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Original Research: OBSTRUCTIVE LUNG DISEASES |

The Effect of Secondhand Smoke Exposure on Markers of Elastin DegradationSecondhand Smoke Exposure and Elastin Degradation

Natalie Slowik, MD; Shuren Ma, PhD; Jiangtao He, PhD; Yong Y. Lin, PhD; Offie P. Soldin, PhD; Richard A. Robbins, MD, FCCP; Gerard M. Turino, MD
Author and Funding Information

From the Department of Medicine (Drs Slowik, Ma, He, Lin, and Turino), St. Luke’s Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, NY; the Departments of Oncology and Medicine (Dr Soldin), Georgetown University Medical Center, Washington, DC; and the University of Arizona (Dr Robbins), Phoenix, AZ.

Correspondence to: Gerard M. Turino, MD, Department of Medicine, St. Luke’s Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, 1000 Tenth Ave, New York, NY 10019; e-mail: gmt1@columbia.edu


Funding/Support: This work was supported by funds from the James P. Mara Center for Lung Diseases, the Flight Attendant Medical Research Institute, the Charles A. Mastronardi Foundation, the Ned Doyle Foundation, and the Alpha-1 Foundation, and by funds from Ethel Kennedy, John Kennedy, and Judith Sulzberger.

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(4):946-953. doi:10.1378/chest.10-2298
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Background:  Tobacco smoke is a major risk factor in the development of COPD. Secondhand smoke (SHS) exposure is a known risk factor in asthma, bronchitis, and coronary artery disease. Elastin is a recognized target for injury in COPD, and the amino acids desmosine and isodesmosine (D/I), which are specific for elastin degradation, are elevated in COPD. This study determined whether exposure to SHS affects elastin degradation in asymptomatic individuals.

Methods:  Two cohorts of asymptomatic individuals without evidence of respiratory or circulatory disease, exposed to SHS, were studied. Both cohorts comprised normal nonsmokers, active smokers, and those exposed to SHS. D/I were measured in plasma and quantified by high-performance liquid chromatography and tandem mass spectrometry by published methods. Plasma cotinine, a metabolite of nicotine, was also measured.

Results:  In each cohort, the levels of D/I in plasma were statistically significantly higher in secondhand-smoke-exposed subjects than in the normal nonexposed subjects. Smokers had the highest levels of D/I but their levels were not statistically significantly higher than those of the secondhand-smoke-exposed. Cotinine levels were elevated in secondhand-smoke-exposed subjects and active smokers but not in most nonsmoking control subjects.

Conclusions:  Results indicate a tissue matrix effect of degradation of body elastin from SHS exposure and possible lung structure injury, which may result in COPD. Long-term studies of individuals exposed to SHS for the development of COPD are warranted.

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