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  1. Jian-Qing He1,
  2. Loubna Akhabir1,
  3. Don D Sin1,
  4. S F Paul Man1,
  5. Peter D Paré1,
  6. Andrew J Sandford1,
  7. Marilyn G Foreman2,3,
  8. Dawn L DeMeo2,3,
  9. Edwin K Silverman2,3
  1. 1The UBC James Hogg Research Center, St Paul's Hospital, University of British, Columbia, Vancouver, BC, Canada
  2. 2Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
  3. 3Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
  1. Correspondence to Jian-Qing He, UBC James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of BC, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada; jhe{at}

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van den Borst and colleagues present interesting data regarding the role of the interleukin 6 (IL6)-74G/C promoter polymorphism (rs1800795) in determining the level of lung function.1 We have shown that the C allele of the -174 polymorphism was associated with more rapid decline of lung function in the Lung Health Study (LHS) and with chronic obstructive pulmonary disease in the National Emphysema Treatment Trial (NETT).2 However, there was no association of this polymorphism with baseline lung function in the LHS, and we hypothesised that this may have been due to the younger age of the participants of the LHS compared with the NETT group. Specifically, the baseline lung function in the LHS participants may have been strongly influenced by the maximal attained lung function, whereas lung function in the NETT group (on average two decades older) may be more reflective of the rate of decline of lung function. In this model, the -174G/C polymorphism primarily affects the rate of decline of lung function in response to cigarette smoke and not the maximal level attained during development.

The data from van den Borst et al show an association of the -174C allele with lower forced vital capacity in young adults who were on average 23 years younger than the LHS cohort which we studied. Thus, their results are more reflective of the effect of this polymorphism during lung development than ours, and this may partly explain the differences in results with regard to baseline lung function values. However, we agree with van den Borst and colleagues that further studies are warranted to clarify the mechanism underlying these observations.


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