Carbon monoxide assessment of smoking in chronic obstructive pulmonary disease

Crowley, Thomas J.; Andrews, Amy; Cheney, Joyce; Zerbe, Gary O.; Petty, Thomas L.

doi:10.1016/0306-4603(89)90069-5

Cited by 25 publications

(17 citation statements)

References 16 publications

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“…The standard values of nonsmoker, light-smoker and heavy-smoker are 1-7, 8-19 and 20 ppm or more, respectively, according to the manufacture's protocol. These data are consistent with the data of Crowley et al (1989). Levels of cotinine are generally reported to remain relatively constant in active smokers over long periods of time, and are reported to be in higher concentrations than nicotine.…”

Section: Discussionsupporting

confidence: 91%

Smoking cessation increases gingival blood flow and gingival crevicular fluid

Morozumi

Kubota

Satô

et al. 2004

J Clinic Periodontology

117

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Section: Discussionsupporting

confidence: 91%

Smoking cessation increases gingival blood flow and gingival crevicular fluid

Morozumi

Kubota

Satô

et al. 2004

J Clinic Periodontology

117

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“…The mean level of breath CO was 22 (range = 3–51 ppm, identical to the mean previously measured in a group of still‐smoking COPD patients 9 ). Two patients had normal CO levels (< 10); one patient stated she no longer inhaled, and the other said he was only smoking 2–3 cigarettes daily.…”

Section: Resultssupporting

confidence: 84%

“…About 90% of cases of chronic obstructive pulmonary disease (COPD), an often debilitating lung illness that is the fifth most common cause of death in this country, are attributable to cigarette smoking 7,8 . Many COPD patients continue to smoke, often in spite of severe medical problems 9 . Although they may admit to an addiction to nicotine, they often deny that cigarette smoking is related to their declining health.…”

mentioning

confidence: 99%

Substance Use Diagnoses in Smokers With Lung Disease

et al. 1993

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Will medically ill smokers meet criteria for nicotine dependence using current diagnostic criteria (especially concerning tolerance and withdrawal)? The authors interviewed smokers with chronic obstructive pulmonary disease (COPD) to determine the following: 1) Will they meet DSM‐III‐R criteria? 2) Will requiring withdrawal or tolerance change prevalence? 3) Will denial of health consequences due to smoking change prevalence? and 4) How prevalent are comorbid substance use disorders? In 50 COPD smokers, 94% met nicotine dependence criteria. Because all had tolerance or withdrawal, prevalence was unaffected by these symptoms. Denial reduced prevalence by 8%. Lifetime alcohol dependence was 52%; other substance use disorders were uncommon.

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“…It was concluded that underlying airway disease might be misleading for distinguishing smokers from non-smokers. However, as in our study, there are some studies that show that the exhaled CO level is not related to COPD but to the state of smoking in COPD patients (15,16). In one of these studies, Montuschi et al (16) found that the exhaled CO level was significantly higher in smokers with COPD than in non-smokers with COPD and they could not demonstrate a relationship between the exhaled CO level and pulmonary functions.…”

Section: Discussionmentioning

confidence: 53%

“…If there is underlying an airway disease such as COPD or asthma in active smokers, exhaled CO level is suggested to be higher than expected (14). In other studies that suggest the opposite, it was detected that the exhaled CO level was related to the current level of smoking in COPD patients but did not exhibit a correlation with the severity of COPD (15,16). On the other hand, in a study of a large population, it was concluded that the exhaled CO level could not be an indicator of pulmonary functions (17).…”

Section: Introductionmentioning

confidence: 80%

Does the Finding of Small Airway Obstruction in Pulmonary Function Tests Effect End-Expiratory Carbonmonoxide Level?

Salepçi¹

2015

Eurasian J Pulmonol

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Objective: End-expiratory CO level, which is used to test smoking cessation is known to be effected by many factors. We aimed to evaluate effect of small airway obstruction (SAO) on end-expiratory CO levels. Methods:The study population consisted of cases who applied to smoking cessation clinic between April-December 2014. The duration of smoking (pack-years), pulmonary function tests (PFT) and end-expiratory carbonmonoxide (CO) were noted at first visit. The cases were questioned for last time of smoking and amount of cigarettes they smoked within past 12 hours. Pearson correlation test was used to determine factors effecting CO levels.Results: Mean age of 167 cases -112 male (67.1%), 55 female (32.9%) was 38.7±12.7 years. Mean duration of smoking was 23.3±16.4 pack-years, mean CO level was 14.1±6.9 ppm, mean FEF25-75% was 77.2±28.2. Mean period elapsed after last cigarette was 1.5±1.8 hours, mean number of cigarettes smoked within past 12 hours was 7.2±5.0. SAO was found in 50 cases (34.1%). Correlation analyses revealed that CO levels were correlated positively to duration of smoking and amount of cigarettes they smoked within past 12 hours (p=0.03, r=0.228; p=0.000, r=0.511, respectively) and negatively to the last time of smoking (p=0.023, r=0.176). SAO and in PFT was not correlated to CO level (p>0.05). Conclusion:End-expiratory CO level is closely related to duration of smoking, number of cigarettes smoked within past 12 hours and period elapsed after last cigarette. Presence of SAO does not seem to effect CO levels.

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Carbon monoxide assessment of smoking in chronic obstructive pulmonary disease

Cited by 25 publications

References 16 publications

Smoking cessation increases gingival blood flow and gingival crevicular fluid

Smoking cessation increases gingival blood flow and gingival crevicular fluid

Substance Use Diagnoses in Smokers With Lung Disease

Does the Finding of Small Airway Obstruction in Pulmonary Function Tests Effect End-Expiratory Carbonmonoxide Level?

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