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PubMed2005

Mass spectrometric profile of exhaled breath--field study by PTR-MS.

Recently, increased interest has focused on the diagnostic potential of volatile organic compounds (VOC) exhaled in human breath as this substance group has been conjectured in indoor air quality and disease screening. Proton transfer reaction-mass spectrometry (PTR-MS) has been established as a new tool for a rapid determination of exhaled air profile. However, no investigations have been carried out into the profile of exhaled air as determined by PTR-MS. Therefore, it was the aim of the present study to determine the profile of exhaled breath in a field survey enrolling 344 persons. Analysis was performed using PTR-MS. No significant correlations with age, blood pressure, and body mass index could be observed with any molecular mass. The present study delineates possible reference values for PTR-MS investigations into exhaled air profile. In conclusion, the present study was the first to delineate mass spectrometric characteristics of an average patient sample as possible reference values.

Aged↗
PubMed2006

Exhaled nasal nitric oxide output is reduced in humans at night during the sleep period.

The physiologic function of nasal nitric oxide (NO) release is unknown. In prior experiments, topical NG-nitro-L-arginine methyl ester (L-NAME) on nasal mucosa reduced exhaled nasal NO output and caused daytime sleepiness. We hypothesized that nasal NO output is reduced at night during the sleep period. We measured exhaled nasal NO concentration and minute ventilation and calculated nasal NO output in humans over 24 h. Daytime awake NO output was greater than NO output at night during sleep or transient wakefulness. Exhaled NO concentration decreased during sleep along with minute ventilation. A daytime voluntary reduction in minute ventilation also decreased nasal NO output but exhaled NO concentration increased. Nasal NO output was not changed by body position. We conclude that exhaled nasal NO output is decreased at night due to decreased mass flow of NO into nasal air in addition to decreased minute ventilation. Our findings suggest a role of nasal NO in sleep or in the physiologic processes accompanying sleep.

Adult↗
PubMed2003

Elemental and ion composition of exhaled air condensate in cystic fibrosis.

BACKGROUND: In cystic fibrosis (CF) the exact ion composition of the airway surface fluid is still debated and it is not clear if it differs from healthy subjects. The air that we exhale contains small droplets, which are generated by shear forces from the airway surface fluid and very likely mirror its ion composition. We hypothesized that differences between CF-patients and healthy controls would be reflected by differences in their exhaled air. METHODS: In nasally collected exhaled breath condensate from 20 children and young adults with cystic fibrosis and 20 healthy subjects, the elements and anions were determined by optical emission spectroscopy and ion-exchange chromatography. RESULTS: The concentrations of the major components Na and Cl- did not differ, Zn was higher and NO3- was lower in CF-patients. During a given time period, CF-patients produced a slightly larger volume of breath condensate and they exhaled more Na, K and Zn. Fluoride was detected in half of all samples, whereas copper, iron, magnesium, phosphorus and sulfur were present only sporadically, with no differences. CONCLUSIONS: These data detail the composition of exhaled breath condensate and suggest a similar Na and Cl- concentration in CF-airway surface fluid as in healthy subjects.

Adolescent↗
PubMed2004

Inhaling to mitigate exhaled bioaerosols.

Humans commonly exhale aerosols comprised of small droplets of airway-lining fluid during normal breathing. These "exhaled bioaerosols" may carry airborne pathogens and thereby magnify the spread of certain infectious diseases, such as influenza, tuberculosis, and severe acute respiratory syndrome. We hypothesize that, by altering lung airway surface properties through an inhaled nontoxic aerosol, we might substantially diminish the number of exhaled bioaerosol droplets and thereby provide a simple means to potentially mitigate the spread of airborne infectious disease independently of the identity of the airborne pathogen or the nature of any specific therapy. We find that some normal human subjects expire many more bioaerosol particles than other individuals during quiet breathing and therefore bear the burden of production of exhaled bioaerosols. Administering nebulized isotonic saline to these "high-producer" individuals diminishes the number of exhaled bioaerosol particles expired by 72.10 +/- 8.19% for up to 6 h. In vitro and in vivo experiments with saline and surfactants suggest that the mechanism of action of the nebulized saline relates to modification of the physical properties of the airway-lining fluid, notably surface tension.

Administration, Inhalation↗
PubMed2006

Exhaled nitric oxide in asthma: variability, relation to asthma severity, and peripheral blood lymphocyte cytokine expression.

Exhaled nitric oxide has been used as a means of indirectly measuring the underlying inflammation in asthma. The objectives of the study were to measure exhaled nitric oxide levels in asthma patients and healthy volunteers, to study peripheral blood lymphocyte cytokine expression, and to study the relationship between exhaled nitric oxide and intracellular cytokine expression. Exhaled nitric oxide was elevated in patients with moderate to severe asthma and with treatment decreased in the first week reaching to a near normal level by 4 weeks. Elevated exhaled nitric oxide was associated with decreased IL-4 and IL-13 cytokine expression by CD8 lymphocytes.

Adult↗
PubMed2004

Effects of Ginkgo biloba on exhaled nasal nitric oxide during normobaric hypoxia in humans.

Ginkgo biloba, an extract of the ginkgo tree, may prevent or lessen symptoms of acute mountain sickness in humans. The mechanism of this effect is poorly understood. One hypothesis is that ginkgo alters nitric oxide (NO) metabolism, possibly by scavenging NO or altering nitric oxide synthase expression and thereby lessening the vasodilatory effects of NO. To date, an effect of Ginkgo biloba on NO metabolism has not been demonstrated in humans. We measured exhaled nasal NO output in humans (n = 9) during normoxia and then during acute normobaric hypoxia (goal oxyhemoglobin saturation 75% to 85%) before and after administration of a standardized extract of Ginkgo biloba (120 mg twice daily for 5 days). Oxygen saturation, heart rate, and minute ventilation were similar before and after Ginkgo biloba administration. Exhaled nasal NO output was increased during normoxia following ginkgo (p < 0.02) and reduced during normobaric hypoxia both before (p < 0.02) and following (p < 0.003) ginkgo. Exhaled nasal NO output during normobaric hypoxia was lowest following ginkgo (p < 0.003). We conclude that Ginkgo biloba increases exhaled nasal NO output during normoxia and enhances reduced exhaled nasal NO output during normobaric hypoxia. Our results suggest that Ginkgo biloba may act to reduce AMS through an effect on NO metabolism.

Adult↗
PubMed2003

Elective haemodialysis increases exhaled isoprene.

BACKGROUND: Uraemic odour is a characteristic feature of patients with end-stage renal disease (ESRD). However, few investigations have been carried out into the composition of exhaled air in ESRD patients undergoing haemodialysis (HD). Increases of exhaled isoprene levels by a factor of up to 2.7 following HD have been reported. METHODS: We attempted to confirm these findings in 50 patients undergoing HD using haemophan (n=23) or polysulphone (n=27) dialysis membranes. Parallel evaluation of ambient air, calorie intake, medication and haemodynamic variables was performed. Samples were analysed using proton transfer reaction-mass spectrometry (PTR-MS). RESULTS: Significant changes in breath isoprene concentration were observed when comparing patients before [39.14+/-14.96 parts per billion (ppbv)] and after (63.54+/-27.59 ppbv) dialysis (P<0.001). The quotient of values before and after dialysis was 1.84 (SD 1.41). No significant differences in isoprene kinetics were found between the use of haemophan and polysulphone membranes. No significant correlations were observed between isoprene quotients and variations in blood pressure during HD, calorie intake, ingestion of lipid-lowering drugs or serum lipid levels. CONCLUSIONS: Isoprene concentration was higher in the exhaled air of patients after HD as compared with values before HD. Large interindividual variability existed in isoprene kinetics. Oxidative stress appears to be an unlikely cause for this rise. An alternative hypothesis is an influence of respiratory variables on isoprene exhalation based upon Henry's law constant. We therefore propose to perform online monitoring of isoprene exhalation by PTR-MS during the HD session to investigate the possible influence of respiratory variables.

Adult↗
PubMed2003

Exhaled nitric oxide and acute lung injury in a rat model of extracorporeal circulation.

Exhaled nitric oxide (NO) concentration, a marker of pulmonary inflammation, has been shown to be elevated in various models of acute lung injury (ALI). This study was undertaken to evaluate the pulmonary NO production in a rat model of postextracorporeal circulation (ECC) ALI. Wistar rats underwent either a partial femorofemoral ECC in normothermia for 3 h (n = 10) or a sham procedure (n = 10). The extracorporeal circuit consisted of a roller pump and a membrane oxygenator. Exhaled NO concentration was monitored with a chemiluminescence analyzer. After sacrifice, lungs were harvested for microscopic studies and to analyze the inducible nitric oxide synthase (iNOS) activity and expression (Western blot). ECC was responsible for an ALI characterized by a decreased arterial blood oxygen saturation (88.9% [51.7-94.2] vs. 93.7% [91.4-98.6] P = 0.005) and pulmonary histological changes (marked alveolar neutrophil infiltration; interstitial edema; intraalveolar hemorrhage). The lung injury score was significantly higher in the ECC group (n = 5; 3.0 [2-4]) in comparison to the sham group (n = 5; 1.0 [0-2]). Exhaled NO concentration remained stable throughout the experiment in all sham rats whereas it significantly increased in the ECC group from baseline (2 ppb [1-5]) until the end of experiment (33.5 ppb [1-47]). Lung iNOS activity and expression were also significantly increased in the ECC group. An increase in exhaled NO, however, did not correlate with the decrease in arterial oxygen pressure. ECC was responsible for an ALI in rats and for an elevated pulmonary NO production. Determination of the relationship between exhaled NO and the severity of the inflammatory process in ALI will require further studies.

Acute Disease↗
PubMed2004

Decreased exhaled nitric oxide as a marker of postinsult immune paralysis.

Nitric oxide (NO) regulates neutrophil migration and alveolar macrophage functions such as cytokine synthesis and bacterial killing, both of which are impaired in immune paralysis associated with critical illness. The aim of this study was to determine whether NO is involved in immune paralysis and whether exhaled NO measurement could help to monitor pulmonary defenses. NO production (protein expression, enzyme activity, end products, and exhaled NO measurements) was assessed in rats after cecal ligation and puncture to induce a mild peritonitis (leading to approximately 20% mortality rate). An early and sustained decrease in exhaled NO was found after peritonitis (from 1 to 72 h) compared with healthy rats [median (25th-75th percentile), 1.5 parts per billion (ppb) (1.2-1.7) vs. 4.0 ppb (3.6-4.3), P < 0.05], despite increased NO synthase-2 and unchanged NO synthase-3 protein expression in lung tissue. NO synthase-2 activity was decreased in lung tissue. Nitrites and nitrates in supernatants of isolated alveolar macrophages decreased after peritonitis compared with healthy rats, and an inhibitory experiment suggested arginase overactivity in alveolar macrophages bypassing the NO substrate. Administration of the NO synthase-2 inhibitor aminoguanidine to healthy animals reproduced the decreased neutrophil migration toward alveolar spaces that was observed after peritonitis, but L-arginine administration after peritonitis failed to correct the defect of neutrophil emigration despite increasing exhaled NO compared with D-arginine administration [4.8 (3.9-5.7) vs. 1.6 (1.3-1.7) ppb, respectively, P < 0.05]. In conclusion, the decrease in exhaled NO observed after mild peritonitis could serve as a marker for lung immunodepression.

Animals↗
PubMed2005

Exhaled 8-isoprostane in childhood asthma.

BACKGROUND: Exhaled breath condensate (EBC) is a non-invasive method to assess airway inflammation and oxidative stress and may be useful in the assessment of childhood asthma. METHODS: Exhaled 8-isoprostane, a stable marker of oxidative stress, was measured in EBC, in children (5-17 years) with asthma (13 steroid-naïve and 12 inhaled steroid-treated) and 11 healthy control. RESULTS: Mean exhaled 8-isoprostane concentration was significantly elevated in steroid-naïve asthmatic children compared to healthy children 9.3 (SEM 1.7) vs. 3.8 (0.6) pg/ml, p < 0.01. Children on inhaled steroids also had significantly higher 8-isoprostane levels than those of normal subjects 6.7 (0.7) vs. 3.8 (0.6) pg/ml, p < 0.01. Steroid-naïve asthmatics had higher exhaled nitric oxide (eNO) than those of controls 28.5 (4.7) vs. 12.6 (1.5) ppb, p < 0.01. eNO in steroid-treated asthmatics was similar to control subjects 27.5(8.8) vs. 12.6(1.5) ppb. Exhaled 8-isoprostane did not correlate with duration of asthma, dose of inhaled steroids or eNO. CONCLUSION: We conclude that 8-isoprostane is elevated in asthmatic children, indicating increased oxidative stress, and that this does not appear to be normalized by inhaled steroid therapy. This suggests that 8-isoprostane is a useful non-invasive measurement of oxidative stress in children and that antioxidant therapy may be useful in the future.

Adolescent↗
PubMed2004

Does the use of leucocyte depletion during cardiopulmonary bypass affect exhaled nitric oxide production?

Fifty patients undergoing elective coronary revascularisation were prospectively randomised to receive either a leucocyte-depleting or a control filter inserted into the arterial line of the cardiopulmonary bypass (CPB) circuit. The concentration of exhaled nitric oxide (NO) was measured 15 min before and 30 min after CPB using a real-time chemiluminescence analyser (Logan Research, Northampton, UK). The baseline rate of exhaled NO production was 2.14 +/- 0.83 ppb/s in the control group, and 2.58 +/- 0.53 ppb/s in leucocyte-depleted group (p = 0.17). Following CPB, the mean rate of exhaled NO production in the control group had increased by 1.51 +/- 0.45 ppb/s to 3.65 +/- 0.81 ppb/s and in the leucocyte- depletion group had increased by 1.05 +/- 0.45 ppb/s to 3.64 +/- 0.62 ppb/s. The increase in exhaled NO production was significantly lower in the leucocyte depleted group (p = 0.002), indicating that leucocyte depletion suppressed the increase in exhaled NO production seen following CPB.

Aged↗
PubMed2003

Effect of montelukast on exhaled nitric oxide and nonvolatile markers of inflammation in mild asthma.

STUDY OBJECTIVES: Leukotriene receptor antagonists appear to exert anti-inflammatory activity in asthma. We undertook the present study to evaluate the effect of montelukast on levels of exhaled nitric oxide (ENO) and two inflammatory markers, hydrogen peroxide (H(2)O(2)), and cysteinyl leukotrienes (cys-LTs), in the exhaled breath condensate of subjects with mild asthma. PATIENTS: Twenty stable subjects with mild asthma (15 women and 5 men; mean [+/- SD] age, 34.8 +/- 12.6 years) were included in the study. INTERVENTION: A 1-week run-in period was followed by 2 weeks of treatment (with montelukast or placebo) that was administered in randomized, double-blind, crossover fashion. One week of washout followed each treatment arm. RESULTS: Montelukast significantly reduced the levels of ENO from baseline (median, 52.5 parts per billion [ppb]; 25th to 75th percentile, 37.8 to 101.8 ppb) during the entire treatment period (ie, day 1 to day 14), with the effect measurable as early as day 1 (median, 45.9 ppb; 25th to 75th percentile, 29.3 to 92.5 ppb) and with the maximal effect being observed on day 7 (median, 35.7 ppb; 25th to 75th percentile, 27.6 to 66.6 ppb). The levels of ENO did not change significantly with placebo therapy. Montelukast improved symptom score and reduced peak expiratory flow (PEF) variability. Changes in PEF variability correlated positively with changes in ENO (r = 0.46; p = 0.04). No significant changes in FEV(1) or concentration of H(2)O(2) in the exhaled breath condensate were observed. Levels of cys-LTs were undetectable in the exhaled breath condensate. CONCLUSIONS: We concluded that montelukast reduces the levels of ENO in patients with mild asthma, a finding that is compatible with an anti-inflammatory effect of montelukast, and that ENO appears to be more sensitive in detecting this effect than FEV(1) and H(2)O(2) levels in the exhaled breath condensate.

Acetates↗
PubMed2005

Effect of montelukast on exhaled leukotrienes and quality of life in asthmatic patients.

STUDY OBJECTIVES: In some patients with asthma treated with inhaled corticosteroids, suppression of inflammation is incomplete. This may be because the effect of corticosteroids on cysteinyl-leukotriene (cys-LT) biosynthesis is limited. Montelukast is a cys-LT antagonist that significantly improves asthma control in corticosteroid-treated asthmatic patients. However, not all patients treated with cys-LT antagonists show a clinical improvement. DESIGN: We have studied the effect of treatment for 4 weeks with montelukast (10 mg/d) on exhaled cys-LTs and leukotriene B4 (LTB4), exhaled nitric oxide, asthma quality of life (AQL), and respiratory function in patients with stable asthma. SETTING: Asthma clinics in general practice. PATIENTS: We studied 50 patients (30 men; mean +/- SEM age, 53 +/- 2 years) who were treated with inhaled corticosteroids. MEASUREMENTS AND RESULTS: We detected cys-LTs in exhaled breath condensate in 25 of 50 patients; however, in the normal nonasthmatic subjects, cys-LTs were below the limit of detection. After treatment with montelukast, there was a fall in cys-LT concentrations from 14.6 +/- 3.3 to 8.5 +/- 2.6 pg/mL after 2 weeks (p > 0.05) and to 3.9 +/- 1.3 pg/mL after 4 weeks (p < 0.01). Exhaled LTB4 levels were also elevated. After treatment with montelukast, LTB4 levels fell from 33.0 +/- 3.9 to 20.4 +/- 2.5 pg/mL after 2 weeks of treatment (p < 0.05), and to 17.0 +/- 2.2 pg/mL after 4 weeks of treatment (p < 0.01). These changes in exhaled cys-LT and LTB4 were associated with significant improvements in AQL scores. CONCLUSIONS: It appears that in some patients with stable asthma treated with inhaled corticosteroids, the suppression of inflammation is incomplete. Adding a leukotriene receptor antagonist can provide a complementary effect of controlling inflammation, with a significant improvement in quality of life.

Acetates↗
PubMed2005

Exhaled breath condensate as a method of sampling airway nitric oxide and other markers of inflammation.

Most of the methods of investigating lung diseases have been invasive until the discovery that exhaled nitric oxide can be used as a surrogate marker of airway inflammation, particularly in asthma. Exhaled nitric oxide (NO) is now established as a marker of airway inflammation. It has been shown to correlate well with eosinophilic asthmatic airway inflammation, and to be able to predict decline in asthma control and airway function. Altered levels of NO are also associated with other inflammatory lung diseases. In addition, polymorphisms of the genes encoding the three nitric oxide synthases are associated with phenotypic differences associated with lung diseases. Exhaled NO is, however, non-specific. It is therefore of importance that collecting exhaled breath condensate (EBC) has emerged as a potential tool in the study of pulmonary diseases. The exhaled breath is collected in a cooling system which allows water vapour to condense. The EBC contains a number of mediators relating to the NO pathway, including nitrite as a metabolite of nitric oxide, nitrotyrosine, nitrosothiols plus small molecular mediators associated with oxidative stress, including hydrogen ions, and hydrogen peroxide. In addition, reports are emerging of the detection of larger molecules which not only include leukotrienes, prostaglandins, albumin and other proteins, such as cytokines, but also macromolecules, for example, DNA. EBC is becoming a technique which will allow repeated non-invasive sampling from the respiratory tract thus assisting pulmonary research and possibly the monitoring of lung diseases.

Animals↗
PubMed2005

Exhaled breath analysis: from occupational to respiratory medicine.

Breath analysis is a technique rapidly gaining ground as a non-invasive tool to diagnose and monitor various aspects of lung diseases. Measurement of exhaled breath is safe, rapid, simple to perform, and effort independent. Given that human breath contains upwards of 250 chemicals, the potential for developing new applications is high. Much of the current knowledge on breath analysis in respiratory medicine derives from years of experience gained in occupational settings, where breath analysis has been used mainly to assess exposure to volatile chemicals. Laboratory based analysis of exhaled air is a complex, expensive and time consuming process and thus is not in wide spread use in occupational medicine. However, recent knowledge of exhaled breath analysis in pulmonology, in particular in bronchial asthma and lung cancer, and the development of fast, and easy to perform non-invasive procedures for breath analysis, re-opened possible application of exhaled breath as a novel approach for biological monitoring of inhaled pneumotoxic substances. The simultaneous quantification of biomarkers of dose and effect in exhaled air may provide new insights into lung damage occurring in workers exposed to inhaled toxicants, thus representing a new and fascinating application in risk assessment strategies.

Breath Tests↗
PubMed2005

[Exhaled nitric oxide as a marker of diseases].

Recently a method to measure nitric oxide (NO) concentration in exhaled air has been developed. The method is non-invasive and easy to perform and it provides information on a fascinating molecule, with such extensive respiratory functions, ranging from bronchial and vascular dilation to ciliary motion and antibacterial defense. Nasal and sinus cavities are the site of major NO production, followed by airway and alveolar compartment. A very low nasal NO production is associated with ciliary dyskinesia, a disease characterized by severe chronic sinusitis and bronchiectasis. An increased concentration of NO in exhaled air has been reported in airway diseases, characterized by airway inflammation, such as bronchial asthma, where its concentration is related to bronchial hyperresponsiveness and sputum eosinophilia. Exhaled NO concentration in asthma is a sensitive marker of airway inflammation that reacts rapidly in response to treatment or exacerbation of disease. Clinical application of exhaled NO measurement include monitoring compliance and response to treatment, disease activity, diagnosis of asthma, and the prediction of acute exacerbations. Exhaled NO concentration may be increased also in other diseases, as COPD, bronchiectasis and some connective tissue diseases (SLE and systemic sclerosis). An increased NO production from alveolar source has been shown to be involved in oxygenation impairment of patients with liver disease, particularly in case of hepato-pulmonary syndrome.

Asthma↗
PubMed2006

Moderate exercise decreases nitric oxide exhalation in patients with stable coronary artery disease.

Nitric oxide (NO) is present in exhaled air in humans and its level may decrease in heart diseases. Nitrates are metabolised to NO. In the present study we prospectively investigated how coronary disease treated with oral nitrates and physical exercise influence the exhaled NO concentration (exNO). The study was performed in 44 patients with stable coronary artery disease (CAD) treated with oral nitrates (31 nonsmokers and 13 smokers). End-tidal concentration of exhaled NO was measured by the use of a chemiluminescence method. The Bruce protocol of an exercise test was performed in 21 coronary patients and 11 volunteers. NO was measured before and 2-5 min after the test. We found no significant differences in the exNO level between healthy controls and CAD patients as analyzed either for the whole groups or non-smoker and smoker subgroups (6.01 parts per billion (ppb) vs. 4.91 ppb; 7.02 ppb vs. 5,89 ppb; 3.62 ppb vs. 3.33 ppb, respectively). However, the coronary patients group, as a whole, had lower exNO after exercise (4.22 ppb vs. 3,84 ppb, P<0.01). The difference persisted after division of this group into non-smokers and smokers; 5.19 ppb vs. 4,79 ppb, P<0.05 and 3.63 ppb vs. 3.27 ppb, P<0.05, respectively). The level of exNO changed inappreciably after exercise in control subjects. We conclude that coronary disease and oral nitrates, in themselves, do not influence the exhaled NO concentration. Physical exercise, on the other side, lowers the exhaled NO level in coronary patients.

Breath Tests↗
PubMed2000

Exhaled nitric oxide in children measured by tidal breathing method: differences between asthmatics and nonasthmatic controls.

The single-breath maneuver used to measure nitric oxide (NO) in adults cannot be performed by young children. We, therefore, developed a method of measuring NO in mixed exhaled gas collected during tidal breathing. NO was measured in mixed exhaled gas during 5 min of tidal breathing in 113 children 4-14 years of age: 22 nonasthmatics, 21 asthmatic children not taking inhaled corticosteroids, and 70 asthmatic children using inhaled corticosteroids. Exhaled NO levels (median, range) were significantly lower in nonasthmatic controls (median, range: 7, 2-10 ppb) than in asthmatic children on inhaled corticosteroids (8, 3-25 ppb; 95% CI for difference in medians with those of controls, 0-4 ppb), and in those not on inhaled corticosteroids (13, 6-37, ppb; 95% CI for difference in medians, 5-17 ppb). Asthmatic children not using inhaled corticosteroids had significantly higher exhaled NO levels than asthmatic children using inhaled corticosteroids (95% CI for difference in medians, 3-10 ppb). The tidal breathing method is a useful and practical way of measuring exhaled NO levels in children regardless of their age.

Administration, Inhalation↗