Given that SP-A plays a critical role in assisting phagocytosis in the lung, we hypothesized that either the absence of SP-A expression in the lung of SP-A (-/-) mice or a decrease in SP-A function after oxidation of SP-A in WT mice is one of the factors that contribute to increased susceptibility of mice to pneumonia if exposed to air pollutants, such as ozone. This evidence concerns the gene SFTPA2 and pneumonia.