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Early life origins of chronic obstructive pulmonary disease
  1. Cecilie Svanes (cecilie.svanes{at}
  1. Haukeland Hospital, Norway
    1. Jordi Sunyer (jsunyer{at}
    1. CREAL, Spain
      1. Estel Plana (eplana{at}
      1. CREAL, Spain
        1. Shyamali Dharmage
        1. University of Melbourne, Australia
          1. Joachim Heinrich
          1. GSF-Neuherberg, Germany
            1. Debbie Jarvis (d.jarvis{at}
            1. Imperial College, United Kingdom
              1. Roberto deMarco
              1. University of Verona, Italy
                1. Dan Norback
                1. University of Uppsala, Sweden
                  1. Chantal Raherison
                  1. INSERM, France
                    1. Simona Villani
                    1. University of Pavia, Italy
                      1. Matthias Wjst
                      1. GSF-Neuherberg, Germany
                        1. Knut Svanes
                        1. University of Bergen, Norway
                          1. Josep Anto
                          1. CREAL, Spain


                            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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