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Pulmonary functional parameters and blood cotinine level in chronic obstructive pulmonary disease
Hatice Kozluca1, Emrah Dural2, Gülseren Karabıyıkoğlu1
1Department of Chest Diseases, Faculty of Medicine, Ankara University, Ankara, Turkey.
Tuberkuloz Ve Toraks
|January 27, 2019
Summary
Cotinine reliably indicates tobacco exposure, showing a negative correlation with peripheral airway function (FEF25-75%) in smokers, potentially reflecting early COPD effects. This study confirms cotinine
Area of Science:
- Pulmonary Medicine
- Clinical Chemistry
- Toxicology
Background:
- Smoking is the primary cause of Chronic Obstructive Pulmonary Disease (COPD).
- Cotinine is a validated biomarker for assessing tobacco exposure.
- Understanding the link between smoking biomarkers and lung function is crucial for COPD management.
Purpose of the Study:
- To investigate the correlation between pulmonary function tests (PFTs) and blood cotinine levels.
- To assess cotinine as a marker of tobacco exposure in COPD patients and healthy controls.
- To explore the relationship between smoking history, cotinine levels, and lung function parameters.
Main Methods:
- Included 102 COPD patients and 106 healthy volunteers.
- Performed spirometry to assess pulmonary function (FVC%, FEV1, FEV1/FVC, FEF25-75%).
- Quantified blood cotinine levels using gas chromatography-mass spectrometry (GC-MS).
Main Results:
- Established a cotinine cut-off value of 41.12 ng/mL for tobacco exposure (97.2% sensitivity, 100% specificity).
- Found a significant correlation between smoking pack-years and cotinine levels in current smokers (p<0.05).
- Observed a negative correlation between FEF25-75% and cotinine in healthy smokers (p<0.05, r=-0.372), suggesting early peripheral airway changes.
Conclusions:
- Cotinine is a reliable biomarker for quantifying tobacco exposure.
- The negative correlation between FEF25-75% and cotinine suggests smoking impacts peripheral airways early in COPD development.
- Further research can elucidate the early mechanisms of smoking-induced lung damage.
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