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Title: Some effects of nitrogen dioxide on the lung

Abstract

Nitrogen dioxide (NO/sub 2/) when inhaled in different concentrations and for varying times produces pulmonary injuries which are dependent on the anatomic site in the lung and the duration of exposure. Single exposures to high concentrations of NO/sub 2/ for 5 to 6 hr produce an intense cellular proliferation which regresses within 48 hr in all lung regions except the terminal respiratory bronchiole region and the alveoli where the proliferation persists for 4 to 7 days. This same delayed response is also observed in more chronic exposures. Histologically, the lesion in the terminal and respiratory bronchioles may resemble an obliterative bronchiolitis, but the lesion clears if further exposure is terminated. Prolonged exposure to 20 ppM NO/sub 2/, 20 to 22 hr per day for 7 days per wk, produces an increase in total pulmonary and upstream resistance in animals killed immediately after exposure; this resistence returns to normal values within 3 mo after removal from exposure. The internal surface area (ISA) is decreased after 12 mo exposure to NO/sub 2/, but this loss of surface progresses during the recovery period in air, suggesting an autonomous progression of the tissue destructive process. Exposure to 3.64 ppM NO/sub 2/ with and withoutmore » fly ash for periods of 12 to 14 mo causes no increase in pulmonary resistance and no alteration in lung surface. Lung phospholipids and protein synthesis appear to be depressed following exposure to NO/sub 2/. Lecithin is significantly increased. The synthesis of proteases by alveolar macrophages is increased during NO/sub 2/ exposure. Pigmented alveolar macrophages present in animals exposed to NO/sub 2/ simulate those found in human lungs of young cigarette smokers in the terminal and respiratory bronchioles. The mechanism of tissue injury by oxidants such as NO/sub 2/ may involve free radical formation, and peroxidation of lipids or proteins.« less

Authors:
Publication Date:
Research Org.:
Case Western Reserve Univ., Cleveland
OSTI Identifier:
7215257
Resource Type:
Journal Article
Journal Name:
Fed. Proc.; (United States)
Additional Journal Information:
Journal Volume: 36:5
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; 59 BASIC BIOLOGICAL SCIENCES; NITROGEN DIOXIDE; BIOLOGICAL EFFECTS; BIOSYNTHESIS; DOSE-RESPONSE RELATIONSHIPS; ENZYMES; FLY ASH; INHALATION; LECITHINS; LUNGS; MACROPHAGES; PROTEINS; TOBACCO SMOKES; AEROSOL WASTES; AEROSOLS; ANIMAL CELLS; BODY; CHALCOGENIDES; COLLOIDS; CONNECTIVE TISSUE CELLS; DISPERSIONS; ESTERS; INTAKE; LIPIDS; NITROGEN COMPOUNDS; NITROGEN OXIDES; ORGANIC COMPOUNDS; ORGANIC PHOSPHORUS COMPOUNDS; ORGANS; OXIDES; OXYGEN COMPOUNDS; PHAGOCYTES; PHOSPHOLIPIDS; RESIDUES; RESPIRATORY SYSTEM; SMOKES; SOLS; SOMATIC CELLS; SYNTHESIS; WASTES; 560305* - Chemicals Metabolism & Toxicology- Vertebrates- (-1987); 550900 - Pathology

Citation Formats

Kleinerman, J. Some effects of nitrogen dioxide on the lung. United States: N. p., 1977. Web.
Kleinerman, J. Some effects of nitrogen dioxide on the lung. United States.
Kleinerman, J. Fri . "Some effects of nitrogen dioxide on the lung". United States.
@article{osti_7215257,
title = {Some effects of nitrogen dioxide on the lung},
author = {Kleinerman, J},
abstractNote = {Nitrogen dioxide (NO/sub 2/) when inhaled in different concentrations and for varying times produces pulmonary injuries which are dependent on the anatomic site in the lung and the duration of exposure. Single exposures to high concentrations of NO/sub 2/ for 5 to 6 hr produce an intense cellular proliferation which regresses within 48 hr in all lung regions except the terminal respiratory bronchiole region and the alveoli where the proliferation persists for 4 to 7 days. This same delayed response is also observed in more chronic exposures. Histologically, the lesion in the terminal and respiratory bronchioles may resemble an obliterative bronchiolitis, but the lesion clears if further exposure is terminated. Prolonged exposure to 20 ppM NO/sub 2/, 20 to 22 hr per day for 7 days per wk, produces an increase in total pulmonary and upstream resistance in animals killed immediately after exposure; this resistence returns to normal values within 3 mo after removal from exposure. The internal surface area (ISA) is decreased after 12 mo exposure to NO/sub 2/, but this loss of surface progresses during the recovery period in air, suggesting an autonomous progression of the tissue destructive process. Exposure to 3.64 ppM NO/sub 2/ with and without fly ash for periods of 12 to 14 mo causes no increase in pulmonary resistance and no alteration in lung surface. Lung phospholipids and protein synthesis appear to be depressed following exposure to NO/sub 2/. Lecithin is significantly increased. The synthesis of proteases by alveolar macrophages is increased during NO/sub 2/ exposure. Pigmented alveolar macrophages present in animals exposed to NO/sub 2/ simulate those found in human lungs of young cigarette smokers in the terminal and respiratory bronchioles. The mechanism of tissue injury by oxidants such as NO/sub 2/ may involve free radical formation, and peroxidation of lipids or proteins.},
doi = {},
url = {https://www.osti.gov/biblio/7215257}, journal = {Fed. Proc.; (United States)},
number = ,
volume = 36:5,
place = {United States},
year = {1977},
month = {4}
}