TY - JOUR
T1 - Evaluation of exhaled breath condensate pH as a biomarker for COPD
AU - MacNee, William
AU - Rennard, Stephen I.
AU - Hunt, John F.
AU - Edwards, Lisa D.
AU - Miller, Bruce E.
AU - Locantore, Nicholas W.
AU - Tal-Singer, Ruth
N1 - Funding Information:
We would like to express our thanks to all subjects who took part in these studies. All three studies were funded by GlaxoSmithKline .
Funding Information:
Professor William MacNee: WMcN has been reimbursed for travel by GlaxoSmithKline, AstraZeneca, Boehringer Ingelheim, Pfizer and Micromet for attending conferences. WMcN has received honoraria from GlaxoSmithKline and AstraZeneca for participating as a speaker in scientific meetings. WMcN serves on advisory boards for GlaxoSmithKline, Pfizer, Almirall, Amgen, Bayer and Micromet. WMcN serves as a consultant for Pfizer and SMB Pharmaceuticals. Research grants to support work carried out in WMcN’s laboratory comes from SMB, Pfizer, GlaxoSmithKline and Novartis.
Funding Information:
Please note that StIR has had tobacco industry funding. Specifically, StIR has received funding from the tobacco industry for studies relating to harm reduction and to the impact of tobacco smoke on stem cells. StIR has also consulted with RJ Reynolds without personal fee on the topic of harm reduction. StIR received funding from RJ Reynolds to evaluate the effect of a harm reduction product in normal smokers (1996) and in subjects with chronic bronchitis (1999) and to assess the effect of smoking cessation on lower respiratory tract inflammation (2000); StIR participated in a Philip Morris multi-center study to assess biomarkers of smoke exposure (2002); StIR received funding for a clinical trial from the Institute for Science and Health (2005), which receives support from the tobacco industry, to evaluate biomarkers in exhaled breath associated with smoking cessation and reduction. This study was supplemented with funding from Lorillard and RJ Reynolds. StIR has received a grant from the Philip Morris External Research Program (2005) to assess the impact of cigarette smoking on circulating stem cells in the mouse. StIR has consulted with RJ Reynolds on the topic of harm reduction until 2007, but did not receive personal remuneration for this. There are no active tobacco-industry funded projects. All ties with tobacco industry companies and entities supported by tobacco companies were terminated in 2007.
Funding Information:
John Hunt, MD: JH is a co-founder of Respiratory Research, Inc., which develops exhaled breath assays and manufactures the RTubes used in this study. Respiratory Research has also provided funding for his laboratory. His University of Virginia research lab receives funding indirectly from Philip Morris through the University of Virginia Phillip Morris Tobacco Research Program, over which Phillip Morris has no supervision authority.
PY - 2011/7
Y1 - 2011/7
N2 - Introduction: We assessed the utility of EBC pH as a biomarker in COPD in a large cohort of well-characterised individuals with COPD and control subjects from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study. We also determined short term reproducibility and the response of EBC to oral prednisolone. Methods: EBC was collected with R-TubesTM, using techniques for sampling and measurement that have been shown to be reproducible. Results: EBC pH was lower in COPD (n = 676, 7.29 ± SD 0.60) and in smoking controls (n = 31, 7.18 ± 0.85), compared with non-smoking controls (n = 50, 7.59 ± 0.44, p = 0.0008 and 0.0033 respectively), but was not different between COPD and smoking controls. There was no relationship between EBC pH and disease severity, as assessed by the percent predicted FEV1, nor with airway inflammation as assessed by sputum leukocyte counts. Treatment with 20 mg.day-1 prednisolone for 4 weeks did not change EBC pH. Conclusion: EBC pH is lower in COPD than in healthy control non-smokers, but does not differentiate COPD from smokers without COPD, relate to disease severity or to airway inflammation, and does not respond to corticosteroids. EBC pH therefore does not appear to be a useful biomarker in COPD.
AB - Introduction: We assessed the utility of EBC pH as a biomarker in COPD in a large cohort of well-characterised individuals with COPD and control subjects from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study. We also determined short term reproducibility and the response of EBC to oral prednisolone. Methods: EBC was collected with R-TubesTM, using techniques for sampling and measurement that have been shown to be reproducible. Results: EBC pH was lower in COPD (n = 676, 7.29 ± SD 0.60) and in smoking controls (n = 31, 7.18 ± 0.85), compared with non-smoking controls (n = 50, 7.59 ± 0.44, p = 0.0008 and 0.0033 respectively), but was not different between COPD and smoking controls. There was no relationship between EBC pH and disease severity, as assessed by the percent predicted FEV1, nor with airway inflammation as assessed by sputum leukocyte counts. Treatment with 20 mg.day-1 prednisolone for 4 weeks did not change EBC pH. Conclusion: EBC pH is lower in COPD than in healthy control non-smokers, but does not differentiate COPD from smokers without COPD, relate to disease severity or to airway inflammation, and does not respond to corticosteroids. EBC pH therefore does not appear to be a useful biomarker in COPD.
KW - Biomarkers
KW - COPD
KW - Exhaled breath condensate
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U2 - 10.1016/j.rmed.2011.02.009
DO - 10.1016/j.rmed.2011.02.009
M3 - Article
C2 - 21377342
AN - SCOPUS:79957521375
VL - 105
SP - 1037
EP - 1045
JO - Respiratory Medicine
JF - Respiratory Medicine
SN - 0954-6111
IS - 7
ER -