Prospective Evaluation of Airways Reactivity

BACKGROUND: 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. This study was a subproject in a Specialized Center of Research in Chronic Diseases of the Airways. The East Boston cohort was developed in 1975 under contract issued by the Division of Lung Diseases. DESIGN NARRATIVE: In 1975 a stratified, random sample of propositus children ages 5-9 living in the East Boston area of Boston, Massachusetts was selected as were their family members to form the cohort. In the longitudinal study, each member of the propositus cohort and all family members five years of age and older residing in the household were visited at home annually by study personnel. Data collected included: a respiratory illness history; demographic data on type of heating, fuel for cooking, types of air-purifying devices, and area of residence; cigarette smoking history; disability from cardiac disease; age of puberty in female children; pulmonary function tests; and anthropometric data. The study helped to determine the extent to which airways responsiveness was a risk factor for chronic airflow obstruction, was acquired as a result of other exposures or as a consequence of chronic symptoms or lower levels of pulmonary function. Each year study families were requested to participate in the cold air challenge protocol. Subjects participating in this protocol were studied in a laboratory at the community health center. Forced expiratory volumes were obtained followed by a cold air challenge test using the technique of eucapneic hyperventilation with subfreezing air. The cold air challenge test separated normals from asthmatics. Two inhalations of isoproterenol were administered one minute apart after which three forced vital capacity maneuvers were performed. After pulmonary function tests were completed, allergy tests were conducted for ragweed, trees, house dust, and grasses. The study was renewed in 1992 to examine the relationship of respiratory symptoms and illnesses, cigarette smoking, airways responsiveness, and markers of inflammation to growth and decline in lung function in two well-characterized and investigated community-based populations of children and adults. Data were available in two populations: the Childhood Respiratory Disease Study in East Boston (CRD) and the Normative Aging Study Population (NAS). This group has shown that increased airway responsiveness was associated with altered patterns of lung growth (in children) and reduced levels of lung function (in adults). They also have shown that airway responsiveness was cross-sectionally associated with chronic respiratory symptoms in both children and adults. However, asymptomatic airway responsiveness was extremely common, occurring in 20 percent to 60 percent of responsive subjects, depending on how responsiveness and chronic symptoms were defined. Asymptomatic bronchial responsiveness was thought to represent subclinical or mild airway inflammation. Alternatively, it may have represented differences in mechanical factors leading to airway narrowing. Funding represented approximately 15 percent of the dollars of the Specialized Center of Research in Chronic Diseases of the Airways (P50HL19170) used to support this study. The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) rec