Lung cancer is the leading cause of cancer death. Results of therapeutic interventions are particularly discouraging when the disease is discovered in an advanced stage. Early diagnosis is limited by the fact that the disease usually develops asymptomatically and available screening methods do not fulfil the requirements for reliable discrimination between patients with lung cancer and subjects not suffering from the disease. Breath sampling is completely noninvasive and provides a potentially useful approach to screening lung cancer. Exhaled biomarkers contain both volatile and nonvolatile molecules. The profile of volatile organic compounds is different in patients with lung cancer than in control subjects. In exhaled breath condensate, the proteomic profile of breath from cancer patients differs from that of healthy smokers. We reviewed the scientific evidence demonstrating that a unique chemical signature can be detected in the breath of patients with lung cancer and that the exhaled breath biomarker profile could aid clinical decision making.

Exhaled breath condensate (EBC) pH is considered to reflect the acid-base balance of the airways. Current pH measurements do not take into account the effect of CO₂. The aim of the present study was to determine the effect of condensate CO₂partial pressure on pH and to provide a more precise mode of EBC pH determination.Condensate pH and CO₂partial pressure were measured in parallel from 12 healthy volunteers and 12 asthmatics using a blood gas analyser in neat, argon de-aerated and CO₂-loaded samples. The regression analysis was used to test the relationship between pH and CO₂, and to calculate the pH at a CO₂level of 5.33 kPa (physiological alveolar CO₂partial pressure). Reproducibility of different pH readings was compared using the Bland–Altman test.Condensate CO₂concentration was variable both in neat and argon de-aerated samples. There was a close negative logarithmic relationship between CO₂and pH. Calculation of pH at a CO₂level of 5.33 kPa provided reproducibility approximately six times as good as that of the currently used measurements.Condensate CO₂partial pressure influences pH measurements. Determination of pH at a standard CO₂level provides the most reproducible condensate pH values to date.

Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder that may lead to gas exchange abnormalities, including hypercapnia. Chronic hypercapnia is an independent risk factor of mortality in COPD, leading to epithelial dysfunction and impaired lung immunity. Moreover, chronic hypercapnia affects the cardiovascular physiology, increases the risk of cardiovascular morbidity and mortality, and promotes muscle wasting and musculoskeletal abnormalities. Noninvasive ventilation is a widely used technique to remove carbon dioxide, and several studies have investigated its role in COPD. In the present review, we aim to summarize the causes and effects of chronic hypercapnia in COPD. Furthermore, we discuss the use of domiciliary noninvasive ventilation as a treatment option for hypercapnia while highlighting the controversies within the evidence. Finally, we provide some insightful clinical recommendations and draw attention to possible future research areas.

Rationale: Exhaled breath condensate pH has been proposed as a noninvasive marker of airway inflammation. However, due to standardization difficulties in pH measurement techniques, different pH readings were obtained in previous studies. Objectives: In this longitudinal study we assessed condensate pH in patients with an exacerbation of asthma or chronic obstructive airway disease using the very precise carbon dioxide standardization method that negates the effect of this gas on condensate acidity. Methods: Condensate pH, fractional exhaled nitric oxide, lung function, and blood gases were measured in 20 nonsmoking patients with asthma and 21 smoking and 17 ex-smoking patients with chronic obstructive airway disease first at hospital admission due to an acute exacerbation of the disease and again at discharge after treatment. Condensate pH was also assessed in 18 smoking and 18 nonsmoking healthy control subjects. Measurements and Main Results: In patients with asthma, condensate pH was significantly decreased at the time of exacerbation compared with nonsmoking control subjects and increased with treatment. In patients with chronic obstructive airway disease, condensate pH remained unchanged during exacerbation, both in smokers and ex-smokers. Nevertheless, condensates collected from smokers were more acidic than those of ex-smokers. A similar difference was observed between smoker and nonsmoker healthy control subjects. No correlations were found between condensate pH and fractional exhaled nitric oxide or lung function variables measured either at admission or discharge. Conclusions: Our data suggest that exacerbation of asthma, but not chronic obstructive airway disease, is associated with acidification of breath condensate.

Electronic noses (e-noses) represent an easy and cheap method for exhaled volatile compound analysis. Various electronic noses are available which differ in material and thus analytical performance. In this review, we describe a wide range of electronic noses and summarize data on the methodological issues in electronic nose research. We also review studies which show the ability of electronic noses to distinguish pulmonary and extrapulmonary disorders from health.

Myeloid and plasmacytoid dendritic cells (mDCs, pDC) are crucial to the immune system, detecting microorganisms and linking the innate and adaptive immunity. pDC are present in small quantities in tissues that are in contact with the external environment; mainly the skin, the inner lining of the nose, lungs, stomach and intestines. They produce large amounts of IFN-α after stimulation and are pivotal for the induction of antiviral responses. Chronic obstructive pulmonary disease (COPD) patients are known to be more susceptible to viral infections. We have demonstrated that exposure of mDC to cigarette smoke extract (CSE) leads to the release of chemokines, however, not much is known about the role of pDC in COPD. In this study, we addressed several key questions with respect to the mechanism of action of CSE on human pDC in an in vitro model. Human pDCs were isolated from normal healthy volunteers and subjected to fresh CSE and the levels of IL-8, TNF-α, IP-10, IL-6, IL-1, IL-12 and IL-10 and IFN-α were studied by both ELISA and real time PCR methods. We observed that CSE augmented the production of IL-8 and suppressed the release of TNF-α, IL-6 and IFN-α. Moreover, CSE suppressed PI3K/Akt signalling in pDC. In conclusion, our data indicate that CSE has both the potential to diminish anti-viral immunity by downregulating the release of IFN-α and other pro-inflammatory cytokines while, at the same time, augmenting the pathogenesis of COPD via an IL-8 induced recruitment of neutrophils.