Correlation of exhaled carbon monoxide level with disease severity in chronic obstruction pulmonary disease

Ejazi, Arshad; Shameem, Mohammad; Bhargava, Rakesh; Ahmad, Zuber; Akhtar, Jamal; Khan, Nafeees A; Alam, M S; Alam, Arif; Wafi, C G Adil

doi:10.4103/lungindia.lungindia_11_18

Cited by 7 publications

(12 citation statements)

References 43 publications

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“…The difference between the exhaled CO level of non-smokers and current smokers was statistically significant (Studen's t-test; P˂0.0001). The values found in our study were comparable to the data recorded for healthy adult non-smokers (1.5 ± 0.6 ppm) and healthy adult smokers (9.7 ± 5.7 ppm) in a recent independent study using the same type of CO monitor [69].…”

Section: Exhaled Carbon Monoxide In Healthy Smokers and Non-smokerssupporting

confidence: 91%

A case study of salivary microbiome in smokers and non-smokers in Hungary: analysis by shotgun metagenome sequencing

Wirth

Maróti

Mihók

et al. 2020

Journal of Oral Microbiology

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Objective: To investigate the role of cigarette smoking in disease-development through altering the composition of the oral microbial community. Periodontitis and oral cancer are highly prevalent in Hungary; therefore, the salivary microbiome of smoker and non-smoker Hungarian adults was characterized. Methods: Shotgun metagenome sequencing of salivary DNA samples from 22 individuals (11 non-smokers and 11 current smokers) was performed using the Ion Torrent PGM TM platform. Quality-filtered reads were analysed by both alignment-based sequence similarity searches and genome-centric binning. Results: Prevotella, Veillonella and Streptococcus were the predominant genera in the saliva of both groups. Although the overall composition and diversity of the microbiota were similar, Prevotella was significantly more abundant in salivary samples of current smokers compared to non-smokers. Members of the genus Prevotella were implicated in the development of inflammatory diseases and oral cancer. The abundance of the genus Megasphaera also increased in current smokers, whereas the genera Neisseria, Oribacterium, Capnocytophaga and Porphyromonas were significantly reduced. The data generated by read-based taxonomic classification and genome-centric binning mutually validated the two distinct metagenomic approaches. Conclusion: Smoking-associated dysbiosis of the salivary microbiome in current cigarette smokers, especially increased abundance of Prevotella and Megasphaera genera, may facilitate disease development.

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Section: Exhaled Carbon Monoxide In Healthy Smokers and Non-smokerssupporting

confidence: 91%

A case study of salivary microbiome in smokers and non-smokers in Hungary: analysis by shotgun metagenome sequencing

Wirth

Maróti

Mihók

et al. 2020

Journal of Oral Microbiology

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Section: Resultsmentioning

confidence: 99%

“…Papers published before 2000, not in English, or reporting only data on nonadult subjects or only data on pregnant women were excluded from the analysis. 14 papers addressing the topic accordingly to the inclusion criteria were included in our final analysis [2][3][4][5][6][7][8][9][10][11][12][13][14][15]. For each article, we extracted information from the main texts of those reporting data in the abstracts on the cut-offs of at least one of the investigated biomarkers in at least one of the populations of interest.…”

Section: Search Methodsmentioning

confidence: 99%

“…The optimal cut-off to distinguish COPD patients who are current smokers from those who are former smokers or nonsmokers was 11 ppm, with 73.1% sensitivity and 84.7% specificity. The lower sensitivity and specificity values might be explained by the disease-related inflammatory environment, which may have altered such measurements, as confirmed by EJAZI et al [8] As for SHS exposure, an exhaled CO cut-off in COPD patients has still to be determined.…”

Section: Healthy Controlsmentioning

confidence: 97%

“…Moreover, exhaled CO showed a positive correlation with the number of smoked cigarettes per day [12]. Exhaled CO was ∼1.5 ppm in healthy nonsmokers; nevertheless, no evidence about a precise cut-off for SHS exposure was provided [8]. COPD patients SATO et al [14] analysed smoking status in COPD patients who were nonsmokers, former smokers or current smokers, correlating exhaled CO levels with serum cotinine concentrations.…”

Section: Healthy Controlsmentioning

confidence: 99%

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Smoking status and second-hand smoke biomarkers in COPD, asthma and healthy controls

Bradicich

Schuurmans

2020

ERJ Open Res

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IntroductionTobacco smoke worsens COPD and asthma. For healthy individuals, quantifying active and second-hand smoke (SHS) exposure clarifies the epidemiology of tobacco consumption and the efficacy of nonsmoking measures. Identifying tobacco exposure biomarkers and cut-offs might allow the creation of sensitive and specific tests.AimWe describe the state-of-the-art serum, urinary cotinine and exhaled carbon monoxide (CO) cut-offs for assessing smoking status and SHS exposure in adult patients with COPD or asthma, and healthy controls.MethodologyAfter a keyword research in the PubMed database, we included papers reporting on the cut-offs of the investigated biomarkers in one of the populations of interest. Papers published before 2000, not in English, or reporting only data on nonadult subjects or on pregnant women were excluded from the analysis. 14 papers were included in the final analysis. We summarised diagnostic cut-offs for smoking status or SHS exposure in COPD, asthmatic and healthy control cohorts, reporting sensitivity and specificity when available.ConclusionSerum and urinary cotinine and exhaled CO are easy-to-standardise, affordable and objective tests for assessing smoking status and SHS exposure. Evidence on cut-offs with good sensitivity and specificity values is available mainly for healthy controls. For COPD and asthmatic patients, most of the currently available evidence focuses on exhaled CO, while studies on the use of cotinine with definite sensitivity and specificity values are still missing. Solid evidence on SHS exposure is available only for healthy controls. An integrated approach with a combination of these markers still needs evaluation.

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The role of oxidised self-lipids and alveolar macrophage CD1b expression in COPD

Ween

White

Tran

et al. 2021

Sci Rep

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In chronic obstructive pulmonary disease (COPD) apoptotic bronchial epithelial cells are increased, and their phagocytosis by alveolar macrophages (AM) is decreased alongside bacterial phagocytosis. Epithelial cellular lipids, including those exposed on uncleared apoptotic bodies, can become oxidized, and may be recognized and presented as non-self by antigen presenting cells. CD1b is a lipid-presenting protein, previously only described in dendritic cells. We investigated whether CD1b is upregulated in COPD AM, and whether lipid oxidation products are found in the airways of cigarette smoke (CS) exposed mice. We also characterise CD1b for the first time in a range of macrophages and assess CD1b expression and phagocytic function in response to oxidised lipid. Bronchoalveolar lavage and exhaled breath condensate were collected from never-smoker, current-smoker, and COPD patients and AM CD1b expression and airway 8-isoprostane levels assessed. Malondialdehyde was measured in CS-exposed mouse airways by confocal/immunofluorescence. Oxidation of lipids produced from CS-exposed 16HBE14o- (HBE) bronchial epithelial cells was assessed by spectrophotometry and changes in lipid classes assessed by mass spectrometry. 16HBE cell toxicity was measured by flow cytometry as was phagocytosis, CD1b expression, HLA class I/II, and mannose receptor (MR) in monocyte derived macrophages (MDM). AM CD1b was significantly increased in COPD smokers (4.5 fold), COPD ex-smokers (4.3 fold), and smokers (3.9 fold), and AM CD1b significantly correlated with disease severity (FEV1) and smoking pack years. Airway 8-isoprostane also increased in smokers and COPD smokers and ex-smokers. Malondialdehyde was significantly increased in the bronchial epithelium of CS-exposed mice (MFI of 18.18 vs 23.50 for control). Oxidised lipid was produced from CS-exposed bronchial epithelial cells (9.8-fold of control) and showed a different overall lipid makeup to that of control total cellular lipid. This oxidised epithelial lipid significantly upregulated MDM CD1b, caused bronchial epithelial cell toxicity, and reduced MDM phagocytic capacity and MR in a dose dependent manner. Increased levels of oxidised lipids in the airways of COPD patients may be responsible for reduced phagocytosis and may become a self-antigen to be presented by CD1b on macrophages to perpetuate disease progression despite smoking cessation.

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Correlation of exhaled carbon monoxide level with disease severity in chronic obstruction pulmonary disease

Cited by 7 publications

References 43 publications

A case study of salivary microbiome in smokers and non-smokers in Hungary: analysis by shotgun metagenome sequencing

A case study of salivary microbiome in smokers and non-smokers in Hungary: analysis by shotgun metagenome sequencing

Smoking status and second-hand smoke biomarkers in COPD, asthma and healthy controls

The role of oxidised self-lipids and alveolar macrophage CD1b expression in COPD

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