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Correspondence |

Why Conventional Exhaled Breath Condensate pH Studies Cannot Provide Reliable Estimates of Airway AcidificationExhaled Breath Condensate pH FREE TO VIEW

Richard M. Effros, MD; Richard Casaburi, MD, PhD, FCCP; Janos Porszasz, MD; Virender Rehan, MD; for the National Heart, Lung, and Blood Institute Severe Asthma Research Program (SARP)
Author and Funding Information

From the Department of Medicine (Drs Effros, Casaburi, and Porszasz) and the Department of Pediatrics (Dr Rehan), Los Angeles Biomedical Research Institute at Harbor, University of California, Los Angeles Medical Center.

Correspondence to: Richard M. Effros, MD, LABiomed, 1124 W Carson St, Bldg J4, Torrance, CA 90502; e-mail: reffros@labiomed.org


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Funding/Support: This work was supported by the National Institutes of Health [Grants HL75405 and HD51857].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(4):1099. doi:10.1378/chest.11-0974
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In a recent article in CHEST (February 2011), the failure of Liu et al1 to confirm earlier reports of decreased exhaled breath condensate (EBC) pH among patients with asthma2 is disappointing but may have been inevitable because of some fundamental misconceptions in conventional EBC pH studies. Although EBC acidification is used to detect acidification of airway lining fluid (ALF), ALF pH cannot be estimated from EBC pH unless the buffer capacities of ALF and EBC are also known. It is likely that the principal buffers in ALF are nonvolatile and similar to those in plasma, primarily proteins and phosphates. In contrast, NH4+/NH3 usually accounts for ∼ 90% of buffering in EBC.3,4 Most of this volatile constituent is derived from the diffusion of gaseous NH3 from saliva into exhaled air, and it is associated with the equilibration of CO2/bicarbonate (HCO3) at ambient Pco2.3,4 Unfortunately, the relatively high concentrations of NH4+/NH3 and CO2/HCO3 found in most EBC samples overwhelm any effects that metabolic acids in the miniscule amounts of ALF present in EBC can have on EBC pH. It has been argued that because changes in NH4+ concentration have a relatively modest effect on EBC pH, they can be ignored.5 This is patently incorrect because changes in buffer concentrations typically have modest effects on pH but have profound effects on buffer capacity. The buffer capacity of EBC must increase with NH4+, thereby reducing any impact that ALF acids have on EBC pH.

Conventional EBC pH studies also fail to consider or measure the dilution of ALF by condensed water vapor, which is large and variable (∼ 5,000-20,000 fold). The effect of nonvolatile acids in ALF on EBC pH will obviously be less when the dilution is increased. In view of the dominance of oral NH3 on EBC pH, investigators should measure specific ions in EBC (eg, lactate), indicating metabolic acids from the ALF. Furthermore, sensitive amylase measurements should be routinely made to estimate salivary contamination.3 Some low EBC pH values that have been reported may reflect acid reflux, suggesting that gastric markers should also be measured. Efforts to remove CO2 by bubbling argon through the EBC1,2 are unwise because measurements are not made of the effects of purging on CO2, NH4+/NH3, water, or other volatile constituents. Unless these problems are addressed, it is unlikely that EBC pH will ever become a reliable indicator of pulmonary airway acidosis or inflammation. The expenditure of additional time and scarce resources on conventional EBC pH measurements would, therefore, seem unjustified.

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscript.

Other contributions: This work was performed at the Los Angeles Biomedical Research Institute at Harbor, University of California, Los Angeles Medical Center.

Liu L, Teague WG, Erzurum S, et al; for the National Heart, Lung, and Blood Institute Severe Asthma Research Program (SARP) for the National Heart, Lung, and Blood Institute Severe Asthma Research Program (SARP) Determinants of exhaled breath condensate pH in a large population with asthma. Chest. 2011;1392:328-336 [CrossRef] [PubMed]
 
Hunt JF, Fang K, Malik R, et al. Endogenous airway acidification. Implications for asthma pathophysiology. Am J Respir Crit Care Med. 2000;1613 pt 1:694-699 [PubMed]
 
Effros RM, Casaburi R, Su J, et al. The effects of volatile salivary acids and bases on exhaled breath condensate pH. Am J Respir Crit Care Med. 2006;1734:386-392 [CrossRef] [PubMed]
 
Effros RM, Casaburi R, Porszasz J. Assessment of exhaled breath condensate pH. Am J Respir Crit Care Med. 2011;1837:952 [PubMed]
 
Wells K, Vaughan J, Pajewski TN, et al. Exhaled breath condensate pH assays are not influenced by oral ammonia. Thorax. 2005;601:27-31 [CrossRef] [PubMed]
 

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References

Liu L, Teague WG, Erzurum S, et al; for the National Heart, Lung, and Blood Institute Severe Asthma Research Program (SARP) for the National Heart, Lung, and Blood Institute Severe Asthma Research Program (SARP) Determinants of exhaled breath condensate pH in a large population with asthma. Chest. 2011;1392:328-336 [CrossRef] [PubMed]
 
Hunt JF, Fang K, Malik R, et al. Endogenous airway acidification. Implications for asthma pathophysiology. Am J Respir Crit Care Med. 2000;1613 pt 1:694-699 [PubMed]
 
Effros RM, Casaburi R, Su J, et al. The effects of volatile salivary acids and bases on exhaled breath condensate pH. Am J Respir Crit Care Med. 2006;1734:386-392 [CrossRef] [PubMed]
 
Effros RM, Casaburi R, Porszasz J. Assessment of exhaled breath condensate pH. Am J Respir Crit Care Med. 2011;1837:952 [PubMed]
 
Wells K, Vaughan J, Pajewski TN, et al. Exhaled breath condensate pH assays are not influenced by oral ammonia. Thorax. 2005;601:27-31 [CrossRef] [PubMed]
 
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