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Maarten van den Berge, MD, PhD; Nick H. T. ten Hacken, MD, PhD; Judith Cohen, MD, PhD; W. Rob Douma, MD, PhD; Dirkje S. Postma, MD, PhD
Author and Funding Information

From the Department of Pulmonology, University Medical Center Groningen, University of Groningen.

Correspondence to: Dirkje S. Postma, MD, PhD, Department of Pulmonology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands; e-mail: d.s.postma@long.umcg.nl


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr van den Berge has received a research grant from GlaxoSmithKline. Dr Postma has received grants from AstraZeneca, GlaxoSmithKline, and Nycomed for research and has been a consultant to AstraZeneca, GlaxoSmithKline, Nycomed, and TEVA. Drs ten Hacken, Cohen, and Douma have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(2):562. doi:10.1378/chest.11-0858
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To the Editor:

We have read with great interest the comments of Drs Siafakas and Tzortzaki regarding our article on small airway disease in asthma and COPD.1 They suggest excluding the term “abnormal inflammatory response to cigarette smoke” from the definition currently used for COPD.

Although smoking is the most important risk factor for COPD, only approximately 20% to 30% of smokers will ultimately develop COPD.2 A key unanswered question is why smoking causes irreversible and progressive obstructive changes in these susceptible subjects and how they differ in their response to smoking from nonsusceptible subjects.

To clarify the abnormal response to smoking in susceptible individuals, several possible mechanisms have been put forward with respect to airway inflammation, oxidative stress, protease-antiprotease imbalance, tissue injury, and repair and remodeling.3 Thus far in research, patients with established COPD have been compared with control subjects without COPD. Therefore, any observed difference between these groups will as likely reflect a cause as a consequence of COPD. For this reason, it is presently unknown whether susceptible smokers exhibit a different or abnormal inflammatory response when compared with nonsusceptible smokers who will not develop COPD over time.

In this context, the findings of Silverman et al4 are of interest. They demonstrated that susceptible subjects can be identified based on family history. When first-degree relatives of patients with severe early-onset COPD (defined by lung function, ie, FEV1 <40% predicted and age <53 years) smoked, their FEV1 was significantly lower than in subjects who smoked and were not first-degree relatives.4

A study is now needed that investigates if there are differences in the response to smoking between young healthy subjects who are susceptible according to the criteria of Silverman et al4 and young healthy subjects who are nonsusceptible. Such a study will certainly generate highly valuable new insights in the mechanisms that contribute to COPD pathogenesis. Only then can we decide to definitively exclude the possibility that a different or abnormal response to cigarette smoking contributes to the development of COPD.

van den Berge M, ten Hacken NHT, Cohen J, Douma WR, Postma DS. Small airway disease in asthma and COPD: clinical implications. Chest. 2011;1392:412-423. [CrossRef] [PubMed]
 
Eisner MD, Balmes J, Katz PP, Trupin L, Yelin EH, Blanc PD. Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease. Environ Health. 2005;41:7. [CrossRef] [PubMed]
 
van der Vaart H, Postma DS, Timens W, ten Hacken NH. Acute effects of cigarette smoke on inflammation and oxidative stress: a review. Thorax. 2004;598:713-721. [CrossRef] [PubMed]
 
Silverman EK, Chapman HA, Drazen JM, et al. Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis. Am J Respir Crit Care Med. 1998;1576 pt 1:1770-1778. [PubMed]
 

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van den Berge M, ten Hacken NHT, Cohen J, Douma WR, Postma DS. Small airway disease in asthma and COPD: clinical implications. Chest. 2011;1392:412-423. [CrossRef] [PubMed]
 
Eisner MD, Balmes J, Katz PP, Trupin L, Yelin EH, Blanc PD. Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease. Environ Health. 2005;41:7. [CrossRef] [PubMed]
 
van der Vaart H, Postma DS, Timens W, ten Hacken NH. Acute effects of cigarette smoke on inflammation and oxidative stress: a review. Thorax. 2004;598:713-721. [CrossRef] [PubMed]
 
Silverman EK, Chapman HA, Drazen JM, et al. Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis. Am J Respir Crit Care Med. 1998;1576 pt 1:1770-1778. [PubMed]
 
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