Early life origins of chronic obstructive pulmonary disease
- C Svanes1,2,
- J Sunyer2,3,
- E Plana2,
- S Dharmage4,
- J Heinrich5,
- D Jarvis6,
- R de Marco7,
- D Norbäck8,
- C Raherison9,
- S Villani10,
- M Wjst5,
- K Svanes11,
- J M Antó2,3
- 1Section of Thoracic Medicine, Institute of Medicine, University of Bergen, Norway
- 2Centre Recerca Epidemiologia Ambiental (CREAL-IMIM), Barcelona, Spain
- 3Universitat Pompeu Fabra, Barcelona, Spain
- 4Centre for MEGA Epidemiology, School of Population Health, The University of Melbourne, Australia
- 5Helmholtz Zentrum Munchen, National Research Center for Environmental Health, Institute of Epidemiology, Germany
- 6Department of Public Health Sciences, Imperial College, London, UK
- 7Department of Medicine and Public Health/Epidemiology and Medical Statistics, University of Verona, Italy
- 8Department of Medical Science/Occupational and Environmental Medicine, Uppsala University, Sweden
- 9INSERM U700 – Epidémiologie, Faculté de Médecine Xavier Bichat, Paris, France
- 10Department of Health Sciences, Section of Medical Statistics of Epidemiology, University of Pavia, Italy
- 11Institute of Surgery, University of Bergen, Norway
- Correspondence to Dr C Svanes, Department of Occupational Medicine, 5021 Haukeland University Hospital, Norway;
- Received 3 January 2009
- Accepted 4 August 2009
- Published Online First 2 September 2009
Background: Early life development may influence subsequent respiratory morbidity. The impact of factors determined in childhood on adult lung function, decline in lung function and chronic obstructive pulmonary disease (COPD) was investigated.
Methods: European Community Respiratory Health Survey participants aged 20–45 years randomly selected from general populations in 29 centres underwent spirometry in 1991–3 (n = 13 359) and 9 years later (n = 7738). Associations of early life factors with adult forced expiratory volume in 1 s (FEV1), FEV1 decline and COPD (FEV1/FVC ratio <70% and FEV1 <80% predicted) were analysed with generalised estimating equation models and random effects linear models.
Results: Maternal asthma, paternal asthma, childhood asthma, maternal smoking and childhood respiratory infections were significantly associated with lower FEV1 and defined as “childhood disadvantage factors”; 40% had one or more childhood disadvantage factors which were associated with lower FEV1 (men: adjusted difference 95 ml (95% CI 67 to 124); women: adjusted difference 60 ml (95% CI 40 to 80)). FEV1 decreased with increasing number of childhood disadvantage factors (⩾3 factors, men: 274 ml (95% CI 154 to 395), women: 208 ml (95% CI 124 to 292)). Childhood disadvantage was associated with a larger FEV1 decline (1 factor: 2.0 ml (95% CI 0.4 to 3.6) per year; 2 factors: 3.8 ml (95% CI 1.0 to 6.6); ⩾3 factors: 2.2 ml (95% CI −4.8 to 9.2)). COPD increased with increasing childhood disadvantage (1 factor, men: OR 1.7 (95% CI 1.1 to 2.6), women: OR 1.6 (95% CI 1.01 to 2.6); ⩾3 factors, men: OR 6.3 (95% CI 2.4 to 17), women: OR 7.2 (95% CI 2.8 to 19)). These findings were consistent between centres and when subjects with asthma were excluded.
Conclusions: People with early life disadvantage have permanently lower lung function, no catch-up with age but a slightly larger decline in lung function and a substantially increased COPD risk. The impact of childhood disadvantage was as large as that of heavy smoking. Increased focus on the early life environment may contribute to the prevention of COPD.
See Editorial, p 1
▸ Additional information is published online only at http://thorax.bmj.com/content/vol65/issue1
Funding A list of investigators and funding sources is given in the online supplement.
Competing interests None.
Provenance and Peer review Not commissioned; externally peer reviewed.
Ethics approval Ethical approval was obtained for each centre from the appropriate institutional or regional ethics committee and written informed consent was obtained from each participant.