A 72-year-old man, an ex-smoker (26.3 packs a year), had a mild cough for several years. Obstructive lung damage (FEV₁/FVC < 70%, % FEV₁ < 80%) was shown in the spirometry that was performed because of clinical symptoms and his history of smoking. No obvious findings were seen on a chest roentgenogram; in contrast, low attenuation areas were spread out at the bilateral upper lobes in the lungs on a chest high-resolution chest tomography (HRCT). The number of eosinophils was increased modestly (2%) in the quantitative analysis by using sputum expectorated spontaneously. This case was diagnosed as chronic obstructive pulmonary disease (COPD), stage II, as a result of smoking-induced emphysema. A long-acting anticholinergic agent and a long-acting β₂-agonist were inhaled daily. However, two months later this case was hospitalized because a wheeze and dyspnea had developed. The percentage of eosinophils had markedly increased to 36%. This exacerbation seemed to be mediated by eosinophilic inflammation in the airways similar to that of bronchial asthma. After an administration of glucocorticoids, the symptoms improved promptly, and the infiltration of eosinophils had roughly returned to normal. To determine whether bronchial asthma is complicated in this case of COPD, we performed an acethylcholine provocation test. The result of this examination indicated no airway hyperresponsiveness. In conclusion, this patient's disease was diagnosed as COPD with eosinophilic airway inflammation, not bronchial asthma. This case may be a novel phenotype of COPD.