Childhood Respiratory Risk Factor Profiles and Middle-Age Lung Function: A Prospective Cohort Study from the First to Sixth Decade
Year: 2018
Type: article
Study design: Observational Study
Abstract: Rationale Childhood risk factors for long-term lung health often coexist and their specific patterns may affect subsequent lung function differently. Objectives To identify childhood risk factor profiles and their influence on lung function and chronic obstructive pulmonary disease (COPD) in middle age, and potential pathways. Methods Profiles of 11 childhood respiratory risk factors, documented at age 7, were identified in 8,352 participants from the Tasmanian Longitudinal Health Study using latent class analysis. We investigated associations between risk profiles and post-bronchodilator lung function and COPD at age 53, mediation by childhood lung function and adult asthma, and interaction with personal smoking. Results Six risk profiles were identified: 1) unexposed or least exposed (49%); 2) parental smoking (21.5%); 3) allergy (10%); 4) frequent asthma, bronchitis (8.7%); 5) infrequent asthma, bronchitis (8.3%); and 6) frequent asthma, bronchitis, allergy (2.6%). Profile 6 was most strongly associated with lower forced expiratory volume in 1 second (FEV1) (−261; 95% confidence interval, −373 to −148 ml); lower FEV1/forced vital capacity (FVC) (−3.4; −4.8 to −1.9%) and increased COPD risk (odds ratio, 4.9; 2.1 to 11.0) at age 53. The effect of profile 6 on COPD was largely mediated by adult active asthma (62.5%) and reduced childhood lung function (26.5%). Profiles 2 and 4 had smaller adverse effects than profile 6. Notably, the effects of profiles 2 and 6 were synergistically stronger for smokers. Conclusions Profiles of childhood respiratory risk factors predict middle-age lung function levels and COPD risk. Specifically, children with frequent asthma attacks and allergies, especially if they also become adult smokers, are the most vulnerable group. Targeting active asthma in adulthood (i.e., a dominant mediator) and smoking (i.e., an effect modifier) may block causal pathways and lessen the effect of such established early-life exposures.
Authors: Dinh S. Bui, Haydn E. Walters, John A. Burgess, Jennifer L. Perret, Minh Q. Bui, Gayan Bowatte, Adrian J. Lowe, Melissa A. Russell, Bruce R. Thompson, Garun S. Hamilton, Alan L. James, Graham G. Giles, Paul S. Thomas, Debbie Jarvis, Cecilie Svanes, Judith Garcia-Aymerich, Bircan Erbas, Peter A. Frith, Katrina J. Allen, Michael J. Abramson, Caroline J. Lodge, Shyamali C. Dharmage
Institutions: The University of Melbourne, Institute for Breathing and Sleep, The Alfred Hospital, Monash University, Monash Health, The University of Western Australia, Sir Charles Gairdner Hospital, Cancer Council Victoria, UNSW Sydney, Public Health England, MRC Centre for Environment and Health, Imperial College London, Haukeland University Hospital, University of Bergen, Universitat Pompeu Fabra, Center for Research in Environmental Epidemiology, Centro de Investigación Biomédica en Red, Barcelona Institute for Global Health, Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública, La Trobe University, Flinders University, Royal Children's Hospital, Murdoch Children's Research Institute
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2807870020