Acute Bronchoconstriction Triggers
All of these conditions—exposure to allergens, cold air, and particulate matter—can trigger acute bronchoconstriction in affected individuals. 1, 2
Allergen Exposure
Allergen inhalation causes acute bronchoconstriction beginning within 15-30 minutes and lasting 1-3 hours in sensitized individuals. 3
- IgE-mediated inhalant allergen exposures induce both airway inflammation with eosinophils and airway hyperresponsiveness, triggering bronchoconstriction through mast cell degranulation and release of inflammatory mediators including histamine, tryptase, and leukotrienes. 2, 4
- Indoor allergens (house-dust mites, animal proteins, cockroaches, fungi) and outdoor allergens (pollen, outdoor molds) are well-established triggers. 2
- Individuals who develop both early and late responses after allergen exposure have more marked increases in airway hyperresponsiveness and greater airway inflammation, particularly with eosinophils and basophils. 3
Cold Air Exposure
Cold air exposure triggers bronchoconstriction through both direct airway effects and cutaneous reflex mechanisms. 1, 5
- Whole-body exposure to cold air (-17°C) during resting nasal breathing induces statistically significant bronchoconstriction, with maximal decrements in FEV1 of approximately 9-10% in both COPD patients and healthy subjects. 5
- Cooling of facial skin is predominantly responsible for cold weather-induced bronchoconstriction through reflex mechanisms. 5
- At high ventilation levels (during heavy exercise), the direct airway effects of cold air contribute additional bronchoconstriction by creating a hyperosmolar environment through water loss from the airway surface. 1, 4
- Cold, dry air inhalation during exercise is a particularly potent trigger, explaining the 30% prevalence of exercise-induced bronchoconstriction in ice rink athletes and high rates in Nordic skiers. 4, 6
Particulate Matter Exposure
Particulate matter and air pollutants are recognized exacerbants of asthma that trigger acute bronchoconstriction. 1, 7
- Workplace exposures to dusts, fumes, and sprays trigger bronchoconstriction in workers with hyperreactive airways, accounting for 15-25% of asthma in adults. 1, 2
- High outdoor exposures to alkaline dust (calcium oxide) from events like the World Trade Center collapse were associated with occupational airway irritant responses, increased airway responsiveness, and "World Trade Center cough" in exposed workers. 1
- Components of particulate matter including transition metals, diesel exhaust, and biologicals such as endotoxin activate inflammatory pathways (NF-κB) that lead to airway inflammation and bronchoconstriction. 7
- Ozone and various PM components are active exacerbants of asthma through their ability to induce airway inflammation. 7
Common Pathophysiologic Mechanism
All three triggers share a common pathway involving mast cell degranulation and release of inflammatory mediators (predominantly leukotrienes, but also histamine, tryptase, and prostaglandins) that act on airway smooth muscle to cause bronchoconstriction. 1, 2, 4
Clinical Caveat
Patients with poorly controlled underlying asthma or severe airway hyperresponsiveness are at greatest risk for bronchoconstriction from these triggers. 1 Protective measures include avoiding known triggers, using face masks or scarves in cold weather to warm and humidify air, and appropriate pharmacologic prophylaxis with short-acting β2-agonists 15 minutes before anticipated exposure. 1, 4, 5