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Eur Respir J 2004; 23:961-962
Copyright ©ERS Journals Ltd 2004


Exhaled breath condensate pH

R.M. Effros

Harbor-UCLA Medical Center, Torrance, USA.

To the Editor:

Vaughan et al. 1 are to be congratulated for the most extensive study of the pH of exhaled breath condensates (EBC) yet reported. However, there is reason to doubt that the pH of the condensate provides a reliable measure of the pH of fluid lining the airways. As noted in our recent study 2, the average concentration of NH4+ is 20 times greater than that of any other EBC cation in normal condensates, and NH4+ accounts for most of the ions and buffer in the condensate (as judged by total conductivity).

Several previous studies have shown that most of this NH4+ is derived from NH3 generated in the mouth, in part from the bacterial degradation of urea 24. In the study by Vaughan et al. 1, collection of condensates through endotracheal tubes did not seem to have an effect upon average pH. Since both intubation and tracheostomy significantly reduce NH4+ concentrations of the EBC 2, they should be associated with more acidic condensates. This paradox could only be explained if intubation also reduced concentrations of some atmospheric or oral acid (e.g. residual CO2 or acetic acid) in the EBC. It must be concluded that the pH of normal condensates reflects buffering by these volatile constituents from the mouth, rather than buffers in the airway fluid, and therefore EBC pH cannot provide reliable estimates of airway pH.

Although the normal condensate pH is set by oral and atmospheric buffers, Hunt and coworkers 5 observed "acidopnoea" in asthmatics, which they attributed to airway acidification. We have suggested that reductions in exchange of NH3 in the mouth and condenser are responsible in part for the reduction in EBC NH4+ seen in asthmatics 7, and consequently contribute to acidification. It is also possible that reflux of gastric fluid, which is extraordinarily common in asthmatics 8, is responsible for EBC acidification. Aerosolisation of tiny quantities of gastric acid (pH often 1–2) from the stomach or pharynx would be difficult to avoid or detect in these patients but could have a profound effect on EBC pH.

References

  1. Vaughan J, Ngamtrakulpanit L, Pajewski TN, et al. Exhaled breath condensate pH is a robust and reproducible assay of airway acidity. Eur Respir J 2003;22:889–894.[Abstract/Free Full Text]
  2. Effros RM, Biller J, Foss B, et al. A simple method for estimating respiratory solute dilution in exhaled breath condensates. Am J Respir Crit Care Med 2003;168:1500–1505.[Abstract/Free Full Text]
  3. Norwood DM, Wainman T, Lioy PJ, Waldman JM. Breath ammonia depletion and its relevance to acidic aerosol exposure studies. Arch Environ Health 1992;47:309–313.[ISI][Medline] [Order article via Infotrieve]
  4. Vass G, Huszar E, Barat E, et al. Comparison of nasal and oral inhalation during exhaled breath condensate collection. Am J Respir Crit Care Med 2003;167:850–855.[Abstract/Free Full Text]
  5. Hunt J, Fang K, Malik R, et al. Endogenous airway acidification: implications for asthma pathophysiology. Am J Respir Crit Care Med 2000;161:694–699.[Abstract/Free Full Text]
  6. Hunt JF, Erwin E, Palmer L, et al. Expression and activity of pH-regulatory glutaminase in the human airway epithelium. Am J Respir Crit Care Med 2002;165:101–107.[Abstract/Free Full Text]
  7. Effros RM. Do low exhaled NH4+ concentrations in asthma reflect reduced pulmonary production?. Am J Respir Crit Care Med 2003;167:91–92.[Free Full Text]
  8. Harding SM. Recent clinical investigations examining the association of asthma and gastroesophageal reflux. Am J Med 2003;115:137–143.[CrossRef]




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