Thunderstorm asthma: causes, risks, and mitigation

As climate change drives increased aeroallergen prevalence and more extreme weather, incidence of thunderstorm asthma could become more frequent and unpredictable.

On November 21, 2016, Melbourne experienced the largest and deadliest episode of thunderstorm asthma recorded to date. This catastrophic event overwhelmed local health care services, leading to 3,365 excess public hospital emergency department presentations for respiratory illnesses, 476 excess asthma-related hospital admissions, and 10 associated fatalities.

Thunderstorm asthma, a potentially catastrophic phenomenon, is a specialised form of asthma exacerbation that clinicians should heed, especially during high-pollen seasons. The term refers to observed episodes of respiratory distress, bronchospasm, or asthma exacerbations that are temporally associated with local thunderstorm activity

Thunderstorm asthma phenomena are not new; outbreaks, ranging from isolated episodes to epidemics have been documented globally for over four decades, with reports from Europe, North America, the Middle East, Africa, and Australasia.

While uncommon, thunderstorm asthma events are becoming more frequent and their potential for disaster was tragically underlined in the Melbourne event. Since then, global awareness and research focused on understanding and mitigating thunderstorm asthma risk have significantly increased.

Pathophysiology: When three factors coincide

Thunderstorm asthma arises from a complex interaction between environmental and meteorological factors, coupled with intense aeroallergen exposure in susceptible individuals. For an event to occur, a specific trifecta of conditions must coincide: a high concentration of aeroallergen; an exposed and susceptible population; and particular weather conditions that maximise the dispersal of the aeroallergen to that population.

The central mechanism revolves around the behaviour of pollen grains when exposed to moisture. Intact pollen grains, such as those from temperate grasses, are generally large (typically greater than 20 µm in diameter) and are usually trapped in the upper airways.

However, when it rains or when there is high humidity, these intact pollen grains absorb moisture, causing them to swell and burst open liberating hundreds of ultrafine, allergen-containing starch particles. These resulting submicronic particles (less than 2.5 µm diameter) are small enough to be pushed down to ground level by strong thunderstorm winds and enter the very small airways of the lungs. Once inhaled deep into the lungs, these potent allergen-carrying particles trigger asthma symptoms and potentially cause a severe asthma attack.

The specific aeroallergen triggers vary regionally. In Southeastern Australia, thunderstorm asthma episodes have been linked almost exclusively to sensitisation to ryegrass pollen (Lolium perenne). Globally, triggers include certain weeds (eg, Parietaria, Artemisia), olive pollen, and fungal spores (including Cladosporium, Alternaria spp., and Didymella exitalis). Fungal spores alone have also been observed causing an increase in asthma and other respiratory symptoms during thunderstorms.

In Australia, the eleven documented events (likely an underreporting) have consistently occurred during the spring season when temperate grass pollen levels are naturally high.

Identifying At-Risk Groups: Epidemiology and risk factors

The ability of thunderstorm asthma to affect individuals, even those without a prior asthma diagnosis, makes accurate risk stratification essential. Key risk factors include:

1. Allergic rhinitis (hay fever)

Allergic rhinitis is a major risk factor and a more sensitive predictor for thunderstorm asthma presentation than an asthma diagnosis alone. The prevalence of allergic rhinitis in thunderstorm asthma cohorts globally typically ranges between 70% and 100%. Adults who are sensitive to grass pollen and experience seasonal hay fever are considered to be at highest risk.

2. Pre-existing asthma and poor control

A prior asthma diagnosis is predictive of all severity levels of thunderstorm asthma. All 35 patients admitted to intensive care and all 10 patients who died during the Melbourne epidemic had known previous asthma. Poor asthma control, such as not regularly using a preventer or a recent asthma admission, significantly increases the odds of requiring hospitalisation.

3. Demographics and Ethnicity

Studies of thunderstorm asthma events reveal that young adults and older children are most susceptible. This susceptibility is likely mediated by atopy, aligning with the peak ages for expression of allergic rhinitis. Specifically, those in their third and fourth decades of life are disproportionately affected.

A notable finding from the Melbourne event was the significantly increased risk among individuals of Asian and Indian descent. Six of the ten people who died were of Asian or Indian descent. This increased prevalence suggests potential gene-environment interactions.

Prediction and Biomarkers

Early warning systems are vital for mitigating risk. Environmental modelling based on meteorological factors and pollen monitoring allow for the development of prediction models. Factors used to forecast “high asthma admission days” include the presence of thunderstorms, rainfall, certain wind directions, and high pollen counts over preceding days.

For individual patients with seasonal allergic rhinitis, specific biomarkers can help identify those at the highest risk for severe thunderstorm asthma. Detailed analysis of high-risk individuals following the Melbourne event identified four key variables namely total eosinophil count; serum specific ryegrass IgE concentration; fractional exhaled nitric oxide (FeNO) level; and Asthma Control Questionnaire(ACQ) score, a validated patient-reported symptom score.

Lower lung function (as measured by forced expiratory volume in 1 second, FEV1) when available, is also a strong candidate biomarker. Furthermore, measuring specific IgE sensitivity to the dominant ryegrass allergen Lol p 5 (via component-resolved diagnostics) may improve the predictive sensitivity for severe thunderstorm asthma risk.

Clinical Management and Prevention Strategies

Individual patient management focuses on preventative treatment and rapid intervention at onset of symptoms.

Preventative Therapy

Since allergic rhinitis is a strong risk factor, effective treatment is essential. Current advice for those suffering seasonal allergic rhinitis is to ensure symptoms are under good control using preventative therapy, such as intranasal steroid sprays with or without an antihistamine.

For patients diagnosed with asthma, adherence to an up-to-date asthma management plan is vital. Preventative therapy and acute therapy must be available at all times during the vulnerable spring period. Regular use of preventer medication, particularly inhaled corticosteroids, is highly recommended during high pollen seasons or when thunderstorms are predicted, as research suggests these reduce the risk of presentation during an acute episode. Even management of mild asthma has evolved to recommend the use of inhaled budesonide / LABA therapy instead of as-needed SABA therapy.

Advanced options for high-risk individuals include allergen immunotherapy which has demonstrated apparent protection in non-randomised studies. The use of modern biologic agents for those with severe asthma (targeting IgE or IL-4/IL-13 pathways), also hold strong promise for thunderstorm asthma prevention.

Acute Management

Patients should use their asthma inhaler as prescribed for mild or moderate symptoms. However, if breathing problems are severe or if usual reliever medication does not ease symptoms during or following a thunderstorm, the patient must seek immediate emergency medical help.

Public health initiatives and early warning systems are important in the management framework. Susceptible individuals (those with asthma or allergic rhinitis) should be advised to take protective measures just before, during, and after thunderstorms, including staying inside, closing doors and windows, and setting air conditioners to recirculate air.

Future Risk

Unfortunately, changes associated with climate change suggest that thunderstorm asthma events may become more frequent and more severe. Climate change increases the unpredictability of extreme weather events, including the frequency and distribution of severe thunderstorms — a necessary component for thunderstorm asthma.

Furthermore, aerobiological surveys have shown that the pollen season for many weeds and tree pollen has lengthened, and predictions suggest that some grass species will have increased pollen production over the next few decades.

As climate change drives increased aeroallergen prevalence and more extreme weather, the frequency and geographic distribution of thunderstorm asthma may change in the coming decades, underscoring the necessity for robust public health initiatives, early warning systems based on regular pollen and weather monitoring and targeted preventive therapies.

Constance H Katelaris is Senior Staff Specialist of Immunology & Allergy, Campbelltown Hospital and Western Sydney University.

The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.  

The statements or opinions expressed in this article reflect the views of the authors and do not necessarily represent the official policy of the AMA, the MJA or InSight+ unless so stated. 

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