The ultrastructure of the lung of mice exposed to a supra-lethal dose of ionizing radiation on the thorax.
TL;DR: Mice were exposed to 2000 R of x-rays to the whole chest or to the right hemithorax at various periods, from 0 to 15 months after exposure, and the changes in the ultrastructure of the lung were studied.
Abstract: Mice were exposed to 2000 R of x-rays to the whole chest or to the right hemithorax. At various periods, from 0 to 15 months after exposure, the changes in the ultrastructure of the lung were studi...
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TL;DR: In this paper, the authors present an Ionizing Radiation Sources and Biological Effects (IRBE) study, in which the sources and biological effects of ionizing radiation are investigated and compared.
Abstract: (1983). Ionizing Radiation: Sources and Biological Effects. International Journal of Radiation Biology and Related Studies in Physics, Chemistry and Medicine: Vol. 43, No. 5, pp. 585-586.
769 citations
TL;DR: The cellular effects of irradiating the lungs are rleated to the histologic and clinical sequelae, and characteristic changes in pulmonary function and radiographic appearance are described, and management is reviewed.
Abstract: The cellular effects of irradiating the lungs are rleated to the histologic and clinical sequelae. The occurrence and severity of damage rare semiquantitatively related to the volume of lung irradiated, and the dose rate of irradiation. The clinical syndrome occurs in up to about 10% of patients and consists of an acute transient phase, radiation pneumonitis, usually occurring 6 to 12 weeks after radiation therapy. This is followed by clinical remission except in the most severe cases and gradula radiologic progression to the stage of radiation fibrosis over the next 6 to 12 months. Concommittant chemotherapy, repeat courses of radiation, and steroid wihtdrawal are exacerbating factors. Characteristic changes in pulmonary function and radiographic appearance are described, and management is reviewed.
551 citations
TL;DR: The LD/50 between 40 and 180 days after irradiation of the thorax has been taken as a measure of lung damage in mice and the method has been used to derive the relationship between total dose, number of fractions (N) and overall treatment time (T).
Abstract: The LD/50 between 40 and 180 days after irradiation of the thorax has been taken as a measure of lung damage in mice. The method has been used to derive the relationship between total dose, number of fractions (N) and overall treatment time (T). For X rays the results fit an Ellis type of relationship, i.e. total dose ∝N0·25 T0·07. This only applies for more than 8 fractions, below which N0·39 becomes a good fit to the results. For neutrons, the best fit is total dose ∝T0·07. Various possible explanations for the T factor are discussed, but for lung damage we attribute it to a slow repair process which possibly may only be observed in slowly proliferating tissues. Slow repair is about 100 times less rapid than Elkind-type of repair of sublethal damage and whereas Elkind repair is greatly reduced for irradiation with fast neutrons, relative to X rays, slow repair is not.
175 citations
TL;DR: The principles of radiobiology that can explain the time of onset, duration, and severity of the complex reactions of the lung to ionizing radiation are outlined and emphasis is placed on the data showing that alpha emitters are at least an order of magnitude more hazardous than beta/gamma radiation.
Abstract: This article outlines the principles of radiobiology that can explain the time of onset, duration, and severity of the complex reactions of the lung to ionizing radiation. These reactions have been assayed biochemically, cell kinetically, physiologically, and pathologically. Clinical and experimental data are used to describe the acute and late reactions of the lung to both external and internal radiation including pneumonitis, fibrosis and carcinogenesis. Acute radiation pneumonitis, which can be fatal, develops in both humans and animals within 6 months of exposure to doses greater than or equal to 8 Gy of low LET radiation. It is divisible into a latent period lasting up to 4 weeks; an exudative phase (3-8 weeks) and with an acute pneumonitic phase between 2 and 6 months. The latter is an inflammatory reaction with intra-alveolar and septal edema accompanied by epithelial and endothelial desquamation. The critical role of type II pneumonocytes is discussed. One favored hypothesis suggests that the primary response of the lung is an increase in microvascular permeability. The plasma proteins overwhelm the lymphatic and other drainage mechanisms and this elicits the secondary response of type II cell hyperplasia. This, in its turn, produces an excess of surfactant that ultimately causes the fall in compliance, abnormal gas exchange values, and even respiratory failure. The inflammatory early reaction may progress to chronic fibrosis. There is much evidence to suggest that pneumonitis is an epithelial reaction and some evidence to suggest that this early damage may not be predictive of late fibrosis. However, despite detailed work on collagen metabolism, the pathogenesis of radiation fibrosis remains unknown. The data on radiation-induced pulmonary cancer, both in man and experimental animals from both external and internal irradiation following the inhalation of both soluble and insoluble alpha and beta emitting radionuclides are reviewed. Emphasis is placed on the data showing that alpha emitters are at least an order of magnitude more hazardous than beta/gamma radiation and on recent data showing that the more homogeneous the irradiation of the lung, the greater is the carcinogenic hazard which contradicts the so-called "hot particle" theory.
163 citations
TL;DR: Comparison of dose-response curves for the pathological changes and for breathing frequency 16, 36, and 52 weeks after irradiation indicated that increases in breathing frequency were associated with increases in the severity of the histological changes scored.
Abstract: TRAVIS, E. L., DOWN, J. D., HOLMES, S. J., AND HOBSON, B. Radiation Pneumonitis and Fibrosis in Mouse Lung Assayed by Respiratory Frequency and Histology. Radiat. Res. 84, 133-143 (1980). The response of mouse lung to radiation was assessed by measuring breathing frequency up to 52 weeks after graded single doses of X rays to both lungs. Breathing frequency was increased after both lethal and sublethal doses, with damage appearing sooner after higher doses. Dose-response curves were obtained after 14 weeks with a threshold of 12 Gy. All mice given doses greater than 15 Gy died by 22 weeks. Some return of function was observed in the lower dose groups by 36 weeks, but breathing frequency remained elevated for 52 weeks after a nonlethal dose. The changes in breathing frequency were compared with histological changes in the same mice at sacrifice. The increased breathing frequency between 14 and 24 weeks was associated with radiation pneumonitis seen histologically. After 36 weeks, the elevation in breathing frequency above the control value was associated with fibrosis. Comparison of dose-response curves for the pathological changes and for breathing frequency 16, 36, and 52 weeks after irradiation indicated that increases in breathing frequency were associated with increases in the severity of the histological changes scored.
163 citations
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TL;DR: Pulmonary-function studies of a patient with severe radiation-induced changes of the lungs showed marked lung restriction and an "alveolar-capillary block," with no evidence of airway obstruction.
Abstract: IRRADIATION of the thoracic region can induce pathologic changes in normal lung tissue. Although this reaction to radiation has been known for over thirty years, clinical recognition occurs infrequently, and neither the pathologic physiology nor effective treatment has been clearly established. Recently, pulmonary-function studies of a patient with severe radiation-induced changes of the lungs showed marked lung restriction and an "alveolar-capillary block," with no evidence of airway obstruction. During a course of adrenocorticosteroid therapy there was impressive amelioration of subjective respiratory symptoms. Repetition of the pulmonary-function studies, however, showed progression of the physiologic defect. Case Report A 46-year-old Negro was . . .
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