Dinh S Bui1, Haydn E Walters1, John A Burgess1, Jennifer L Perret1,2, Minh Q Bui1, Gayan Bowatte1, Adrian J Lowe1, Melissa A Russell1, Bruce R Thompson3,4, Garun S Hamilton5,6, Alan L James7,8, Graham G Giles9, Paul S Thomas10,11, Debbie Jarvis12,13, Cecilie Svanes14,15, Judith Garcia-Aymerich16,17,18, Bircan Erbas19, Peter A Frith20, Katrina J Allen21, Michael J Abramson22, Caroline J Lodge1, Shyamali C Dharmage1. 1. 1 Allergy and Lung Health Unit, University of Melbourne, Melbourne, Victoria, Australia. 2. 2 Institute for Breathing and Sleep, Heidelberg, Victoria, Australia. 3. 3 Allergy, Immunology and Respiratory Medicine, The Alfred Hospital, Melbourne, Victoria, Australia. 4. 4 Central Clinical School, Monash University, Melbourne, Victoria, Australia. 5. 5 Monash Lung and Sleep, Monash Health, Melbourne, Victoria, Australia. 6. 6 School of Clinical Sciences and. 7. 7 Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia. 8. 8 School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australia. 9. 9 Cancer Epidemiology Centre, Cancer Council Victoria, Melbourne, Victoria, Australia. 10. 10 Prince of Wales Clinical School and. 11. 11 School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia. 12. 12 Department of Epidemiology & Biostatistics, MRC-PHE Centre for Environment and Health, School of Public Health, and. 13. 13 Respiratory Epidemiology and Public Health Group, National Heart and Lung Institute, Imperial College London, London, United Kingdom. 14. 14 Centre for International Health, Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. 15. 15 Department of Occupational Medicine, Haukeland University Hospital, Bergen, Norway. 16. 16 ISGlobal, Centre for Research in Environmental Epidemiology, Barcelona, Spain. 17. 17 Universitat Pompeu Fabra, Barcelona, Spain. 18. 18 CIBER Epidemiología y Salud Pública, Barcelona, Spain. 19. 19 School of Psychology and Public Health, La Trobe University, Melbourne, Victoria, Australia. 20. 20 Department of Respiratory Medicine, School of Medicine, Flinders University, Adelaide, South Australia, Australia; and. 21. 21 Murdoch Children's Research Institute, Royal Children's Hospital and University of Melbourne, Melbourne, Victoria, Australia. 22. 22 School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia.
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.
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: Elizabeth C Oelsner; Victor E Ortega; Benjamin M Smith; Jennifer N Nguyen; Ani W Manichaikul; Eric A Hoffman; Xiuqing Guo; Kent D Taylor; Prescott G Woodruff; David J Couper; Nadia N Hansel; Fernando J Martinez; Robert Paine; Meilan K Han; Christopher Cooper; Mark T Dransfield; Gerard Criner; Jerry A Krishnan; Russell Bowler; Eugene R Bleecker; Stephen Peters; Stephen S Rich; Deborah A Meyers; Jerome I Rotter; R Graham Barr Journal: Am J Respir Crit Care Med Date: 2019-09-15 Impact factor: 21.405
Authors: Engi F Attia; Hellen Moraa; Elizabeth Maleche-Obimbo; Dalton Wamalwa; Laurén A Gómez; Sarah Rylance; Rumbidzayi Vundla; Rashida A Ferrand; Catherine J Karr; Grace C John-Stewart; Sarah F Benki-Nugent Journal: J Acquir Immune Defic Syndr Date: 2022-01-01 Impact factor: 3.771