This paper discusses the lung response to irradiation in the context of accidental radiation exposure. The lung is a relatively radiation sensitive organ with a response to irradiation that is complex, involving killing of lung cells, death of endothelial cells, influx of inflammatory cells, and waves of inflammatory cytokines and reactive oxygen species (ROS) production. Two major functional outcomes are observed, radiation pneumonitis and radiation fibrosis. Elevated levels of the cytokine, transforming growth factor-β (TGF-β), appear to play an important role in the development of radiation-induced lung injury, particularly fibrosis. There is limited evidence from animal studies that irradiation of the bone marrow and bone marrow transplantation may affect the lung response, but information regarding irradiation of other organs is lacking. Protection against functional and histopathological damage has been demonstrated for a number of different agents when given before (and after) irradiation (e.g. amifostine, captopril, manganese superoxide dismutase (MnSOD), superoxide dismutase (SOD) mimetic). To what extent protection can be provided by agents given only after irradiation is uncertain and although steroids can relieve the symptoms of pneumonitis, it remains unclear whether they can protect against the development of late fibrosis.
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Rićhard P. Hill (2005) studied this question.
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