Radiation therapy in children younger than 3 years of age results in increased toxi-city. Radiation therapy to the lungs can cause impairment of the proliferation and maturation of alveoli, resulting in chronic respiratory insufficiency. This is thought to be consistent with a proportionate interference with the growth of both the lungs and chest wall. It also causes damage to the type II pneumocyte, which is responsible for the production of surfactant and the maintenance of patency of the alveoli. As a result of changes in surfactant production, there is a decrease in alveolar surface tension and compliance. These children exhibit decreased mean total lung volumes and DLCO (diffusion capacity of carbon monoxide) that is approximately 60% of predicted values.

The effects of direct radiation to the lungs also include damage to the endothelial cells of the capillaries, resulting in alterations of perfusion and permeability of the vessel wall. Currently, this complication is thought to be mediated by cytokine production that stimulates septal fibroblasts increasing collagen production and pulmonary fibrosis. The late radiation injury to the lung is characterized by the presence of progressive fibrosis of alveolar septa and obliteration of collapsed alveoli with connective tissue.

In adolescents treated for Hodgkin disease who are asymptomatic, chest radiographic findings or pulmonary function tests consistent with fibrosis have been found in 30-100% of patients. The changes have been detected months to years after radiation therapy. The incidence of radiation-induced fibrosis has decreased due to refinements in radiation therapy.

Children with malignant brain tumors receiving craniospinal radiation therapy have a significant risk of developing late restrictive lung disease.

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