How many asthma triggers do you know? Several stimuli trigger airway narrowing, wheezing, and dyspnea in asthmatic patients. While the previous view held that these should be avoided, it is now seen as evidence for poor control and an indicator of the need to increase controller therapy.

Allergens, commonest of the asthma triggers

Inhaled allergens are able to activate mast cells with bound IgE directly
leading to the immediate release of bronchoconstrictor mediators, resulting in the early response reversed by bronchodilators. Often, experimental allergen challenge is followed by a late response when there is airway edema and an acute inflammatory response with increased eosinophils and neutrophils that is not very reversible with bronchodilators. The most common allergen to trigger asthma is Dermatophagoides sp., and environmental exposure leads to low-grade chronic symptoms that are perennial. Perennial allergens are derived from cats and other domestic pets, as well as cockroaches. Other allergens, including grass pollen, ragweed, tree pollen, and fungal spores, are seasonal. Pollens usually cause allergic rhinitis rather than asthma, but in thunderstorms the pollen grains are disrupted, and the particles that may be released can trigger severe asthma exacerbations (thunderstorm asthma).

Virus infections

Upper respiratory tract virus infections, such as rhinovirus, respiratory syncytial virus, and coronavirus, are the commonest triggers of acute severe exacerbations. The mechanism whereby these viruses cause exacerbations is poorly understood, but there is an increase in airway inflammation with increased numbers of eosinophils and neutrophils. There is evidence for reduced production of type I interferons by epithelial cells from asthmatic patients, resulting in increased susceptibility to these viral infections and a greater inflammatory response.


Several drugs may trigger asthma. Alpha drenergic blockers commonly worsen asthma, and their use may be fatal. The mechanisms are not clear but are mediated through increased cholinergic bronchoconstriction. All beta blockers need to be avoided, and even selective 2 blocker or topical application (e.g., timolol eye drops) may be dangerous. Angiotensin-converting enzyme inhibitors are theoretically detrimental as they inhibit breakdown of kinins, which are bronchoconstrictors; however, they rarely worsen asthma and the characteristic cough is no more frequent in asthmatics than nonasthmatics. Aspirin may worsen asthma in some patients.


Exercise is a common trigger of asthma, particularly in children. The mechanism is linked to hyperventilation, which results in increased osmolality in airway lining fluids and triggers mast cell mediator release, resulting in bronchoconstriction. Exercise-induced asthma (EIA) typically begins after exercise has ended and recovers spontaneously within about 30 minutes. EIA is worse in cold, dry climates than in hot, humid conditions. It is therefore more common in sports such as cross-country running in cold weather, overland skiing, and ice hockey than in swimming. It may be prevented by prior administration of 2-agonists and antileukotrienes, but is best prevented by regular treatment with inhaled glucocorticoids, which reduce the population of surface mast cells required for this response.

Physical factors

Cold air and hyperventilation may trigger asthma through the same mechanisms as exercise. Laughter may also be a trigger. Many patients report worsening of asthma in hot weather and when the weather changes. Some asthmatics become worse when exposed to strong smells or perfumes, but the mechanism of this response is uncertain.

Food, one of the asthma triggers

There is little evidence that allergic reactions to food lead to increased asthma symptoms, despite the belief of many patients that their symptoms are triggered by particular food constituents. Exclusion diets are usually unsuccessful at reducing the frequency of episodes. Some foods, such as shellfish and nuts, may induce anaphylactic reactions that may include wheezing. Patients with aspirin-induced asthma may benefit from a salicylate-free diet, but these are difficult to maintain. Certain food additives may trigger asthma. Metabisulfite, which is used as a food preservative, may trigger asthma through the release of sulfur dioxide gas in the stomach. Tartrazine, a food yellow-coloring agent, was believed to be a trigger for asthma, but there is little convincing evidence for this.

Occupational factors

Several substances found in the workplace may act as sensitizing agents, as discussed above, but may also act as triggers of asthma symptoms. Occupational asthma is characteristically associated with symptoms at work with relief on weekends and holidays. If removed from exposure within the first 6 months of symptoms there is usually complete recovery. More persistent symptoms lead to irreversible airway changes, and therefore early detection and avoidance are important.

Hormonal factors

Some women show premenstrual worsening of asthma, which can occasionally be very severe. The mechanisms are not completely understood but are related to a fall in progesterone and in severe cases may be improved by treatment with high doses of progesterone or gonadotropin-releasing factors. Thyrotoxicosis and hypothyroidism can both worsen asthma, although the mechanisms are uncertain.

Gastroesophageal reflux

Gastroesophageal reflux is common in asthmatic patients as it is increased by bronchodilators. While acid reflux might trigger reflex bronchoconstriction, it rarely causes asthma symptoms, and anti-reflux therapy fails to reduce asthma symptoms in most patients.


Many asthmatics report worsening of symptoms with stress. There is no doubt that psychological factors can induce bronchoconstriction through cholinergic reflex pathways. Paradoxically, very severe stress, such as bereavement, usually does not worsen, and may even improve, asthma symptoms.

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Air pollution

Increased ambient levels of sulfur dioxide, ozone, and nitrogen oxides are associated with increased asthma symptoms.


Culled from Harrison’s Principle of Internal Medicine, 17th Edition.

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