Epidemiologic models for growth and decline in lung function have been developed from longitudinal studies in adults. The development of chronic obstructive lung disease appeared to be the result of both an abnormally rapid rate of decline in level of lung function in early adult life. Thus factors in early childhood influenced adult pulmonary function in either of two ways. First, it was hypothesized that childhood factors diminished the maximally attained level of lung function in early adult life, thus increasing the likelihood that, with a fixed rate of decline in adult life, these individuals would be more likely to develop symptoms. Alternatively, childhood events might act directly to increase the risk of developing a more rapid rated decline in pulmonary function in adult life. The above theory had a plausible patho-anatomic basis. The lung is one of the last organs in the body to mature and children continue to make alveoli up until the age of six or seven. Thus risk factors both environmental, such as respiratory illness, active and passive cigarette smoke, and host airways responsiveness and atopy, could adversely influence lung growth and lead to less maximal lung growth and/or increased sensitivity to cigarette smoking in adult life.