Dinh S Bui1,2, Jennifer L Perret1,3, E Haydn Walters1, Michael J Abramson4, John A Burgess1, Minh Q Bui1, Gayan Bowatte1, Adrian J Lowe1, Melissa A Russell1, Sheikh M Alif4, Bruce R Thompson5,6, Garun S Hamilton7,8, Graham G Giles9,10, Paul S Thomas11, Stephen Morrison12, David P Johns13, Luke D Knibbs14, Jan-Paul Zock15,16,17, Alessandro Marcon18, Judith Garcia-Aymerich15,16,17, Bircan Erbas19, Deborah Jarvis20,21, Cecilie Svanes22,23, Caroline J Lodge1, Shyamali C Dharmage1. 1. Allergy and Lung Health Unit, The University of Melbourne, Melbourne, Victoria, Australia. 2. Department of Analytical Chemistry and Toxicology, Hanoi University of Pharmacy, Hanoi, Vietnam. 3. Institute for Breathing and Sleep, Heidelberg, Melbourne, Victoria, Australia. 4. School of Public Health and Preventive Medicine. 5. Central Clinical School. 6. Allergy, Immunology, and Respiratory Medicine, The Alfred Hospital, Melbourne, Victoria, Australia. 7. School of Clinical Sciences, and. 8. Monash Lung and Sleep, Monash Health, Melbourne, Victoria, Australia. 9. Precision Medicine, School of Clinical Sciences at Monash Health, Medicine, Nursing and Health Sciences, Monash University, Melbourne, Victoria, Australia. 10. Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia. 11. Prince of Wales Hospital Clinical School and School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia. 12. University of Queensland, Brisbane, Queensland, Australia. 13. Department of Respiratory Medicine, School of Medicine, Flinders University, Adelaide, South Australia, Australia. 14. School of Public Health, the University of Queensland, Brisbane, Queensland, Australia. 15. ISGlobal, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain. 16. Universitat Pompeu Fabra (UPF), Barcelona, Spain. 17. CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain. 18. Unit of Epidemiology and Medical Statistics, Department of Diagnostics and Public Health, University of Verona, Verona, Italy. 19. School of Psychology and Public Health, La Trobe University, Melbourne, Victoria, Australia. 20. Department of Epidemiology and Biostatistics, MRC-PHE Centre for Environment and Health, School of Public Health and. 21. Respiratory Epidemiology and Public Health Group, National Heart and Lung Institute, Imperial College London, London, United Kingdom. 22. Centre for International Health, Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway; and. 23. Department of Occupational Medicine, Haukeland University Hospital, Bergen, Norway.
Abstract
Rationale: Interactions between early life and adult insults on lung function decline are not well understood, with most studies investigating prebronchodilator (pre-BD) FEV1 decline. Objectives: To investigate relationships between adult risk factors and pre- and post-BD lung function decline and their potential effect modification by early life and genetic factors. Methods: Multiple regression was used to examine associations between adult exposures (asthma, smoking, occupational exposures, traffic pollution, and obesity) and decline in both pre- and post-BD spirometry (forced expiratory volume in 1 s [FEV1], forced vital capacity [FVC], and FEV1/FVC) between ages 45 and 53 years in the Tasmanian Longitudinal Health Study (n = 857). Effect modification of these relationships by childhood respiratory risk factors, including low childhood lung function and GST (glutathione S-transferase) gene polymorphisms, was investigated. Results: Baseline asthma, smoking, occupational exposure to vapors/gases/dusts/fumes, and living close to traffic were associated with accelerated decline in both pre- and post-BD FEV1. These factors were also associated with FEV1/FVC decline. Occupational exposure to aromatic solvents was associated with pre-BD but not post-BD FEV1 decline. Maternal smoking accentuated the effect of personal smoking on pre- and post-BD FEV1 decline. Lower childhood lung function and having the GSTM1 null allele accentuated the effect of occupational exposure to vapors/gases/dusts/fumes and personal smoking on post-BD FEV1 decline. Incident obesity was associated with accelerated decline in FEV1 and more pronounced in FVC.Conclusions: This study provides new evidence for accentuation of individual susceptibility to adult risk factors by low childhood lung function, GSTM1 genotype, and maternal smoking.
Rationale: Interactions between early life and adult insults on lung function decline are not well understood, with most studies investigating prebronchodilator (pre-BD) FEV1 decline. Objectives: To investigate relationships between adult risk factors and pre- and post-BD lung function decline and their potential effect modification by early life and genetic factors. Methods: Multiple regression was used to examine associations between adult exposures (asthma, smoking, occupational exposures, traffic pollution, and obesity) and decline in both pre- and post-BD spirometry (forced expiratory volume in 1 s [FEV1], forced vital capacity [FVC], and FEV1/FVC) between ages 45 and 53 years in the Tasmanian Longitudinal Health Study (n = 857). Effect modification of these relationships by childhood respiratory risk factors, including low childhood lung function and GST (glutathione S-transferase) gene polymorphisms, was investigated. Results: Baseline asthma, smoking, occupational exposure to vapors/gases/dusts/fumes, and living close to traffic were associated with accelerated decline in both pre- and post-BD FEV1. These factors were also associated with FEV1/FVC decline. Occupational exposure to aromatic solvents was associated with pre-BD but not post-BD FEV1 decline. Maternal smoking accentuated the effect of personal smoking on pre- and post-BD FEV1 decline. Lower childhood lung function and having the GSTM1 null allele accentuated the effect of occupational exposure to vapors/gases/dusts/fumes and personal smoking on post-BD FEV1 decline. Incident obesity was associated with accelerated decline in FEV1 and more pronounced in FVC.Conclusions: This study provides new evidence for accentuation of individual susceptibility to adult risk factors by low childhood lung function, GSTM1 genotype, and maternal smoking.
Authors: Andrew J Halayko; Christopher D Pascoe; Jessica D Gereige; Michael C Peters; Robyn T Cohen; Prescott G Woodruff Journal: Am J Respir Crit Care Med Date: 2021-08-15 Impact factor: 21.405
Authors: Andy I Ritchie; Jonathon R Baker; Trisha M Parekh; James P Allinson; Surya P Bhatt; Louise E Donnelly; Gavin C Donaldson Journal: Am J Respir Crit Care Med Date: 2021-07-01 Impact factor: 21.405
Authors: James G Krings; Charles W Goss; Daphne Lew; Maanasi Samant; Mary Clare McGregor; Jonathan Boomer; Leonard B Bacharier; Ajay Sheshadri; Chase Hall; Joshua Brownell; Ken B Schechtman; Samuel Peterson; Stephen McEleney; David T Mauger; John V Fahy; Sean B Fain; Loren C Denlinger; Elliot Israel; George Washko; Eric Hoffman; Sally E Wenzel; Mario Castro Journal: J Allergy Clin Immunol Date: 2021-02-09 Impact factor: 14.290