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Early life origins of chronic obstructive pulmonary disease
  1. Cecilie Svanes1,*,
  2. Jordi Sunyer2,
  3. Estel Plana2,
  4. Shyamali Dharmage3,
  5. Joachim Heinrich4,
  6. Debbie Jarvis5,
  7. Roberto deMarco6,
  8. Dan Norback7,
  9. Chantal Raherison8,
  10. Simona Villani9,
  11. Matthias Wjst4,
  12. Knut Svanes10,
  13. Josep Anto2
  1. 1 Haukeland Hospital, Norway;
  2. 2 CREAL, Spain;
  3. 3 University of Melbourne, Spain;
  4. 4 Helmholtz Zentrum Munchen, Australia;
  5. 5 Imperial College, Germany;
  6. 6 University of Verona, United Kingdom;
  7. 7 University of Uppsala, Italy;
  8. 8 INSERM, Sweden;
  9. 9 University of Pavia, France;
  10. 10 University of Bergen, Italy
  1. Correspondence to: cecilie svanes, Thoracic Medicine, Haukeland Hospital, Thoracic Medicine, Outpatient Clinic, 5021 Haukeland Hospital, /Bergen, 5021, Norway; cecilie.svanes{at}med.uib.no

Abstract

Background: Early life development may influence subsequent respiratory morbidity. We addressed the impact of factors determined in childhood on adult lung function, lung function decline and chronic obstructive pulmonary disease (COPD).

Methods: European Community Respiratory Health Survey participants aged 20-45 years, randomly selected from general populations in 29 centres, had a spirometry in 1991-93 (n=13,359) and nine years later (n=7,738). Associations of early life factors with adult FEV1, FEV1 decline and COPD (FEV1/FVC ratio<70% and FEV1<80% predicted) were analysed with Generalized 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 "childhood disadvantage". Forty percent had one or more childhood disadvantage factor, which was associated with lower FEV1 (men: adjusted difference 95ml[95%CI=67-124]; women (60ml[40-80]). FEV1 decreased with increasing childhood disadvantage (≥3 factors men: 274ml[154-395], women: 208ml[124-292]. Childhood disadvantage was associated with larger FEV1 decline (one factor 2.0ml [0.4-3.6] per year; two factors 3.8ml [1.0-6.6]; ≥3 factors 2.2ml[-4.8-9.2]). COPD increased with increasing childhood disadvantage (one factor men: OR=1.7[95%CI=1.1-2.6], women: 1.6[1.01-2.6]; ≥3 factors: men: 6.3[2.4-17], women: 7.2[2.8-19]). These findings were consistent between centres, and when excluding subjects with asthma.

Conclusions: People with early life disadvantage had permanently lower lung function, no catch-up with age but slightly larger lung function decline, and substantially increased COPD risk. The impact of childhood disadvantage was as large as that of heavy smoking. Increased focus on early life environment may contribute to prevent COPD.

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