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Predicting development and progression of COPD
  1. P H Quanjer1,
  2. I Steenbruggen2,
  3. G Ruppel3,
  4. M P Swanney4
  1. 1
    Erasmus University, Rotterdam, The Netherlands
  2. 2
    Isala Klinieken, Zwolle, The Netherlands
  3. 3
    St Louis University Hospital, St Louis, Missouri, USA
  4. 4
    Respiratory Physiology Laboratory, Christchurch Hospital, New Zealand
  1. Dr P H Quanjer, Erasmus University, Rotterdam, The Netherlands; pquanjer{at}

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Albers and colleagues1 recently concluded that “Lung function below the normal range and early respiratory signs predict the development and progression of COPD”. We have some concerns about the data. Table 2 in their article lists 151 subjects without baseline abnormalities. In 5 years, forced expiratory volume in 1 s (FEV1) fell by 200 ml and FEV1%/vital capacity (VC) by 5.2%, remarkably large declines for such subjects. We computed predicted values at ages 43 and 48 years according to 28 authors who had published predicted values for FEV1%/forced vital capacity (FVC) for Caucasians, and 30 who had done so for FEV1.2 The results are shown in table 1; the values reported by Albers and colleagues1 are in the bottom two rows.

Table 1 Mean FEV1%/FVC and FEV1 values from 28 authors and from the study of Albers and colleagues1

The decline in FEV1/FVC during the study period was more than five times the expected average drop; the fall in FEV1 was larger than expected. If the non-smokers declined at an expected rate (135 ml in 5 years) and we attribute the excess decline to smokers, the decline in smokers must have been 340 ml; as a minority of smokers exhibit an accelerated decline in FEV1 leading to COPD,3 a limited number of smokers must have had a decline in FEV1 far in excess of this. In that case, one would expect an increase in the scatter, but the SD of FEV1 did not increase. The decreased scatter in FEV1/VC over the 5 year period suggests that the group became more homogeneous, which makes it unlikely that the excess decline was caused by a subgroup. In any study, the ratio of average FEV1 and average VC is not exactly equal to the average FEV1/VC ratio; however, in 4557 observations from a random sample of a Dutch population, the difference was very small: 0.7623 vs 0.7635. Thus if we reconstruct the VC in the study of Albers and colleagues1 from FEV1 and FEV1/VC, VC at baseline was about 4.18 l, and 5 years later 4.21 l, so there was at best a trivial change.

One wonders whether these unusual findings are caused by problems with data collection which would invalidate the conclusions of this study. The authors state that variation in spirometer performance was assessed and accounted for; this merits a more detailed account. Measurements were performed according to the American Thoracic Society standards,4 but the study started prior to that report; were measurements recalculated?


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  • Competing interests: None declared.

Linked Articles

  • Letters
    M Albers T Schermer Y Heijdra J Molema R Akkermans C van Weel