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To prospectively identify factors that influence the rate of decline in pulmonary function and to identify predictors of chronic obstructive lung disease (COLD) and asthma in a population sample of older adults.
BACKGROUND: Cigarette smoking is recognized as the most important factor in the development of chronic airflow obstruction, yet only a minority of cigarette smokers develop clinical disease. In 1985, interest focused on the role of increased levels of airways responsiveness and atopy as possible potentiating factors for the development of chronic airflow obstruction. Then current epidemiologic studies had data on only one of these potential risk factors or were too small to adequately address the issues involved. The present study assesses both airways responsiveness and atopy. DESIGN NARRATIVE: The study used the population and data base of the Veterans Administration Normative Aging Study (NAS) which began in 1963. The NAS population consists of over 1,900 men originally selected for good health and their wives. The NAS currently administers a cigarette smoking history questionnaire, the NHLBI-ATS respiratory symptom and illness questionnaire, and spirometry at regularly scheduled examinations three years apart. The current study assessed airways responsiveness as measured by response to methacholine inhalation and atopy as measured by skin test, blood eosinophilia, and serum IgE in NAS participants when they returned for their next two examinations. The data were used to examine the relationship of airways responsiveness, atopy, and cigarette smoking to respiratory symptoms both cross-sectionally and longitudinally. The study was renewed in 1996 to prospectively identify factors that influence the rate of decline in pulmonary function and to identify predictors of chronic obstructive lung disease (COLD) and asthma in a population sample of older adults. The investigators hypothesize that the development of accelerated decline in FEV1 and the occurrence of respiratory symptoms in older adults are determined by two environmental exposures: tobacco smoke-induced injury and IgE-mediated hypersensitivity to inhaled aeroallergens. The extent to which allergen exposure and airway responsiveness lead to fixed airflow obstruction in older adults is unknown. The primary allergens of interest include: house dust mite (Der p I, Der fI), cockroach (Bla g I, Bla g II), cat (Fel d I), and fungi. Airway hyperresponsiveness to bronchoconstricting stimuli is a physiologic characteristic that may be thought of both as a manifestation of airway disease and as an intrinsic host characteristic which predisposes to the development of airway disease and determines its clinical pattern. They are using the extensive longitudinal information on respiratory symptoms and illnesses, cigarette smoking, pulmonary function, airway responsiveness, indices of atopy (skin test, total and antigen-specific IgE), indices of inflammation (eosinophil and leukocyte counts in peripheral blood), and allergen levels in dust and air in NAS participants and their wives to address the following hypotheses: that the association of increased airway responsiveness with accelerated longitudinal decline in pulmonary function is modified by gender, smoking, level of FEV1, and skin test reactivity;. that the level of exposure to common indoor allergens affects the rate of longitudinal decline of pulmonary function; that high levels of exposure to common indoor allergens leads to longitudinal increases in airway responsiveness over time; and that settled dust levels of fungi (culturable and countable organisms) and antigens, cockroach (Bla g l, Bla g II\], and cat (Fel d I) are correlated with airborne levels of these agents. The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.
Age
0 - 100 years
Sex
MALE
Healthy Volunteers
No
Start Date
January 1, 1985
Completion Date
March 1, 2002
Last Updated
March 16, 2016
Lead Sponsor
National Heart, Lung, and Blood Institute (NHLBI)
NCT02327897
NCT07219173
NCT07486401
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