Abstract
The human lungs are relatively radiosensitive organs, requiring a single dose of only 9.0 Gy (corrected lung dose) to produce a 25% incidence of acute radiation pneumonitis syndrome following irradiation of the upper half of the body (Van Dyk et al, 1981). This low tolerance limits the therapeutic potential of whole lung irradiation for pulmonary metastases, and radiation damage may have been responsible for pneumonitis in 30–40% of leukaemic patients receiving total body irradiation (TBI) prior to bone marrow transplantation (Keane et al, 1981). Split-dose experiments in laboratory animals show that the lungs have a considerable capacity for repair of sublethal damage (Field et al, 1976). Peters et al (1979) have proposed that fractionated TBI should lead to therapeutic gain in the treatment of leukaemia with TBI, since cells of haemopoietic origin show less capacity for repair of sublethal radiation injury than the lung.