Nasal challenge with cold, dry air results in release of inflammatory mediators. Possible mast cell involvement

J Clin Invest. 1985 Oct;76(4):1375-81. doi: 10.1172/JCI112113.


The purpose of our study was to assess the effect of cold, dry air (CDA) on the nasal mucosa of selected individuals in relation to the release of inflammatory mediators associated with mast cells. 12 subjects with a history of nasal symptoms of rhinorrhea and congestion upon cold or dry environmental exposure were challenged by nasal breathing of CDA and warm, moist air (WMA). Each subject was tested on two occasions with the order of the challenges reversed. Symptom scores were recorded, and the levels of histamine, prostaglandin (PG) D2, kinins, and [3H]-N-alpha-tosyl-L-arginine methyl ester (TAME)-esterase activity in nasal lavage fluids were measured. CDA caused a significant increase in mediator levels and in symptom scores as compared to baseline or to WMA. No significant increase in symptom scores or mediators was noted after WMA challenge, with the exception of a marginal increase in kinins. The response to CDA was similar, regardless of challenge order. Changes in mediators correlated with one another, and symptom scores correlated significantly with the levels of histamine, kinins, and PGD2. Five subjects without a history of nasal symptoms on cold air exposure had no change in mediators or symptom scores after CDA or WMA challenge. We conclude that CDA causes the release of inflammatory mediators possibly associated with mast cells and speculate that such a mechanism may be involved in the bronchospasm induced by CDA in asthmatics.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Air*
  • Cold Temperature*
  • Histamine Release
  • Humans
  • Humidity*
  • Inflammation
  • Kinins / metabolism
  • Mast Cells / metabolism*
  • Middle Aged
  • Nasal Mucosa / metabolism*
  • Nasal Provocation Tests
  • Peptide Hydrolases / metabolism
  • Prostaglandin D2
  • Prostaglandins D / metabolism
  • Rhinitis / etiology
  • Rhinitis / physiopathology*


  • Kinins
  • Prostaglandins D
  • Peptide Hydrolases
  • tosylarginine methyl ester hydrolase
  • Prostaglandin D2