The etiology of cystic fibrosis remains unknown. It has been generally accepted that the elaboration of an abnormally viscid mucus, leading to obstruction and stasis, accounts for most of the pathology observed in this disease. An alternative hypothesis has been proposed which holds that an altered ionic environment of the mucus is responsible for its atypical physical properties (1, 2). The two hypotheses are not mutually exclusive as a molecular alteration of the mucus might be expressed only in an altered environment. The influence of infection on the chemical composition of pulmonary secretions has been demonstrated previously in this laboratory (3, 4) by a study of three types of pulmonary secretions:(1) secretions from patients with cystic fibrosis in which infection is most marked in degree and diffuseness,(2) secretions from patients with bronchiectasis in which infection is more localized and of a lesser magnitude, and (3) secretions from laryngectomized patients in whom bronchorrhea results from irritation of the mucosa due to exposure to dry air and in which infection is least pronounced. The degree of infection was found to correlate well with an increase in the organic constituents (DNA, protein, lipid, and carbohydrate) and a decrease in total ash content of these secretions. On this basis, it was hypothesized that the observed differences in the ionic environment of the secretions were secondary to the infectious