How does aspirin trigger asthma?

Picture this, you’re enjoying a nice day out and want to take an aspirin for that headache. The last thing you expect is for your airways to constrict making it hard to breathe. This can be the reality of someone experiencing aspirin-triggered asthma (ATA). In this article, we will delve into ATA so buckle up and let’s get started.

What is Aspirin-Triggered Asthma?

Aspirin-Triggered Asthma(AT) is a condition whereby taking aspirin leads to acute attacks of asthma symptoms such as wheezing, coughing, chest tightness, shortness of breath (sob) or even fatal bronchoconstriction.

Asthma Inhaler
Asthma inhaler

Who Gets Affected by Aspirin Triggered-Asthma?

ATA affects approximately five percent of asthmatics typically between ages 20 and 50 years old who also suffer from nasal polyps [^1]. Studies show that women have been more affected than men in case series’ with mild-moderate severity compared to those with severe manifestations.

Allergic Rhinitis

Allergic rhinitis associates with the increased risk of developing ATA [^2]. Specifically – individuals expressing cross-reactive epitopes between mast-cell glycoprotein strongly correlate with persistent upper respiratory allergic symptomatology affecting multiple organ systems including: skin itching/hives; diarrhea/bloated colitis / intermittent rhinosinusitis/asthmatic accentuations exacerbated at night or on awakening.

How Aspirin Triggers Asthma

Allergic asthma is considered the most common type of airway disease worldwide. ATA can be explained by a non-IgE-mediated respiratory hypersensitivity mediated through cyclooxygenase-dependent pathways in inflammatory clearance-branch paths in leucocytes [^4]. In essence, when a patient with ATA takes aspirin, it acutely blocks Cox1 enzyme which leads to an accumulation of leukotrienes that cause inflammation and bronchoconstriction.


Leukotrienes are products of arachidonic acid metabolism selectively synthesized by leukocytes that play vast roles as phagocytic cellular organisms controlling inflammation such as rheumatoid arthritis and acute stages of aspiration pneumonia sepsis induction.

However, for some people with underlying respiratory conditions like asthmatics sinuses polyps predominate leukotriene production released after aspirin ingestion to subsequent activation antigen-presenting cells (APCs) known transiently activate T helper cells leading to COX dependency polarization at high levels inducing local mucosal hyperreactivity [^6].

The Samter’s Triad Hypothesis

ATA is part of a clinical triad made up Chronic rhinosinusitis, nasal polyposis (CRSwNP), and ASA allergy also referred to as Samter’s triad[^5]. Of course we’re not talking about taking pills like Oprah Winfrey was taking Christmas gifts during her show but analyzing changes occurring within the end organs & biochemical imbalance leading fluctuations reduced lincolnic-proneasis constriction initiated dosing effect proportional-to-time releasing internal spaces much more than present ingested dose.

Ok, let me simplify this for you. If one has sinusitis, they would invariably have difficulty breathing since their nasal passages tend towards being clogged up causing undue strain on airflow into the lungs. However, this condition doesn’t just affect our nasal passage or airways but also extends to other organs such as intestines and muscles comprising of internal spaces.

The changes that occur in the bronchial airflow during aspirin ingestion occur due to complex biochemical interactions within these end organs leading to imbalanced fluctuations resulting in constriction proportional-to-time released by both ingested illicit consumption patterns of excess mucous secretion, which further leads to prolonged and difficult breathing.[^7] This can have serious implications contributing significantly towards morbidity associated with Samter’s triad-linked exacerbation synchronous with acute anaphylactic reactions.

Mechanism of COX Inhibition

Aspirin acts by inhibiting cyclooxygenase(COX), responsible for prostaglandins production. Unusually high levels of leukotrienes are produced as a compensatory mechanism when COX-1 is inhibited consequently leading to inflammation and bronchoconstriction [^8]. The mechanism behind this is unclear; however, it has been postulated that COX-2 activation inhibits lipoxin A4 synthesis essential in preventing airway inflammation[^9].


A patient who experiences symptoms upon ingestion or after taking aspirin should meet diagnostic criteria for ATA. Diagnostic tools include often expensive acetylsalicylic reflex testing (ASPIRIN).[^10] Other confirmatory tests using non-selective NSAIDs like indomethacin have used salt challenge tests (JOLT) since iodized crystalized salt intake is absorbed through skin pores breaking down large molecules not able otherwise penetrate cellular descents accessing inflammatory mediators diffusing microchannels recognized through allergic asthma reaction.

An approach commonly employed specifies daily use an inhaler containing either formoterol fumarate diluents combined with budesonide activity usually prescribed ergonomically portable accessible anytime anywhere while limiting incidence incidents identification based on self-symptomatology[^11 ].


Central to the management of ATA is complete avoidance of NSAIDs [^12]. Once a patient has been diagnosed with ATA, they are at risk for severe bronchospasm and anaphylactic reactions. Anti-inflammatory drugs such as inhaled corticosteroids or leukotriene modifiers like montelukast are recommended.[^13]

Here’s a list you may find helpful:
– Inhaled Corticosteroids
– Leukotriene receptor antagonists – Montelukast.
– Cromolyn (mast cell stabilizer)


Desensitization with aspirin immunotherapy may also be used as an alternative approach when nonselective COX inhibitors cannot be avoided [^14].

Treatment Inhaler and Spacer


ATA might not have been something you knew about but now, hopefully, you know your ASA from your Samter’s triad! The importance of avoiding NSAIDS called out like Uncle Sam beckoning never more paramount than before related asthmatic reactions in life-threatening situations should be weighed between risks vs benefits against preventive dosing regiments all individuals avoid causing undue duress when making decisions finalizing medication choices contact always optional rather practicable 😉

Random Posts