Measurement Of Exhaled Carbon Monoxide Research Articles

Smoking Cessation Intervention After Ischemic Stroke or Transient Ischemic Attack. A Randomized Controlled Pilot Trial

Smoking cessation is widely recommended for secondary stroke prevention. However, little is known about the efficacy of smoking cessation intervention after stroke or transient ischemic attack (TIA). Ninety-four smokers under age 76, admitted with ischemic stroke or TIA were randomized to minimal smoking cessation intervention or intensive smoking cessation intervention. All patients attended a 30-min individual counseling by the study nurse. Patients randomized to intensive smoking cessation intervention also participated in a 5-session outpatient smoking cessation program by an authorized smoking cessation instructor, a 30-min outpatient visit after 6 weeks, and 5 telephone counseling sessions by the study nurse. Free samples of nicotine replacement therapy were offered as part of the intensive smoking cessation program. Smoking cessation rates at 6 months were determined by self-report and verified by measurement of exhaled carbon monoxide (CO). Fewer patients than expected were recruited, which renders this report a pilot study. The 6-month self-reported smoking cessation rate was 37.8% in the minimal intervention group and 42.9% in the intensive intervention group. Smoking cessation rates verified by exhaled CO levels in the minimal intervention group and the intensive intervention group were 28.9% and 32.7%, respectively. No difference was found between the two groups (χ(2) = 0.16, p = .69). Overall smoking cessation rates were moderate and comparable to the results from other studies. Intensive smoking cessation intervention was not superior to short smoking cessation intervention. Thus, other factors than intensity of smoking cessation intervention might influence the smoking cessation rates after stroke or TIA.

The JAK2V617F Mutation In Non-MPD Individuals Occurs at a Low Frequency During Erythroid Differentiation and Not In the Stem Cells.

AbstractAbstract 1583A somatic point mutation in the JAK2 gene results in a constitutive activation of the JAK2 kinase in the erythropoietin (epo) signal transduction pathway. The mutation was found in Polycythemia Vera (PV) patients (>95%) as well as in other myeloproliferative disorders (MPD). In MPD the mutation was shown to occur in pluripotential hematopoietic stem cells and to be present in all blood cell lineages. We analyzed DNA of blood donors for the JAK2V617F mutation by allele specific Real Time PCR. The mutation was detected in 9% of 114 samples with a very low mutation frequency of < 0.002% per sample (mutant/wild-type DNA allelic ratio) in comparison to frequency of 50–100% in PV.We speculated that accelerated erythropoiesis with increased erythroid differentiation will result in higher mutation rate. We therefore studied the presence of V617F mutation in two conditions associated with increased erythropoiesis, thalassemia and smoking.In beta-thalassemia major patients, the mutation was found in 22.2% (12/54), a significant 2.4-fold increase in mutation incidence compared to healthy individuals (p=0.016). The mutation frequency was 0.035% per positive sample.The V617F mutation was studied in a case – control study of hospitalized smokers (n=81) and non-smokers (n=61). Smoking was defined as 10 or more cigarettes per day, everyday of the week, for at least 10 consecutive years. Smoking status was assessed by a questionnaire and validated with measurement of exhaled carbon monoxide. Smokers suffered more chronic lung disease than non-smokers (45.7% vs. 6.6%, respectively, p<0.0001) and had a higher hematocrit, RBC and WBC (47.8% vs. 41.7% p<0.0001, 5.2 vs. 4.4×1012 cells/liter, p<0.0001 and 9.4 vs. 7.6×109 cells/liter, p=0.003, respectively). In all subjects epo was within the normal range or higher. The proportion of subjects with higher than normal epo was similar in smokers and non-smokers.The prevalence of the mutation was significantly higher among the smokers (36%) than among the controls (15%) (p= 0.005) The median V617F mutation frequency in smokers was 10 fold higher than in controls (0.032% and 0.0032% respectively; p=0.027).Very low V617F mutation frequency in DNA of non-MPD blood donors led us to question whether in these non-MPD individuals V617F mutation occurs in stem sells as was shown for PV patients. We found that the mutation was more frequent in peripheral blood mononuclear cells than in CD34+ cells purified from these mononuclear cells. Following 3 weeks culturing of CD34+ cells with epo mutation frequency increased by 9-folds (range 6–14) in hemoglobin-containing normoblasts. We next grew individual erythroid colonies from 8 healthy donors in semi-solid culture in the presence of epo. Out of 201 single colonies analyzed 13% contained the JAK2V617F mutation in a very small proportion of the cells (< 0.02%). These results demonstrate that in non-MPD individuals V617F mutation arises in very low frequency during cell differentiation.We established a cell line model to study the occurrence of JAK2V617F mutation during erythroid differentiation. Mouse erythroleukemia (MEL) cells were transfected with the 1kb fragment of human JAK2 gene containing exon 14 sub-cloned into a mammalian expression vector. MEL cells were stimulated to differentiate by hexamethylene bisacetamide and the frequency of sequence changes in the JAK2 exon 14 was investigated. We found that changes in the JAK2 exon 14 sequence occurred at late stages of differentiation.We hypothesize that maintenance of DNA fidelity is down graded with cell differentiation, rendering the cells susceptible for mutations in general and in JAK2 in particular.In summary, accelerated erythropoiesis results in increased V617F mutation frequency such as in beta-thalassemia major patients and in heavy smokers. We demonstrate that unlike in MPD where the JAK2V617F mutation occurs in pluripotential stem cells and expands extensively, in non-MPD individuals it arises at very low frequency during cell differentiation. These differences determine the lack of clinical significance of the JAK2V617F mutation in non-MPD individuals. Disclosures:No relevant conflicts of interest to declare.

Effects of acute hypoventilation and hyperventilation on exhaled carbon monoxide measurement in healthy volunteers

BackgroundHigh levels of exhaled carbon monoxide (eCO) are a marker of airway or lung inflammation. We investigated whether hypo- or hyperventilation can affect measured values.MethodsTen healthy volunteers were trained to achieve sustained end-tidal CO2 (etCO2) concentrations of 30 (hyperventilation), 40 (normoventilation), and 50 mmHg (hypoventilation). As soon as target etCO2 values were achieved for 120 sec, exhaled breath was analyzed for eCO with a photoacoustic spectrometer. At etCO2 values of 30 and 40 mmHg exhaled breath was sampled both after a deep inspiration and after a normal one. All measurements were performed in two different environmental conditions: A) ambient CO concentration = 0.8 ppm and B) ambient CO concentration = 1.7 ppm.ResultsDuring normoventilation, eCO mean (standard deviation) was 11.5 (0.8) ppm; it decreased to 10.3 (0.8) ppm during hyperventilation (p < 0.01) and increased to 11.9 (0.8) ppm during hypoventilation (p < 0.01). eCO changes were less pronounced than the correspondent etCO2 changes (hyperventilation: 10% Vs 25% decrease; hypoventilation 3% Vs 25% increase). Taking a deep inspiration before breath sampling was associated with lower eCO values (p < 0.01), while environmental CO levels did not affect eCO measurement.ConclusionseCO measurements should not be performed during marked acute hyperventilation, like that induced in this study, but the influence of less pronounced hyperventilation or of hypoventilation is probably negligible in clinical practice

Assessing smoking behaviour among medical students by the measurement of expired carbon monoxide (CO)

Smoking behaviour and prevalence rates among medical students and medical professionals are important public health issues, as physicians' attitudes and interventions are decisive for the patients' success in quitting smoking. Studies dealing with prevalence rates of smoking usually use only face-to-face interviews or self-administered questionnaires, which may induce vague findings. Additional measurement of exhaled carbon monoxide is an objective, easy, immediate, non-invasive and inexpensive mode of indicating smoking behaviour and will complement and at some stage replace the usual question regarding the number of cigarettes consumed. CO-measurement of 260 medical students was taken during compulsory public health training at the Medical University Vienna. Definite indication of active smoking was found in 12% of the students, 9.5% showed CO-levels between 6 and 10 ppm and 78% were definitely non-smokers with a CO level between 0 and 5 ppm. The students had the opportunity to get to know an important diagnostic technique and additionally learned about their own smoking habits.

Exhaled Carbon Monoxide Levels: As a Marker of Clinical Severity and Control of Asthma

A study was conducted to evaluate the role of exhaled carbon monoxide (CO) levels in the management of patients with mild and moderate persistent bronchial asthma. Spirometry, exhaled CO measurements and symptom scoring was done before and after four weeks of treatment with inhaled corticosteroids. Exhaled CO levels were significantly elevated in patients of mild as well as moderate persistent asthma as compared to controls but the levels did not correlate with the disease severity. After four weeks of treatment, there was a decrease in exhaled CO levels in both the groups but the decrease was not found to be statistically significant. Therefore, clinically exhaled CO level is not a useful marker in bronchial asthma.

Exhaled carbon monoxide levels in school‐age children with episodic asthma

Carbon monoxide (CO) can be detected in exhaled air and is increased in adult and childhood persistent asthmatic patients. However, little is known about the exhaled CO concentration in episodic childhood asthma. This study aimed to clarify whether measurement of exhaled CO is useful in monitoring disease activity in children with episodic asthma. We measured exhaled CO concentration by modified Micro-Smokerlyzer in 217 elementary school children (132 boys; mean age, 10 +/- 1 (SE) years; range, 9-12 years), in whom 29 had infrequent episodic asthma without current exacerbations. We also measured exhaled CO concentrations in 22 children with episodic asthma (13 boys; mean age, 10 +/- 3 years; range, 8-12 years), who had acute mild asthmatic attacks during examination. In these patients with mild asthmatic attacks, exhaled CO was measured both before and after combination therapy with salbutamol and sodium cromoglycate (SCG) by powered nebulizer. Among 217 schoolchildren, exhaled CO levels in infrequent episodic asthmatic children (1.1 +/- 0.1 parts per million (ppm), n = 29) were not significantly different from those in healthy schoolchildren (1.0 +/- 0.1 ppm, n = 188, P > 0.68). The exhaled CO concentrations during asthma attacks in children with episodic asthma were significantly higher (5.1 +/- 0.4 ppm, n = 22) compared with those in healthy children (P < 0.001) or those in asymptomatic asthmatic children (P < 0.001). The elevated exhaled CO levels were significantly decreased after inhalation therapy of a combination of salbutamol and SCG (3.2 +/- 0.5 ppm, n = 22, P < 0.02). In conclusion, exhaled CO levels were significantly elevated during acute asthma exacerbations, and partially recovered after treatment with beta(2)-agonist and SCG in children with mild episodic asthma. These findings indicate that measurement of exhaled CO might provide another noninvasive measurement of asthma exacerbations that would be suitable for use in children with acute mild episodic asthma.

Self-Reported Smoking Status and Exhaled Carbon Monoxide

To investigate the validity of self-reported responses to questions on current smoking in two cohorts based in Northern England. A cross-sectional population-based study (the Newcastle Heart Project [NHP]) and a follow-up of the Newcastle Thousand Families birth cohort established in 1947. Participants included 1,189 members of the NHP and 410 members of the Newcastle Thousand Families cohort who completed a health and lifestyle questionnaire, including questions on current smoking, and attended a clinical examination, including testing for exhaled carbon monoxide between April 1993 and December 1998. The number of self-reporting smokers for whom very low (ie, < 6 ppm) exhaled carbon monoxide levels were recorded varied between 9% in the Newcastle Thousand Families Study and 26% among the members of the NHP who were of South Asian origin. Using a cutoff of 8 ppm, 80% of self-reported smokers were identified in both the Newcastle Thousand Families study and in the NHP European population, but only 60% were identified in the NHP South Asian population. In each population, < 7% of nonsmokers had exhaled carbon monoxide measurements of > 6 ppm, with nonsmoking men more likely to have higher levels than nonsmoking women. Among the nonsmokers, the levels of exhaled carbon monoxide did not vary with respect to the smoking status of a partner or socioeconomic status. Using a cutoff value of 6 ppm would potentially miss a large number of smokers, although this may vary with ethnicity. Epidemiologic studies should continue to use biochemical markers to validate responses to smoking surveys. However, the use of exhaled carbon monoxide measurements as a method of assessing the validity of self-reported smoking status may require additional analyses of whether the cutoff level should vary for different populations.

Effectiveness of Hospital-Based Smoking Cessation

Smoking cessation for current smokers is a health-care imperative. It is not clear which approaches to smoking cessation are the most effective in the hospital setting and which factors predict long-term abstinence. We hypothesized that a hospital-based smoking cessation program involving behavioral modification and support would provide an effective intervention for smoking cessation. Prospective cohort study. Smoking cessation clinics in a tertiary referral, cardiothoracic hospital. Two hundred forty-three smokers and 187 never-smoker control subjects. Smokers underwent specific sessions of individual counseling on behavioral modification, including written information, advice about quit aids, and support during the quit attempt. Abstinence was confirmed by exhaled carbon monoxide measurements. Compared to never-smoker control subjects, smokers were more likely to have grown up with a smoking father or siblings, and to currently live or socialize with other smokers. Two hundred sixteen smokers attended at least two sessions of the smoking cessation program. Of these, 25% were unavailable for follow-up at 12 months and were assumed to be smoking. The point prevalence abstinence rate at 12 months was 32%. Independent factors associated with abstinence at 12 months were self-belief in quitting ability, having a heart condition, growing up without siblings who smoked, and increasing number of pack-years. This prospective study has demonstrated that this hospital-based smoking cessation program was as effective as programs in other settings. Social and psychological factors were associated with a greater chance of abstinence.

Assessment of smoking status in patients with peripheral arterial disease

To assess the utility of a novel rapid urinary cotinine assay to detect and quantify the level of smoking in patients with peripheral arterial disease. This was a cross-sectional study in a vascular surgical outpatient department of a large teaching hospital. Participants were 100 consecutive subjects presenting to a hospital outpatient clinic with a diagnosis of intermittent claudication confirmed by a positive Edinburgh claudication questionnaire and an ankle-brachial pressure index of less than 0.9. Main outcome measures were patient-offered smoking history, exhaled breath carbon monoxide levels, urinary cotinine levels as measured by a novel rapid assay, and laboratory-measured creatinine-adjusted urinary cotinine levels. Results Fifty-five subjects declared that they were current smokers, 40 declared that they were ex-smokers, and 5 declared that they were never-smokers. Of the 40 ex-smokers, 6 subjects (15%) had urinary cotinine levels greater than 500 ng/mL (regular smokers), and a further 2 (5%) had urinary cotinine levels between 100 and 500 ng/mL (light, irregular, or passive smokers). The rapid urinary cotinine assay had a sensitivity and specificity of 100% and 98%, respectively, in its ability to detect active smoking, and the degree of smoking correlated well with laboratory creatinine-corrected urinary cotinine levels (Spearman coefficient, 0.805; P < .001). By contrast, exhaled carbon monoxide had a sensitivity and specificity of 95% and 89%, respectively, and although it correlated well with urinary cotinine (Spearman coefficient, 0.782; P < .001), it was found on linear regression analysis to be unreliable in differentiating light smokers from nonsmokers. Patient-offered smoking history is unreliable because there is no correlation between the patient-reported number of cigarettes smoked per day and urinary cotinine levels. The novel rapid assay for urinary cotinine described here is superior to exhaled carbon monoxide measurement in detecting the level of smoking exposure among patients with intermittent claudication, and its results correlate well with laboratory-measured cotinine.

The measurement of exhaled carbon monoxide in healthy smokers and non-smokers

The measurement of exhaled carbon monoxide (CO) level may provide an immediate, non-invasive method of assessing smoking status. The aims of this study were to use a portable CO monitor to compare the exhaled CO levels in established smokers and non-smokers. The exhaled CO levels were measured in 322 subjects (243 healthy smokers, 55 healthy non-smokers, 24 passive smokers) who applied to healthy stand during the spring student activity of Fırat University in Elazıǧ. Exhaled CO concentration was measured using the EC50 Smokerlyser. The mean exhaled CO level was 17.13±8.50 parts per million (ppm) for healthy smokers and 3.61±2.15 ppm for healthy non-smokers, and 5.20±3.38 ppm for passive smokers. There were significant positive correlation between CO levels and daily cigarette consumption, and CO levels and duration of smoking in healthy smokers ( r=+0.550, P<0.001, r=+0.265, P<0.001, respectively. Spearman's test). When smokers and non-smokers were looked at as a whole, a cutoff of 6.5 ppm had a sensitivity of 90% and specificity of 83%. In conclusion, exhaled CO level provides an easy, an immediate way of assessing a subject's smoking status.

Repeated validation of parental self-reported smoking during pregnancy and infancy: a prospective cohort study of infants at high risk for allergy development.

Exposure to environmental tobacco smoke (ETS) during fetal life and infancy is closely related to the smoking habits of the parents. Estimates of exposure to ETS require valid and detailed information on changes in cigarette smoking over time. The objective was to test the validity of self-reported smoking among parents during pregnancy and early childhood in a cohort of children at high risk for allergy development by measurement of exhaled carbon monoxide (CO). The cohort comprised 117 families enrolled from the general population of pregnant women at admission to antenatal care. Data on parental tobacco smoking were obtained by interview and exhaled CO was measured (Micro-Smokerlyzer(R)) in parents twice during pregnancy and when the child was 6 and 18 months old. The median (range) exhaled CO levels were 3 (0-10) parts per million (ppm) for non-smokers and 15 (1-39) ppm for smokers (P < 0.0005). A receiver operating characteristic (ROC) analysis was performed at each examination. The areas under the ROC curve were high for both mothers (between 0.88 and 0.99) and fathers (between 0.87 and 0.89), indicating exhaled CO as a good diagnostic tool for determining smoking status. Comparing the ROC areas obtained for mothers from late pregnancy and during infancy with the area from early pregnancy showed no statistical differences (P = 0.21, 0.43 and 0.44 respectively) and the same was true for fathers during infancy (P = 0.81). The level of 8 ppm was used as the cut-off between smokers and non-smokers, based on data from a pilot study. Using CO as a diagnostic tool for smoker status showed very high specificity (between 97 and 100%), indicating that very few persons claiming to be non-smokers had CO levels higher than 8 ppm. In conclusion, the validity of interview-obtained self-reported smoking among parents during pregnancy and early childhood was high. Repeated interviews and CO measurements in a prospective study design did not change the validity, indicating a low risk of information bias. A structured interview combined with measurement of exhaled CO is a valid and reliable method for estimating ETS exposure to the fetus and young infant.

Smoking Cessation Program Using Nicotine Patches Linking Hospital to the Community

Objective: To compare the quit rates achieved by participants in a smoking cessation program, initiated in hospital using nicotine patches and continued in either the community pharmacy or hospital setting, with quit rates in a minimal intervention group.Setting: The medical and surgical units at The Queen Elizabeth Hospital (TQEH), a major teaching hospital located in the western suburbs of Adelaide, South Australia.Participants: Inpatients aged over 18 years who smoked 10 or more cigarettes per day. Of 306 smokers screened, 102 were enrolled.Study Procedures: Participants were randomised to either the minimal intervention arm (n = 33), the hospital‐based program (n = 35), or the community pharmacy‐based program (n = 34). The minimal intervention group received written materials and advice about quitting. The two intervention arms started with a consultation with the research pharmacist and participants were commenced on nicotine patches and were followed after discharge with weekly counselling visits with either the researcher in an outpatient clinic or a community‐based pharmacist. Patches were supplied for $15.00 per week for up to 16 weeks. Exhaled carbon monoxide measurements to confirm abstinence were performed whenever possible. Continuous and point prevalence of abstinence from smoking were assessed 3, 6 and 12 months after enrolment.Results: There was a statistically significant difference in the point prevalence of abstinence between groups at 12 months with 38%, 24% and 4.6% abstinence in the hospital, community pharmacy and minimal intervention arms respectively (X2 = 7 .145, df = 2, p = 0.031 ). The differences seen in continuous abstinence at 12 months (24%, 19% and 4.6% respectively) did not reach statistical significance.Conclusion: A hospital‐based smoking cessation program initiated with nicotine patches was equally effective whether continued by hospital‐ or community‐based pharmacists and was superior to minimal intervention without nicotine patches.

Exhaled Carbon Monoxide and Nitric Oxide in COPD

To investigate whether exhaled carbon monoxide (CO) and nitric oxide (NO) could be used as noninvasive in vivo biomarkers of oxidative stress in the lungs of patients with COPD. Single-center cross-sectional study. Ten healthy nonsmokers, 12 smokers, 15 stable ex-smokers with COPD, and 15 stable current smokers with COPD. Subjects attended the outpatient clinic on one occasion for pulmonary function tests and exhaled CO and NO measurements. Mean (+/- SEM) CO levels in ex-smokers with COPD were higher (7.4 +/- 1.9 ppm; p < 0.05) than in nonsmoking control subjects (3.0 +/- 0.3 ppm) but were lower than in current smokers with COPD (20.0 +/- 2.6 ppm; p < 0.001). There was no correlation between exhaled CO and NO. There was no correlation between CO and lung function tests in any group of patients. Exhaled NO was higher in ex-smokers with COPD (12.0 +/- 1.0 parts per billion [ppb]; p < 0.001) than in healthy nonsmokers (6.5 +/- 0.6 ppb) and in current smokers with COPD (7.6 +/- 1.1 ppb; p < 0.01) compared to healthy smokers (3.3 +/- 0.4 ppb). Ex-smokers with COPD had higher exhaled NO levels than did current smokers with COPD (p < 0.001) There was a negative correlation between exhaled NO and FEV(1) in both ex-smokers with COPD (r = -0.60; p < 0.02) and current smokers with COPD (r = -0.59; p < 0.02). The measurement of exhaled CO and NO may represent a new method for the noninvasive monitoring of airway inflammation and oxidant stress in COPD ex-smokers. Exhaled CO and NO are strongly affected by cigarette smoking, which limits their usefulness as biomarkers in current smokers.

Smoking reduction with oral nicotine inhalers: double blind, randomised clinical trial of efficacy and safety

Objectives: To determine whether use of an oral nicotine inhaler can result in long term reduction in smoking and whether concomitant use of nicotine replacement and smoking is safe.Design: Double...

Increase in exhaled carbon monoxide during exacerbations of cystic fibrosis

BACKGROUNDNon-invasive assessment of inflammation is likely to be useful in the management of cystic fibrosis (CF). Exhaled carbon monoxide (CO) concentrations are increased in patients with clinically stable CF. A...

The measurement of exhaled carbon monoxide is influenced by airflow obstruction.

The concentration of carboxyhaemoglobin (COHb) is often estimated from measurements of carbon monoxide in the exhaled air (COexh). This study investigates whether the presence of airflow obstruction significantly alters the relationship between COexh and COHb. Eighty-one regular smokers were prospectively studied and divided in four groups according to the presence and severity of airflow obstruction (none, mild, moderate, severe). In each subject, the authors measured in this order: 1) arterial blood gases; 2) haemoglobin concentration and COHb (by co-oxymetry); 3) COexh; 4) lung volumes; and 5) forced spirometry. The size of the measurement error (deltaCO) was calculated from the difference between COHb and COexh. Neither the smoking history nor COexh were different in the four groups of subjects studied. In contrast, deltaCO increased in parallel to the degree of airflow obstruction. DeltaCO was >2% (a threshold value normally used in the clinic to separate smokers from nonsmokers) only in patients with severe airflow obstruction. A stepwise multivariate analysis showed that both forced expiratory volume in one second (FEV1) (percentage reference) and COHb contributed significantly (p<0.0001) to predict deltaCO. This study shows that the estimation of carboxyhaemoglobin from exhaled carbon monoxide measurements can be inaccurate in patients with severe airflow obstruction. In these patients, the direct measurement of carboxyhaemoglobin seems advisable in clinical practice.

The measurement of exhaled carbon monoxide is influenced by airflow obstruction

The concentration of carboxyhaemoglobin (COHb) is often estimated from measurements of carbon monoxide in the exhaled air (COexh). This study investigates whether the presence of airflow obstruction significantly alters the relationship between COexh and COHb. Eighty-one regular smokers were prospectively studied and divided in four groups according to the presence and severity of airflow obstruction (none, mild, moderate, severe). In each subject, the authors measured in this order: 1) arterial blood gases; 2) haemoglobin concentration and COHb (by co-oxymetry); 3) COexh; 4) lung volumes; and 5) forced spirometry. The size of the measurement error (deltaCO) was calculated from the difference between COHb and COexh. Neither the smoking history nor COexh were different in the four groups of subjects studied. In contrast, deltaCO increased in parallel to the degree of airflow obstruction. DeltaCO was &gt;2% (a threshold value normally used in the clinic to separate smokers from nonsmokers) only in patients with severe airflow obstruction. A stepwise multivariate analysis showed that both forced expiratory volume in one second (FEV1) (percentage reference) and COHb contributed significantly (p&lt;0.0001) to predict deltaCO. This study shows that the estimation of carboxyhaemoglobin from exhaled carbon monoxide measurements can be inaccurate in patients with severe airflow obstruction. In these patients, the direct measurement of carboxyhaemoglobin seems advisable in clinical practice.

Exhaled carbon monoxide in childhood asthma

Objectives: Oxidative stress and inflammation induce the expression of heme oxygenase-1, which produces carbon monoxide (CO), and nitric oxide synthase, which produces nitric oxide (NO). Exhaled CO and NO levels are elevated in asthmatic patients and are decreased after corticosteroid treatment, suggesting that they may be useful as noninvasive markers of airway inflammation. Study design: We measured forced expiratory volume in the first second, PC 20, and exhaled CO and NO levels in 29 children (18 boys, mean age 11.5 ± 0.53 years) with asthma of different severity and 40 nonsmoking children without asthma (21 boys, mean age 8.1 ± 0.35 years). We also studied whether upper respiratory tract infections were associated with elevated exhaled CO. Results: Exhaled CO levels (ppm) were significantly higher (2.17 ± 0.21) in children with persistent asthma compared with those in children with infrequent episodic asthma (1.39 ± 0.18, P < .05) and healthy children (1.01 ± 0.12, P < .001). The CO levels in children with infrequent episodic asthma and the normal control group, however, were not different. In contrast, exhaled NO levels (ppb) were higher in children with persistent asthma (24.2 ± 5.9, P < .001) and infrequent episodic asthma (14.5 ± 3.73, P < .05) than in normal subjects (5.1 ± 0.24), but no significant difference was seen between the 2 asthmatic groups. In healthy children with upper respiratory tract infections (n = 12), exhaled CO concentrations were significantly elevated (2.16 ± 0.33) during the acute symptomatic phase. No correlation was found between exhaled CO and forced expiratory volume in the first second or PC 20. Conclusions: Noninvasive measurement of exhaled CO may provide complementary data for assessment of asthma control in children. However, elevated CO levels are nonspecific and may be found in association with an acute viral illness. (J Pediatr 1999;135:569-74)

Increased levels of exhaled carbon monoxide in bronchiectasis: a new marker of oxidative stress

BACKGROUNDBronchiectasis is a chronic inflammatory lung disease associated with increased production of oxidants due mostly to neutrophilic inflammation. Induction of heme oxygenase (HO-1) by reactive oxygen species is a general...

Raised levels of exhaled carbon monoxide are associated with an increased expression of heme oxygenase-1 in airway macrophages in asthma: a new marker of oxidative stress

BACKGROUNDChronic inflammatory diseases are associated with an increased production of oxidants. Induction of a stress protein, heme oxygenase (HO) HO-1, is a cytoprotective mechanism against oxidative cellular injury. HO-1 catabolises...