology, Harvard School of Public Health, Boston; the Molecular Disease Branch of the National Heart and Lung Institute, Bethesda, Md; and the Consumer Protection and Environmental Health Service, Division of Health Effects Research, National Air Pollution Control Administration, Cincinnati and Durham, NC.
Footnotes
Received for publication Oct 21, 1970; accepted April 27, 1971.
Read in part before the Tenth Annual Hanford Biology Symposium on Pollution and Lung Biochemistry, Richland, Wash, June 5, 1970, jointly sponsored by the Battelle Memorial Institute-Pacific Northwest Laboratories, National Air Pollution Control Administration, National Institute of Environmental Health Sciences, and the US Atomic Energy Commission.
Reprint requests to Channing Laboratory, Harvard Medical Unit, Boston City Hospital, Boston 02118 (Dr. Huber).
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