Thunderstorm asthma: one airway, one disease

THE Melbourne thunderstorm on 21 November 2016 triggered the world’s most devastating outbreak of epidemic thunderstorm asthma, with more than 9900 patients presenting to hospitals with asthma attacks. In excess of 2300 emergency calls were received, and despite valiant efforts of emergency services, nine deaths are likely attributable to this tragic event.

Since first described 30 years ago, research suggests that thunderstorm asthma events result from a complex interaction of environmental factors and individual susceptibility factors. Environmental factors include:

• high concentrations of an aeroallergen (rye grass pollen [Lolium perenne] in Australia);
• rainwater to rupture rye grass pollen grains, releasing fine (< 2.5 µm) allergen-bearing starch granules respirable to the lower airways; and
• thunderstorm outflows, which bring respirable allergen particles to ground level.

Individual susceptibility factors include:

• prior sensitisation to rye grass pollen allergen;
• history of seasonal allergic rhinitis; and
• lower rate of inhaled corticosteroid use in those with diagnosed asthma.

To mitigate future risk, education is necessary at all levels of health care (from primary care to government), particularly directed at those with seasonal rhinitis. Further research is required to fully understand the pathophysiological signs that may predispose or prime the lung to be triggered by an environmental event.

What is known about the population risk?

Depending on the size of the population at risk, thunderstorm-associated asthma outbreaks may overwhelm the capacity of health services, as happened in Melbourne, London and Wagga Wagga. Melbourne has suffered recurrent outbreaks, with the first Australian report in 1984, and subsequent epidemics of increasing severity in 1987, 1989, 2003 and 2010. The unique topography predisposing to this vulnerability includes widespread rye grass pastures immediately north of the Great Dividing Range, with seasonal thunderstorm weather and hot northerly winds delivering potent allergenic triggers to a concentrated and susceptible urban population.

While prediction of events based on these environmental, aerobiological and meteorological factors would seem simple, current evidence does not support the feasibility of reliably predicting these asthma outbreaks by using just meteorological data and pollen counts. A British study over 4 years found that thunderstorms and high grass pollen counts preceded asthma outbreaks more often than expected by chance, but most thunderstorms, even with high grass pollen levels, do not trigger outbreaks. Hence, an early warning system based on these parameters would generate an unacceptably high rate of false alarms.

Rhinitis and asthma: “one airway, one disease”

Allergic rhinitis is a global health problem. In one Australian study, 42% of participants reported significant work or school interference because of symptoms. Most patients with asthma have rhinitis, leading to the concept of “one airway, one disease”.

As with other allergic disorders, epidemiological studies indicate an increase in prevalence of rhinitis, often faster than the increase in asthma prevalence (here and here), although in some regions this increase may be reaching a plateau. Physician-diagnosed asthma is strongly associated with both allergic and non-allergic rhinitis. The presence of allergic rhinitis commonly exacerbates asthma, increasing the risk of asthma attacks, emergency visits and admissions (here and here). These patients also experience more frequent absences from work and decreased productivity.

The treating physician should think of these conditions as one pathology occurring at different sites along the single airway.

Treating rhinitis improves asthma

Management of allergic rhinitis includes pharmacotherapy with intranasal corticosteroids, antihistamines and specific allergen immunotherapy. Intranasal corticosteroid sprays significantly improve nasal and eye symptoms. Retrospective studies have found that treatment of allergic rhinitis is associated with reduction in health care use for comorbid asthma. There is a risk reduction by half of an asthma-related event (hospitalisation or emergency department visit) for the treated group compared with the untreated group, and reduced risk for emergency department visits in patients with rhinitis who received intranasal corticosteroids. Specific allergen immunotherapy – by subcutaneous injection or sublingual route – is also a highly effective treatment for allergic rhinitis, with significant benefits for comorbid asthma.

The event in Melbourne underlines the importance of thoroughly understanding the severity and duration of rye grass pollen rhinitis as a risk factor for thunderstorm asthma. It also highlights the importance of education of patients on how vital it is that those at risk carry a reliever inhaler in the event of an unexpected asthma attack.

Significant effort at all levels (for patients and medical professionals) needs to be implemented to avert a further catastrophic event. This may include a “Sneeze! Wheeze! Think asthma!” advertising campaign targeting those with seasonal rhinitis in addition to those with known seasonal asthma and urging an annual GP review early in spring.

Bruce Thompson is professor of Allergy, Immunology and Respiratory Medicine at the Central Clinical School, Monash University and Alfred Health, in Melbourne.

Robyn E O’Hehir is professor of Allergy, Immunology and Respiratory Medicine at the Central Clinical School, Monash University and Alfred Health, Melbourne.

Professor Michael J. Abramson is with the School of Public Health and Preventive Medicine, at Monash University, in Melbourne.

Francis Thien is professor of Respiratory Medicine at Eastern Health and Monash University, in Melbourne.

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