The population under study is the cohort from Tucson Children's Respiratory Study (CRS), which began in 1980.
The longitudinal study follows a birth cohort of children, initially established in the 1980s. The study period took the children through their 16th birthday, when a comprehensive respiratory and allergy assessment was conducted. This extended follow-up took the cohort from birth to an age at which lung growth is virtually complete for girls and ending its most rapid phase for boys.
The resulting data set was used to test diverse hypotheses concerned with lower respiratory tract illnesses (LRI), asthma, wheezing, allergy, and smoking. There were four broad areas: 1) effects of LRI during the first three years of life and early and late symptoms and allergic sensitization on the picture of asthma; 2) changes during adolescence in symptoms and airways responsiveness; 3) the natural history of allergic sensitization and its relation to asthma and asthma-like symptoms; and 4) the change in longitudinal lung function and factors affecting the change.
A well documented data set was available to test these hypotheses. LRI were documented during the first three years of life, atopy was evaluated, symptom status tracked, and lung function periodically measured. Infant lung function was assessed for a sample of the children and methacholine challenge was performed at age 11. In the evaluation at age 16 years, symptoms, lung function, including methacholine responsiveness, and atopy and lymphocyte phenotype were assessed. Various methods for longitudinal data analysis were used.
The study was renewed in 2001 to follow the birth cohort into early adulthood in order to generate data on the mechanisms and risk factors associated with asthma in early adult life. Specifically the study will: 1) identify factors that alter persistence and remission of asthma symptoms among young adults who developed asthma in childhood; 2) assess the role of persistent eosinophilia during childhood as a mechanism which determines progression and incidence of asthma in early adult life, and prevalence of persistent bronchial hyperresponsiveness (BHR); 3) measure noninvasive markers of airway inflammation in early adult life, and identify correlates of these markers, both with childhood and current asthma symptoms, BHR and immune system indicators of allergy; 4) predict early (by age 20 ) decline in lung function with reference to childhood lower respiratory tract illnesses, asthma-like symptoms, and the initiation of smoking; and 5) investigate the role of gender in incidence of and risk factors for asthma during adolescence and young adult life.