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.

Radiation effects in the lung.

SummaryMixture models are proposed for simultaneous analysis of the latency and fractionation characteristics of radiation injury in late-responding normal tissues, The method is an extension of the direct analysis for quantal response data Conceptually, the application of the mixture model is based on the biological observation that over a wide range of doses a proportion of the irradiated subjects will never express damage Mixture models allow the time of occurrence to be utilized in the analysis Furthermore, this type of model takes time-censored observations into account in a natural way and provides an adequate framework for modelling and analysis of effect-dependent latencyMixture models with complete and incomplete repair are applied to dose-incidence data for four late endpoints in rodents: death from radiation-induced pneumonitis, leg paralysis after spinal-cord irradiation, and radiation-induced rectal stenosis and anal discharge Radiation-induced pneumonitis had an effect-dependent latency

Direct estimation of latent time for radiation injury in late-responding normal tissues: gut, lung, and spinal cord.

Effect of cancer chemotherapeutic drugs on radiation-induced lung damage in mice.

A method is described for calculating absolute “operational” values of the parameters α and β that characterise dose fractionation data for tissues, by using the steepness of doseincidence curves measured around each dose per fraction investigated The values are deduced from published mouse lethality data after irradiation of the bone marrow (α = 09 Gy−1; β = 006 Gy−2), the lung (α = 014 Gy−1; β = 002 Gy−2), and the oesophagus (α = 006 Gy−1; β = 0004 Gy−2) With bone marrow and other hierarchical renewal tissues, the operational values apply also to the inactivation of target cells which are the stem cells in the tissue For other tissue types the interpretation of the values is unknown The operational values are useful in characterising the steepness of dose-incidence curves for normal tissue injury after different fractionation schedules

Deriving absolute values of alpha and beta for dose fractionation, using dose-incidence data

The history of radiation research shows that clinical problems give rise to experimental studies and that, in turn, radiobiological findings contribute to the improvement of radiotherapeutic procedures. As long ago as 1922 Groover et al. (1922) and Hines (1922) described the clinical features of radiation-induced pneumonitis and fibrosis of the alveolar wall. Wintz (1923) paid special attention to the complications related to pneumonitis after radiotherapy for bronchial and mammary carcinoma. The clinical observation that the lung is a critical tissue in radiotherapy of organs of the chest wall or within the thorax led to intensive experimental investigations. At a relatively early stage the chronology of the pathological alterations was studied in rabbits (Englestad 1940). An excellent and fundamental review of injuries contributing to lung morbidity and organ dysfunction was published by Rubin and Casarett (1968).

Radiation Injury of the Lung: Experimental Studies, Observations After Radiotherapy and Total Body Irradiation Prior to Bone Marrow Transplantation

Male CBA mice were given X-radiation to the thorax in the range 7 to 23 Gy and their response was quantified by measuring ventilation rate and carbon monoxide uptake at intervals up to 2 years thereafter; their survival was also documented. The two functional end-points were similarly sensitive indicators of lung damage. Radiation damage was not observed below 10 Gy. As radiation dose was raised above this level there was a rapid shortening of the time to the appearance of damage and subsequent death. At a dose of 15 Gy the median survival time was 14 weeks but raising the dose above this level only slightly reduced the survival time. The way in which the time of survival after lung damage depends on dose is an important characteristic of the development of radiation-induced lung damage which should be considered when examining factors that may influence the development of radiation-induced lung damage.

Dose-dependence of the time of appearance of lung damage in mice given thoracic irradiation.

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Dose-dependence of the time of appearance of lung damage in mice given thoracic irradiation.