Pulmonary surfactant protein A (SP-A) has been associated with host defense in the lung, and contributes to the pathogenesis of chronic obstructive pulmonary disease (COPD). The present study aimed to determine a non‑invasive method of measurement of SP‑A, and further examine the expression levels of SP‑A in patients with COPD. SP‑A was detected in the exhaled breath condensate (EBC) obtained from patients with COPD and from non‑COPD subjects. The individuals recruited for the present study comprised 60 subjects with and without COPD, who underwent lobectomy for a solitary peripheral lung nodule. EBC was collected using a condenser, and an enzyme‑linked immunosorbent assay (ELISA) was used to measure the levels of SP‑A. Tissue samples were obtained during lobectomy through resection of the adjacent lung tissues, located >5 cm from the nodule. Western blot analysis and immunohistochemistry were used to measure SP‑A and SP‑A‑positive type II pneumocytes. The results demonstrated that SP‑A was detectable in the EBC of all subjects. The results of the ELISA and western blotting demonstrated that the expression levels of SP‑A were significantly decreased in patients with COPD, compared with the non‑COPD subjects. The reduction of SP‑A‑positive type II pneumocytes was associated with the expression levels of SP‑A. Decreased expression levels of SP‑A in EBC were associated with a higher degree of airway limitation. These results suggested that the measurement of SP‑A levels in the EBC may serve as a method for monitoring airway obstruction in patients with COPD. Further investigations are required in order to examine these observations further and to elucidate the underlying mechanisms.