Opinion - (2025) Volume 14, Issue 1
Received: 03-Feb-2025, Manuscript No. MBL-25;
Editor assigned: 05-Feb-2025, Pre QC No. P-165496;
Reviewed: 17-Feb-2025, QC No. Q-165496;
Revised: 24-Feb-2025, Manuscript No. R-165496;
Published:
04-Mar-2025
, DOI: 10.37421/2168-9547.2025.14.476
Citation: Bah, Hassan. “Hydrogen Peroxide in Exhaled Breath Condensate as a Biomarker of Respiratory Inflammation.” Mol Biol 14 (2025): 476.
Copyright: © 2025 Bah H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Hydrogen peroxide plays a central role in host immune defense and inflammatory signaling within the respiratory tract. During episodes of pulmonary inflammation whether triggered by allergens, pathogens, pollutants, or underlying chronic disease activated leukocytes generate Reactive Oxygen Species (ROS) through enzymatic processes involving NADPH oxidase and myeloperoxidase systems. Among these ROS, hydrogen peroxide serves both as a mediator of cellular signaling and a marker of oxidative injury. Its presence in the airway surface liquid can be detected via collection of exhaled breath condensate, a method that involves the non-invasive condensation of humidified exhaled air using cooled surfaces. This technique captures aerosolized particles and volatile biomarkers from the lower respiratory tract, reflecting the biochemical milieu of the airway lining fluid [2].
Numerous studies have demonstrated that Hâ??Oâ?? levels in EBC are significantly elevated in individuals with respiratory conditions characterized by chronic or acute inflammation. In asthmatic patients, for example, elevated EBC hydrogen peroxide concentrations have been positively correlated with disease severity, airway hyperresponsiveness and exacerbation frequency. Similarly, in COPD, increased Hâ??Oâ?? in EBC reflects heightened neutrophilic inflammation and oxidative stress, both of which contribute to progressive airflow limitation and tissue remodeling. Interventional studies further support the utility of Hâ??Oâ?? as a dynamic biomarker; reductions in EBC hydrogen peroxide levels following treatment with inhaled corticosteroids, antioxidants, or anti-inflammatory agents suggest that it may serve as a responsive indicator of therapeutic efficacy [3].
Despite its promise, the clinical application of hydrogen peroxide in EBC faces several methodological and interpretative challenges. The lack of standardized protocols for EBC collection, storage and analysis contributes to inter-study variability and complicates the establishment of diagnostic thresholds. Techniques for quantifying Hâ??Oâ??, such as colorimetric assays using horseradish peroxidase and fluorometric detection, vary in sensitivity, specificity and susceptibility to contamination. Furthermore, Hâ??Oâ?? concentrations in EBC can be influenced by numerous extrinsic factors including ambient air pollution, recent dietary intake, smoking status and recent physical exertion. These confounding variables must be accounted for to ensure accurate and reproducible measurements. Current research efforts are focused on refining analytical methodologies, enhancing assay robustness and developing portable biosensors for point-of-care use [4].
Additionally, the interpretation of EBC hydrogen peroxide levels must be contextualized within a broader clinical and biological framework. It is increasingly recognized that respiratory diseases are phenotypically heterogeneous; thus, Hâ??Oâ?? may serve different diagnostic or prognostic roles across disease subtypes. For instance, in eosinophilic asthma, elevated Hâ??Oâ?? may reflect a distinct inflammatory endotype compared to neutrophilic asthma or non-inflammatory airflow limitation. Integration of Hâ??Oâ?? data with other biomarkers (e.g., nitric oxide, cytokines, lipid peroxidation products) and clinical parameters (spirometry, imaging, symptom scores) could enhance its diagnostic value and allow for a more nuanced understanding of disease activity [5].
Google Scholar Cross Ref Indexed at
Google Scholar Cross Ref Indexed at
Google Scholar Cross Ref Indexed at
Google Scholar Cross Ref Indexed at
Google Scholar Cross Ref Indexed at
Molecular Biology: Open Access received 607 citations as per Google Scholar report