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Communications to the Editor |

Heat It or Wet It? Nasal Symptoms Secondary to the Use of Continuous Positive Airway Pressure in Sleep Apnea FREE TO VIEW

Lee K. Brown, MD, FCCP
Author and Funding Information

New Mexico Center for Sleep Medicine, Lovelace Health Systems, and the University of New Mexico School of Medicine Albuquerque, NM

Correspondence to: Lee K. Brown, MD, FCCP, Clinical Professor of Medicine, University of New Mexico School of Medicine, Medical Director, New Mexico Center for Sleep Medicine, Associate Medical Director (Medical Specialties), Lovelace Health Systems Inc, 4700 Jefferson Blvd NE, Suite 800, Albuquerque, NM 87109; e-mail: lkbrown@alum.mit.edu



Chest. 2001;119(1):310-312. doi:10.1378/chest.119.1.310-a
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Published online

To the Editor:

I thank Dr. Winck and colleagues for their interesting letter on the objective salutary effect of warming nasal continuous positive airway pressure (CPAP) air on their patient’s nasal symptoms. They raise the interesting question of whether nasal symptoms are the result of the low temperature, the low relative humidity (rH), or both. Unfortunately, published studies on this subject do not currently provide the answer, since none specifically address the condition of warm air and low humidity. For instance, Richards and colleagues1 examined nasal airway resistance in patients with mouth leaks using nasal CPAP air conditioned in a variety of ways. This included the following: cold dry air (temperature, 22.4 to 23.2°C; rH, 61 to 67%); cold humidified air (temperature, 22.8 to 23.6°C; rH, 97 to 100%); warmer humidified air (temperature, 30°C; rH, 97 to 100%); and body temperature humidified air (temperature, 37°C; rH, 97 to 100%). They demonstrated that most of the fall in nasal resistance from baseline occurred when rH was increased even if the air remained cool, while further heating of the air while maintaining the same, almost fully saturated, humidity did not result in much additional benefit. Unfortunately, they did not test the condition of heated, relatively dry air as suggested by Winck and coworkers.

Togias and colleagues2have outlined a mechanism by which nasal mucosal drying could cause an inflammatory response resulting in nasal symptoms. They challenged subjects with cold dry air and measured the osmolality of nasal secretions, nasal symptoms, and the concentration of inflammatory mediators. They were able to demonstrate that osmolality correlated with the level of inflammatory mediators in those subjects who developed nasal symptoms in response to the challenge. Other workers have demonstrated that isolated mast cells exposed to a hyperosmolar medium will release inflammatory mediators.34 Finally, a large body of evidence has emerged suggesting that a similar phenomenon, that of exercise-induced asthma, is the result of water loss from the respiratory mucosa rather than heat loss, although this is still somewhat controversial.56

While I applaud the results obtained by Winck and colleagues in treating their patient with warmed, but not humidified, CPAP air, I remain skeptical that this method will be universally applicable. Certainly, there is no harm in asking patients complaining of nasal symptoms from their CPAP to take the simple measure of placing the circuit under the bedclothes; this procedure is, in fact, commonly recommended by durable medical equipment suppliers in our area. However, if symptoms do not resolve readily, then elimination of mouth leaks and heated humidification should be pursued. In addition, since Dr. Winck and coworkers have the technology to pursue objective evidence that warmed, unhumidified CPAP air reduces nasal symptoms, I would encourage them to continue this line of investigation. They should also measure the CPAP air temperature at the mouth to provide evidence that routing the CPAP circuit under the bedclothes does indeed provide significant warming.

References

Richards, GN, Cistulli, PA, Ungar, RG, et al (1996) Mouth leak with nasal continuous positive airway pressure increases nasal airway resistance.Am J Respir Crit Care Med154,182-186
 
Togias, AG, Proud, D, Lichtenstein, LM, et al The osmolality of nasal secretions increases when inflammatory mediators are released in response to inhalation of cold, dry air.Am Rev Respir Dis1988;137,625-629
 
Eggleston, PA, Kagey-Sobotka, A, Schleimer, RP, et al Interaction between hyperosmolar and IgE-mediated histamine release from basophils and mast cells.Am Rev Respir Dis1983;130,86-91
 
Findlay, SR, Dvorak, AM, Kagey-Sobotka, A, et al Hyperosmolar triggering of histamine release from human basophils.J Clin Invest1981;67,1604-1613
 
Brannan, JD, Koskela, H, Anderson, SD, et al Responsiveness to mannitol in asthmatic subjects with exercise- and hyperventilation-induced asthma.Am J Respir Crit Care Med1998;158,1120-1126
 
Hahn, A, Anderson, SD, Morton, AR, et al A reinterpretation of the effect of temperature and water content of the inspired air in exercise-induced asthma.Am Rev Respir Dis1984;130,575-579
 

Figures

Tables

References

Richards, GN, Cistulli, PA, Ungar, RG, et al (1996) Mouth leak with nasal continuous positive airway pressure increases nasal airway resistance.Am J Respir Crit Care Med154,182-186
 
Togias, AG, Proud, D, Lichtenstein, LM, et al The osmolality of nasal secretions increases when inflammatory mediators are released in response to inhalation of cold, dry air.Am Rev Respir Dis1988;137,625-629
 
Eggleston, PA, Kagey-Sobotka, A, Schleimer, RP, et al Interaction between hyperosmolar and IgE-mediated histamine release from basophils and mast cells.Am Rev Respir Dis1983;130,86-91
 
Findlay, SR, Dvorak, AM, Kagey-Sobotka, A, et al Hyperosmolar triggering of histamine release from human basophils.J Clin Invest1981;67,1604-1613
 
Brannan, JD, Koskela, H, Anderson, SD, et al Responsiveness to mannitol in asthmatic subjects with exercise- and hyperventilation-induced asthma.Am J Respir Crit Care Med1998;158,1120-1126
 
Hahn, A, Anderson, SD, Morton, AR, et al A reinterpretation of the effect of temperature and water content of the inspired air in exercise-induced asthma.Am Rev Respir Dis1984;130,575-579
 
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