Forced expiratory volume in 1 second (FEV1) declines normally with aging by approximately 30 mL/yr, but in susceptible smokers, the decline is greater (about 60 mL/yr), resulting in the development of chronic obstructive pulmonary disease (COPD). Smoking cessation usually restores the normal or near-normal rate of FEV1 decline, whereas intermittent quitting provides less benefit. Thus, smoking cessation is a critical component for the prevention of COPD progression. FEV1 is central to the definition of COPD and classification of its severity. FEV1 is a good predictor of exercise tolerance and correlates with survival and quality of life. More rapid FEV1 decline is also predictive of morbidity, mortality, and hospitalization rates. Risk factors for accelerated decline in FEV1, in addition to smoking, include frequent exacerbations, airways reactivity, and possibly chronic systemic inflammation. Genetic components of the decline in FEV1 are being actively explored, but none has been extensively validated other than alpha1-antitrypsin deficiency. To date, only smoking cessation has been definitively shown to be effective in reducing the rate of FEV1 decline, but other therapeutic strategies are under active research. Consequently, FEV1 and its change over time are important outcomes in COPD and valuable measures for the assessment of disease progression.