Scientific background

Scientific background

H2O2 in airway inflammation 

During chronic airway inflammation, the production of reactive oxygen species by activated inflammatory cells, including neutrophils, alveolar macrophages and eosinophils, exceeds neutralization by the body, resulting in oxidative stress. This can lead to further generation of inflammatory mediators, causing damage to epithelial cells, increased bronchial hyperreactivity and potentially aberrant growth of lung epithelial cells. 1

Reactive oxygen species are metabolized in cells to produce highly reactive oxidants such as H2O2, which is volatile and readily equilibrates with air and can be detected in EBC. 2, 3 Measurement of EBC H2O2 can therefore be used a quantitative measure of oxidative stress and airway inflammation,4, 5 but, until now, this has required complex multi-step processing of collected breath samples, limiting its use to research settings. 3

Previous studies have shown that EBC H2O2 levels are significantly higher in patients with COPD than in healthy controls, 6 and that levels rise further during exacerbations; there is also some evidence that EBC H2O2 levels correlate with disease severity. 4 EBC H2O2 levels are also significantly higher in patients with asthma (non-smokers) than in healthy subjects. 7, 8 The level of EBC H2O2 also correlated with asthma severity and phenotype: levels were significantly higher in moderate asthma than mild asthma, and in patients with neutrophil-predominant airway inflammation. 9, 10. Furthermore, levels of EBC H2O2 were higher in patients with uncontrolled asthma than in those with controlled disease and healthy controls. 11

  1. Goldkorn T et al. (2014) Lung injury and lung cancer caused by cigarette smoke-induced oxidative stress: Molecular mechanisms and therapeutic opportunities involving the ceramide-generating machinery and epidermal growth factor receptor. Antioxid Redox Signal 21: 2149-74.
  2. Horvath I et al. (2017) A European Respiratory Society technical standard: exhaled biomarkers in lung disease. Eur Respir J 49.
  3. Konstantinidi EM et al. (2015) Exhaled breath condensate: Technical and diagnostic aspects. ScientificWorldJournal 2015: 435160.
  4. Kostikas K et al. (2003) Oxidative stress in expired breath condensate of patients with COPD. Chest 124: 1373-80.
  5. Sugiura H and Ichinose M (2008) Oxidative and nitrative stress in bronchial asthma. Antioxid Redox Signal 10: 785-97.
  6. Dekhuijzen PN AK, Dekker I, Aarts LP, Wielders PL, van Herwaarden CL, Bast A. (1996) Increased exhalation of hydrogen peroxide in patients with stable and unstable chronic obstructive pulmonary disease. Am J Respir Crit Care Med 154: 813-6.
  7. Al Obaidi AH (2007) Expired breath condensate hydrogen peroxide concentration and pH for screening cough variant asthma among chronic cough. Ann Thorac Med 2: 18-22.
  8. Teng Y et al. (2011) Hydrogen peroxide in exhaled breath condensate in patients with asthma: a promising biomarker? Chest 140: 108-16.
  9. Antczak A et al. (1999) Hydrogen peroxide in expired air condensate correlates positively with early steps of peripheral neutrophil activation in asthmatic patients. Arch Immunol Ther Exp (Warsz) 47: 119-26.
  10. Loukides S et al. (1998) Elevated levels of expired breath hydrogen peroxide in bronchiectasis. American Journal of Respiratory and Critical Care Medicine 158: 991-5.
  11. Trischler J et al. (2012) Fractionated breath condensate sampling: H2O2 concentrations of the alveolar fraction may be related to asthma control in children. Respir Res 13: 14.