Mice received 2400 rads in two fractions to the thorax; 4 months later when radiation pneumonitis occurred, aspects of their phospholipid metabolism were studied and compared to those of unirradiated mice. In the lung tissue there was a consistent and significant increase in the total phospholipids and particularly in the amount of PC. The proportion of the latter which was disaturated remained constant. In the lavaged AF the increase was smaller and not significant, the degree of disaturation again remaining constant. Isotope labelling in vivo with 3H-glycerol, 14C,-palmitate and 3H-choline indicated significantly increased incorporation of each of these precursors into PC and most other phospholipids. This was not due to changes in nutrition, altered precursor pool sizes, or redistribution of isotope insofar as could be determined. Histologic studies showed the type 2 cells to be large and filled with numerous enlarged lamellar bodies. These results suggest that phospholipid synthesis is enhanced in radiation pneumonitis and that the fall in compliance of the alveolar surface layer is not likely to be due to surfactant deficiency in this model.