Abstract
Cold air–induced rhinitis is a common complaint of individuals with chronic allergic or nonallergic rhinitis and those with no chronic nasal disease. It is characterized by rhinorrhea, nasal congestion, and nasal burning that appear within minutes of exposure to cold air and dissipate soon after exposure is terminated. The symptoms of cold-air rhinitis are reproduced experimentally with nasal cold-air provocation. This procedure has shown that nasal mast cell activation and sensory nerve stimulation are associated with the development of nasal symptoms. Sensory nerve activation generates a cholinergic reflex that leads to rhinorrhea; therefore, anticholinergic agents are highly effective in treating cold-air rhinitis. Experimental data suggest that individuals with nasal cold-air sensitivity may have reduced ability to compensate for the water loss that occurs during exposure to cold air. Therefore, the symptoms of cold air–induced rhinitis may reflect the activation of compensatory mechanisms to restore mucosal homeostasis
Individuals with cold air–induced rhinitis largely constitute two categories: those who report cold-air sensitivity among many nasal complaints (ie, who suffer from chronic rhinitis), and those who report nasal cold-air sensitivity as a single problem. Among individuals with chronic rhinitis, more than 50% of those with perennial allergic disease report cold air as a symptom trigger [6], and cold-air challenges elicit stronger responses in these persons compared with healthy controls. Very interestingly, individuals with asthma and allergic rhinitis are more responsive to nasal cold-air challenge, compared with individuals who have only allergic rhinitis [3•]. The prevalence of cold-air sensitivity in nonallergic chronic rhinitis is not known. Like patients with allergic rhinitis, those with chronic nonallergic rhinitis have a stronger response to cold-air challenge compared with healthy controls [47].
Hypothesis
A defect in the ability of the mucosa to compensate for excessive water loss may be primary or acquired. A recent publication suggests that the nasal air-conditioning capacity follows a familial aggregation pattern, supporting the notion of a primary “defect” [51]. One should also raise the question whether such a condition can produce negative long-term consequences, including chronic mucosal inflammation with increased antigen penetration and mucosal innate immunity dysfunction, leading to an increase in infections. This question is also unanswered, but some intriguing observations are worth mentioning.
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First, Assanasen et al. [52] have reported that the air-conditioning capacity of the nose of asthmatic patients with rhinitis is lower than that of individuals with active allergic rhinitis alone.
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Second, we have reported that asthmatic patients with rhinitis have stronger nasal responses to cold air,compared with individuals with rhinitis alone [3•].
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Third,a respiratory epidemiology study published two decades ago reported that cold-air rhinitis is a risk factor for lower forced expiratory volume in 1 second [5]. Although this line of thinking has several gaps, a hypothesis that a nasal air-conditioning “defect” may have a pathogenetic role in the development of chronic lower airways disease deserves examination. This hypothesis may be of particular value given the plethora of reports of elite winter sport athletes developing asthma-like syndromes [53,54].
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A similar hypothesis of pathway-specific hyperresponsiveness could explain the unique sensitivity to cold air in patients with nonallergic, noninfectious rhinitis [47], but could also apply to individuals without chronic rhinitis.
Conclusion
Intriguing observations raise the hypothesis that the clinical sensitivity of the nasal airways to cold air reflects a “defect” in the ability of the mucosa to keep up with excessive water loss.
