Rhinitis, Cold Air-Induced

Basics

Nasal hyperreactivity is an increased sensitivity to everyday nonspecific external stimuli.
Cold air–induced rhinitis can occur in chronic allergic and nonallergic rhinitis and those with no nasal disease.
Symptoms include rhinorrhea, nasal congestion, postnasal drainage, and nasal burning, within minutes after exposure to cold air.
Symptoms resolve soon after exposure is eliminated.

Prevalence

Overall epidemiology of rhinitis conditions is difficult to assess due to challenges in classifying rhinitis.
Prevalence of cold air sensitivity in nonallergic chronic rhinitis is not known (1)[C].
Rhinitis is a very common disorder affecting 20–40% of the Western population (2)[C].
Most ENT clinics report a 50–50 division between allergic and nonallergic patients (2)[C].
Can occur in those with or without nasal disease
Nonallergic rhinitis presents later in life than allergic rhinitis, with 70% of patients presenting after 20 years of age.
The prevalence of nonallergic rhinitis in children is not well studied.

Exact mechanism of cold air–induced rhinitis pathophysiology is uncertain. TRP ion channels appear to be involved.
A major function of the nose is to warm and humidify inhaled air (1)[C].
As the nose warms and humidifies air, the nasal mucosa loses heat and water (1)[C].
Nasal mucosa has a dense subepithelial capillary network, allowing for exchange of heat and water to humidify air.
Cold air–induced rhinorrhea is a state of mucosal hyperresponsiveness.
Mechanism of action is through activation of mast cell and sensory nerve stimulation, which generates a cholinergic secretory response.
Cholinergic stimulation causes anterior glandular activation, producing predominately rhinorrhea (3)[C].
The associated rhinorrhea appears to be largely the result of glandular parasympathetic stimulation, as it is partially blocked by atropine (4)[A].
Physical stimulus causes mast cell activation.
Activation of mast cells causes release of inflammatory mediators, which take part in mediating nasal congestion (4)[A].
Blocking mast cell products with antihistamine does not alter clinical response to cold air.
Symptoms may reflect activation of a compensating mechanism to restore mucosal hemostasis (1)[C].

Nasal hypersensitivity is common in both allergic and nonallergic rhinitis.
Persistent allergic rhinitis is a risk factor for developing sudden temperature change–related rhinitis even in the absence of allergen exposure (2)[B].

Trigger avoidance

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