By Douglas H. K. Lee
Ebook through Lee, Douglas, Editor
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Extra resources for Environmental Factors in Respiratory Disease
W. (1963). Severe irreversible airways obstruction without emphysema. Thorax 18. 361. Larson, R. K. and Gordinier, R. (1965). Pulmonary alveolar proteinosis: report of six cases, review of the literature and formulation of a new theory. Ann. Int. Med. 62: 292. Corrin, B. and King, E. (1970). of experimental pulmonary alveolar Thorax 25: 230. Wood, W. B. (1951). bacteria. Se. Amer. White blood lSk: 20. Pathogenesis proteinosis. cells vs. Pepys, J. (1969). HypersensItIvity Diseases of the Lung Due to Fungi and Organic Dusts.
One day after 13 mg/kg of paraquat was given intraperitoneally. Alveolar epithelial membranes are swollen, into alveolar spaces in upper corners and center of photographs above dark basement membranes. Capillary endothelium is also swollen around erythrocytes and neutrophilic white blood cells in capillaries above, below and on both sides. ) Z c > < 4. ALVEOLAR RESPONSES cadmium fumes, as well as excess metabolic products such as cholesterol or fatty acids. Physical agents such as heat and ionizing radiation, and trauma such as that produced by explosive decompression or rapid deceleration, also produce pulmonary edema.
These include the herbicide paraquat (Weedol) ( 7 ) , dinitrophenol, thiourea, industrial chemicals such as nickel carbonyl, and 44 4. ALVEOLAR RESPONSES Msàh'^iM^^^aìi^MÈ^ùù^&^^ù^É Fig. 2. A higher power electron microscopic picture of a capillary (above) after one hour's exposure of the dog to nitrogen dioxide, 12 parts per million (ppm). Endothelial membranes are vacuolated and pinocytotic vesicles are increased (compare to Fig. IB). The type II cell below and interstitial space filled with collagen fibrils were not affected.
Environmental Factors in Respiratory Disease by Douglas H. K. Lee