Rationale: Recent studies have reported acidification of exhaled breath condensate (EBC) in inflammatory lung diseases. This phenomenon, designated "acidopnea," has been attributed to airway inflammation. Objectives: To determine whether salivary acids and bases can influence EBC pH in chronic obstructive pulmonary disease (COPD). Methods: Measurements were made of pH, electrolytes, and volatile bases and acids in saliva and EBC equilibrated with air in 10 healthy subjects and 10 patients. In 2000, Hunt and colleagues reported that exhaled breath condensates (EBCs) are acidified during asthmatic exacerbations (1). They referred to this phenomenon as "acidopnea" and suggested that it reflected excess acid produced in the airways by inflammation. These observations were confirmed in studies of chronic obstructive pulmonary disease (COPD) and other inflammatory lung disorders (2-10). Subsequently, Hunt and colleagues found that EBC NH 4 ϩ concentrations were reduced in many patients with asthma (11). They postulated that production of NH 3 in the airways was reduced because of impaired glutaminase activity, and suggested that reductions in airway NH 3 production reduced local buffering, thereby promoting airway acidification. They also argued that concentrations of NH 4 ϩ in EBCs did not influence the pH of the EBC samples, which represented an accurate marker of airway acidification (12, 13). This study has analyzed the acid and base concentrations in saliva and EBC from 10 healthy subjects and 10 patients with COPD to determine whether EBC pH is influenced by volatile or nonvolatile constituents in the saliva.
METHODSEleven healthy subjects and 10 subjects with COPD were initially selected but condensate from one healthy subject was deleted because high amylase concentrations indicated salivary contamination (Table 1). Spirometry was performed in all subjects (Sensormedics, Yorba Linda, CA). The patients had COPD (FEV 1 Ͻ 75% predicted, FEV 1 /FVC Ͻ 70%) (14) and an average smoking history of 59 Ϯ 43 (SD) pack-yr. None smoked within an hour of the study. All were taking prescribed maintenance bronchodilators, which were not used during the hour before collections.Patients exhaled for 1 h into an insulated 66-cm polycarbonate condenser cooled with recirculated ice water. One-way valves were used to ensure that subjects inhaled fresh air and exhaled into the condenser. Nose clips were not used. The mouthpiece and condenser were connected by a 450-ϫ 22-mm ID ventilator tubing (Corr-a-Flex 2; Hudson RCI, Temecula, CA) inclined upward to minimize salivary contamination. Condensate was collected using polycarbonate tubes. Collection and analysis of capillary plasma and saliva are described in the online supplement.All samples were stored at Ϫ80ЊC. Before analysis, all samples were allowed to thaw in room air for about 30 min. To minimize potential losses of volatile acids and bases, no attempt was made to remove ambient CO 2 from the EBC or saliva with inert gas (see the online supplement). The buffering capacity of th...