Exhaled carbon monoxide levels in obstructive sleep apnoea

Adrian Kis, Martina Meszaros, David Laszlo Tarnoki, Adam Domonkos Tarnoki, Zsofia Lazar, P. Horváth, Laszlo Kunos, Andras Bikov

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

BACKGROUND: Obstructive sleep apnoea (OSA) is characterised by chronic intermittent hypoxia, which enhances airway inflammation and oxidative stress. Exhaled carbon monoxide (eCO), a marker for oxidative stress, has been investigated in OSA. However, previous studies could be biased as they did not differentiate patients with OSA based on smoking history, a known factor influencing eCO levels. The aim of this study to investigate eCO levels in patients with OSA and non-OSA controls and compare evening to morning results. METHODS: Exhaled carbon monoxide concentration was measured in the evening and in the morning following an in-hospital cardiorespiratory polygraphy in 60 never-smoker OSA patients, 14 ex-smoker OSA patients, 39 current-smoker OSA patients, 10 never-smoker asthmatic patients with OSA, 16 COPD patients with OSA and 20 never-smoker non-OSA controls. OSA was diagnosed based on the apnoea-hypopnoea index (AHI > 5/h). RESULTS: There was no difference between the never-smoker controls and never-smoker patients with OSA either in the evening (1.98 ± 1.00 ppm versus 1.95 ± 1.28 ppm, p = 0.57, OSA versus controls, respectively) or morning (1.95 ± 0.96 ppm versus 1.80 ± 0.95 ppm, p = 0.42), however there was a weak correlation between eCO and AHI in the evening (r = 0.31, p = 0.01). Accordingly, patients with severe OSA had higher eCO levels in the evening (2.43 ± 1.12 ppm) compared to mild OSA patients (1.57 ± 0.87 ppm, p < 0.01). Ex-smoker (3.07 ± 2.23 ppm), current-smoker (13.13 ± 11.35 ppm), asthmatic (2.70 ± 1.16 ppm) and COPD (18.25 ± 18.60 ppm) patients with OSA had higher levels of eCO compared to the non-smoker OSA group. CONCLUSION: Exhaled carbon monoxide is elevated only in severe never-smoker OSA suggesting accelerated oxidative stress. Previous smoking history is a major influencing factor which may explain differences between our findings and those of previous studies. Although our results show some impact of OSA on eCO measurements, the bias is small, and it does not significantly affect the clinical utility of eCO to monitor smoking cessation.

Original languageEnglish
Number of pages1
JournalJournal of breath research
Volume13
Issue number3
DOIs
Publication statusPublished - Jun 7 2019

Fingerprint

Obstructive Sleep Apnea
Carbon Monoxide
Oxidative Stress
Sleep Apnea Syndromes
Chronic Obstructive Pulmonary Disease
Smoking
History
Apnea
Smoking Cessation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Kis, A., Meszaros, M., Tarnoki, D. L., Tarnoki, A. D., Lazar, Z., Horváth, P., ... Bikov, A. (2019). Exhaled carbon monoxide levels in obstructive sleep apnoea. Journal of breath research, 13(3). https://doi.org/10.1088/1752-7163/ab231d

Exhaled carbon monoxide levels in obstructive sleep apnoea. / Kis, Adrian; Meszaros, Martina; Tarnoki, David Laszlo; Tarnoki, Adam Domonkos; Lazar, Zsofia; Horváth, P.; Kunos, Laszlo; Bikov, Andras.

In: Journal of breath research, Vol. 13, No. 3, 07.06.2019.

Research output: Contribution to journalArticle

Kis, A, Meszaros, M, Tarnoki, DL, Tarnoki, AD, Lazar, Z, Horváth, P, Kunos, L & Bikov, A 2019, 'Exhaled carbon monoxide levels in obstructive sleep apnoea', Journal of breath research, vol. 13, no. 3. https://doi.org/10.1088/1752-7163/ab231d
Kis, Adrian ; Meszaros, Martina ; Tarnoki, David Laszlo ; Tarnoki, Adam Domonkos ; Lazar, Zsofia ; Horváth, P. ; Kunos, Laszlo ; Bikov, Andras. / Exhaled carbon monoxide levels in obstructive sleep apnoea. In: Journal of breath research. 2019 ; Vol. 13, No. 3.
@article{e72e310790d4426aaabd60f7541511be,
title = "Exhaled carbon monoxide levels in obstructive sleep apnoea",
abstract = "BACKGROUND: Obstructive sleep apnoea (OSA) is characterised by chronic intermittent hypoxia, which enhances airway inflammation and oxidative stress. Exhaled carbon monoxide (eCO), a marker for oxidative stress, has been investigated in OSA. However, previous studies could be biased as they did not differentiate patients with OSA based on smoking history, a known factor influencing eCO levels. The aim of this study to investigate eCO levels in patients with OSA and non-OSA controls and compare evening to morning results. METHODS: Exhaled carbon monoxide concentration was measured in the evening and in the morning following an in-hospital cardiorespiratory polygraphy in 60 never-smoker OSA patients, 14 ex-smoker OSA patients, 39 current-smoker OSA patients, 10 never-smoker asthmatic patients with OSA, 16 COPD patients with OSA and 20 never-smoker non-OSA controls. OSA was diagnosed based on the apnoea-hypopnoea index (AHI > 5/h). RESULTS: There was no difference between the never-smoker controls and never-smoker patients with OSA either in the evening (1.98 ± 1.00 ppm versus 1.95 ± 1.28 ppm, p = 0.57, OSA versus controls, respectively) or morning (1.95 ± 0.96 ppm versus 1.80 ± 0.95 ppm, p = 0.42), however there was a weak correlation between eCO and AHI in the evening (r = 0.31, p = 0.01). Accordingly, patients with severe OSA had higher eCO levels in the evening (2.43 ± 1.12 ppm) compared to mild OSA patients (1.57 ± 0.87 ppm, p < 0.01). Ex-smoker (3.07 ± 2.23 ppm), current-smoker (13.13 ± 11.35 ppm), asthmatic (2.70 ± 1.16 ppm) and COPD (18.25 ± 18.60 ppm) patients with OSA had higher levels of eCO compared to the non-smoker OSA group. CONCLUSION: Exhaled carbon monoxide is elevated only in severe never-smoker OSA suggesting accelerated oxidative stress. Previous smoking history is a major influencing factor which may explain differences between our findings and those of previous studies. Although our results show some impact of OSA on eCO measurements, the bias is small, and it does not significantly affect the clinical utility of eCO to monitor smoking cessation.",
author = "Adrian Kis and Martina Meszaros and Tarnoki, {David Laszlo} and Tarnoki, {Adam Domonkos} and Zsofia Lazar and P. Horv{\'a}th and Laszlo Kunos and Andras Bikov",
year = "2019",
month = "6",
day = "7",
doi = "10.1088/1752-7163/ab231d",
language = "English",
volume = "13",
journal = "Journal of Breath Research",
issn = "1752-7155",
publisher = "IOP Publishing Ltd.",
number = "3",

}

TY - JOUR

T1 - Exhaled carbon monoxide levels in obstructive sleep apnoea

AU - Kis, Adrian

AU - Meszaros, Martina

AU - Tarnoki, David Laszlo

AU - Tarnoki, Adam Domonkos

AU - Lazar, Zsofia

AU - Horváth, P.

AU - Kunos, Laszlo

AU - Bikov, Andras

PY - 2019/6/7

Y1 - 2019/6/7

N2 - BACKGROUND: Obstructive sleep apnoea (OSA) is characterised by chronic intermittent hypoxia, which enhances airway inflammation and oxidative stress. Exhaled carbon monoxide (eCO), a marker for oxidative stress, has been investigated in OSA. However, previous studies could be biased as they did not differentiate patients with OSA based on smoking history, a known factor influencing eCO levels. The aim of this study to investigate eCO levels in patients with OSA and non-OSA controls and compare evening to morning results. METHODS: Exhaled carbon monoxide concentration was measured in the evening and in the morning following an in-hospital cardiorespiratory polygraphy in 60 never-smoker OSA patients, 14 ex-smoker OSA patients, 39 current-smoker OSA patients, 10 never-smoker asthmatic patients with OSA, 16 COPD patients with OSA and 20 never-smoker non-OSA controls. OSA was diagnosed based on the apnoea-hypopnoea index (AHI > 5/h). RESULTS: There was no difference between the never-smoker controls and never-smoker patients with OSA either in the evening (1.98 ± 1.00 ppm versus 1.95 ± 1.28 ppm, p = 0.57, OSA versus controls, respectively) or morning (1.95 ± 0.96 ppm versus 1.80 ± 0.95 ppm, p = 0.42), however there was a weak correlation between eCO and AHI in the evening (r = 0.31, p = 0.01). Accordingly, patients with severe OSA had higher eCO levels in the evening (2.43 ± 1.12 ppm) compared to mild OSA patients (1.57 ± 0.87 ppm, p < 0.01). Ex-smoker (3.07 ± 2.23 ppm), current-smoker (13.13 ± 11.35 ppm), asthmatic (2.70 ± 1.16 ppm) and COPD (18.25 ± 18.60 ppm) patients with OSA had higher levels of eCO compared to the non-smoker OSA group. CONCLUSION: Exhaled carbon monoxide is elevated only in severe never-smoker OSA suggesting accelerated oxidative stress. Previous smoking history is a major influencing factor which may explain differences between our findings and those of previous studies. Although our results show some impact of OSA on eCO measurements, the bias is small, and it does not significantly affect the clinical utility of eCO to monitor smoking cessation.

AB - BACKGROUND: Obstructive sleep apnoea (OSA) is characterised by chronic intermittent hypoxia, which enhances airway inflammation and oxidative stress. Exhaled carbon monoxide (eCO), a marker for oxidative stress, has been investigated in OSA. However, previous studies could be biased as they did not differentiate patients with OSA based on smoking history, a known factor influencing eCO levels. The aim of this study to investigate eCO levels in patients with OSA and non-OSA controls and compare evening to morning results. METHODS: Exhaled carbon monoxide concentration was measured in the evening and in the morning following an in-hospital cardiorespiratory polygraphy in 60 never-smoker OSA patients, 14 ex-smoker OSA patients, 39 current-smoker OSA patients, 10 never-smoker asthmatic patients with OSA, 16 COPD patients with OSA and 20 never-smoker non-OSA controls. OSA was diagnosed based on the apnoea-hypopnoea index (AHI > 5/h). RESULTS: There was no difference between the never-smoker controls and never-smoker patients with OSA either in the evening (1.98 ± 1.00 ppm versus 1.95 ± 1.28 ppm, p = 0.57, OSA versus controls, respectively) or morning (1.95 ± 0.96 ppm versus 1.80 ± 0.95 ppm, p = 0.42), however there was a weak correlation between eCO and AHI in the evening (r = 0.31, p = 0.01). Accordingly, patients with severe OSA had higher eCO levels in the evening (2.43 ± 1.12 ppm) compared to mild OSA patients (1.57 ± 0.87 ppm, p < 0.01). Ex-smoker (3.07 ± 2.23 ppm), current-smoker (13.13 ± 11.35 ppm), asthmatic (2.70 ± 1.16 ppm) and COPD (18.25 ± 18.60 ppm) patients with OSA had higher levels of eCO compared to the non-smoker OSA group. CONCLUSION: Exhaled carbon monoxide is elevated only in severe never-smoker OSA suggesting accelerated oxidative stress. Previous smoking history is a major influencing factor which may explain differences between our findings and those of previous studies. Although our results show some impact of OSA on eCO measurements, the bias is small, and it does not significantly affect the clinical utility of eCO to monitor smoking cessation.

UR - http://www.scopus.com/inward/record.url?scp=85067588042&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85067588042&partnerID=8YFLogxK

U2 - 10.1088/1752-7163/ab231d

DO - 10.1088/1752-7163/ab231d

M3 - Article

C2 - 31108481

AN - SCOPUS:85067588042

VL - 13

JO - Journal of Breath Research

JF - Journal of Breath Research

SN - 1752-7155

IS - 3

ER -