Martino, David J.Bui, Dinh S.Li, ShuaiIdrose, SabrinaPerret, JenniferLowe, Adrian J.Lodge, Caroline J.Bowatte, GayanMoodley, YubenThomas, Paul S.Zosky, GraemeHansbro, Philip M.Holloway, John W.Svanes, CecilieFaner, RosaWalters, Eugene H.Dharmage, Shyamali C.2024-02-272024-02-272023-11-151073-449Xhttps://hdl.handle.net/2445/208126Understanding the molecular mechanisms of lung function trajectories that progress to chronic obstructive pulmonary disease (COPD) (pre-COPD trajectories), especially those with a rapidly declining phenotype, should inform preventive interventions. The Tasmanian Longitudinal Health Study (TAHS) previously defined life-course lung function trajectories by serial spirometry in a cohort of all seven-year-old school children in the state of Tasmania recruited in 1968 and followed up to age 53 years (1). Of the six pre-bronchodilator FEV1 lifetime trajectories identified, three collectively accounted for 75% of chronic obstructive pulmonary disease (COPD) prevalence at age 53 years (2). These high-risk trajectories were: 1) early below average lung function (with usual rate of subsequent decline), 2) persistently low, and 3) early below average lung function with accelerated decline. The TAHS cohort provides a unique opportunity to investigate molecular factors associated with disadvantaged trajectories, and we conducted a pilot study in this cohort to characterize associations with COPD high-risk trajectories to inform more extensive longitudinal studies in the future.12 p.application/pdfeng(c) American Thoracic Society, 2023Malalties del pulmóGenèticaEpigènesiPulmonary diseasesGeneticsEpigenesisinfo:eu-repo/semantics/article7444512024-02-27info:eu-repo/semantics/openAccess9380576