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Published ahead of print on November 10, 2005, doi:10.1164/rccm.200507-1059OC

Am. J. Respir. Crit. Care Med., Volume 173, Number 4, February 2006, 386-392

A more recent version of this article appeared on February 15, 2006
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Submitted on July 10, 2005
Accepted on November 9, 2005

The Effects of Volatile Salivary Acids and Bases upon Exhaled Breath Condensate pH

Richard M Effros1*, Richard Casaburi2, Jennifer Su2, Marshall Dunning3, John Torday2, Julie Biller3, and Reza Shaker3

1 Department of Medicine, Los Angeles Biomedical Research Institute at Harbor- UCLA Medical Center, Torrance, CA, USA; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA, 2 Department of Medicine, Los Angeles Biomedical Research Institute at Harbor- UCLA Medical Center, Torrance, CA, USA, 3 Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA

* To whom correspondence should be addressed. E-mail: reffros{at}labiomed.org.

Rationale: Recent studies have reported acidification of exhaled breath condensate (EBC) in inflammatory lung diseases. This phenomenon, designated "acidopnea," has been attributed to airway inflammation. Objectives: To determine whether salivary acids and bases can influence EBC pH in chronic obstructive pulmonary disease (COPD). Methods: Measurements were made of pH, electrolytes, and volatile bases and acids in saliva and EBC equilibrated with air of 10 healthy subjects and 10 patients. Results: The average EBC pH in COPD was reduced (normal = 7.24 ± 0.24 SEM., range: 6.11-8.34; COPD = 6.67 ± 0.18, range: 5.74-7.64; p = 0.079). EBCs were well buffered by NH4+/NH3 and CO2/HCO3- in all but 4 patients, who had NH4+ concentrations under 60 micromoles/liter and acetate concentrations that approached or exceeded those of NH4+. Saliva contained high concentrations of acetate (~6,000 µM) and NH4+ (~12,000 µM). EBC acetate increased and EBC NH4+ decreased when salivary pH was low, consistent with a salivary source for these volatile constituents. Nonvolatile acids did not play a significant role in determining pH of condensates because of extreme dilution of respiratory droplets by water vapor (~1:12,000). Transfer of both acetic acid and NH3 from the saliva to the EBC was in the gas phase rather than droplets. Conclusions: EBC acidification in chronic obstructive pulmonary disease can be affected by the balance of volatile salivary acids and bases, suggesting that EBC pH may not be a reliable marker of airway acidification. Salivary acidification may play an important role in acidopnea.
Key words: Exhaled breath condensate, buffer, ammonium, bicarbonate, acetate




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