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Secondhand Smoke Exposure Effect on Elastin Degradation MarkersPassive Smoking Effect on Elastin Degradation: Which Factors Should Be Taken Into Account? FREE TO VIEW

Michiel Spanbroek, MD; Rob Janssen, MD, PhD; Richard Dekhuijzen, MD, PhD
Author and Funding Information

From the Department of Pulmonary Diseases (Drs Spanbroek and Janssen), Canisius-Wilhelmina Ziekenhuis; and the Department of Pulmonary Diseases (Dr Dekhuijzen), Radboud University Nijmegen Medical Centre.

Correspondence to: Michiel Spanbroek, MD, Canisius Wilhelmina Ziekenhuis, Longziekten en Tuberculose, B01, Weg door Jonkerbos 100, Nijmegen, 6532 SZ, The Netherlands; e-mail: m.spanbroek@cwz.nl


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Drs Spanbroek and Janssen received a 3-yr grant from GlaxoSmithKline to set up a reliable method for the measurement of elastine waste products in order to perform research in the field of COPD. Dr Dekhuijzen has reported 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).


© 2012 American College of Chest Physicians


Chest. 2012;141(4):1119-1120. doi:10.1378/chest.11-2396
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To the Editor:

In a recent article in CHEST (October 2011) Slowik et al1 described the effect of secondhand smoking on elastine breakdown products, desmosine and isodesmosine (D/I). The authors concluded that exposure to secondhand smoke causes a significant rise in plasma D/I and, therefore, may be as dangerous and harmful as active smoking on tissue matrix and lung parenchyma.

We applaud the authors’ attempt to show that passive smoking is indeed harmful. Nevertheless, we have a few comments on the study design.

First, it is unclear why the authors chose to examine two cohorts. The composition between the two cohorts differed greatly. The first cohort, which included a group of nonsmokers, passive smokers, and smokers, consisted of women with the average age ≈30 years. The second cohort, again including a group of nonsmokers, passive smokers, and smokers, consisted of both men and women with average ages of 35, 41, and 57 years, respectively. The question arises as to whether the observed difference between the cohorts (in passive smokers and smokers) is confounded by age and sex differences. Stone et al2 previously described a positive correlation between age and D/I excretion. To our best knowledge, there is no difference between men and women in this regard, although studies to date were conducted with small numbers of individuals and thus perhaps were underpowered.

Second, it is unknown which test subjects were former smokers. Previous investigations show that former smokers with COPD continue to have high D/I content.2,3 It is speculative whether the same effect can be found in former smokers without COPD. In this study, it is not clear whether the former smokers are included, nor is it clear whether smokers, including any former smokers, received pulmonary function testing in order to rule out COPD.

Finally, the high pressure liquid chromatography-mass spectrometry/mass spectrometry method is reliable, provided the use of an internal standard (such as deuterized desmosine)4 is used. Slowik et al1 chose not to use an internal (deuterized) standard but instead used the average of two measurements. In doing so, the internal validation and the results may have been compromised.

D/I remains an interesting marker for the evaluation of elastine breakdown.5 However, its role remains small in contemporary literature. More research must follow if the use of D/I is to gather significance. A validated method, with an internal standard, for the measurement of D/I remains a mandate.

Slowik N, Ma S, He J, et al. The effect of secondhand smoke exposure on markers of elastin degradation. Chest. 2011;1404:946-953 [CrossRef] [PubMed]
 
Stone PJ, Gottlieb DJ, O’Connor GT, et al. Elastin and collagen degradation products in urine of smokers with and without chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1995;1514:952-959 [PubMed]
 
Cocci F, Miniati M, Monti S, et al. Urinary desmosine excretion is inversely correlated with the extent of emphysema in patients with chronic obstructive pulmonary disease. Int J Biochem Cell Biol. 2002;346:594-604 [CrossRef] [PubMed]
 
Albarbarawi O, Barton A, Lin Z, et al. Measurement of urinary total desmosine and isodesmosine using isotope-dilution liquid chromatography-tandem mass spectrometry. Anal Chem. 2010;829:3745-3750 [CrossRef] [PubMed]
 
Luisetti M, Ma S, Iadarola P, et al. Desmosine as a biomarker of elastin degradation in COPD: current status and future directions. Eur Respir J. 2008;325:1146-1157 [CrossRef] [PubMed]
 

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References

Slowik N, Ma S, He J, et al. The effect of secondhand smoke exposure on markers of elastin degradation. Chest. 2011;1404:946-953 [CrossRef] [PubMed]
 
Stone PJ, Gottlieb DJ, O’Connor GT, et al. Elastin and collagen degradation products in urine of smokers with and without chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1995;1514:952-959 [PubMed]
 
Cocci F, Miniati M, Monti S, et al. Urinary desmosine excretion is inversely correlated with the extent of emphysema in patients with chronic obstructive pulmonary disease. Int J Biochem Cell Biol. 2002;346:594-604 [CrossRef] [PubMed]
 
Albarbarawi O, Barton A, Lin Z, et al. Measurement of urinary total desmosine and isodesmosine using isotope-dilution liquid chromatography-tandem mass spectrometry. Anal Chem. 2010;829:3745-3750 [CrossRef] [PubMed]
 
Luisetti M, Ma S, Iadarola P, et al. Desmosine as a biomarker of elastin degradation in COPD: current status and future directions. Eur Respir J. 2008;325:1146-1157 [CrossRef] [PubMed]
 
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