Thunderstorm-triggered asthma: what we know so far
Journal of Asthma and Allergy
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Thunderstorm-triggered asthma: what we know
so far
This article was published in the following Dove Press journal:
Journal of Asthma and Allergy
Nur-Shirin Harun 1,2
Philippe Lachapelle 3,4
Jo Douglass 2,3
1
Department of Respiratory and Sleep
Medicine, The Royal Melbourne Hospital,
Melbourne, VIC, 3050, Australia; 2Lung
Health Research Centre, The University
of Melbourne, Melbourne, VIC, 3052,
Australia; 3Department of Immunology
and Allergy, The Royal Melbourne
Hospital, Melbourne, VIC, 3050,
Australia; 4Pulmonary Division, Faculty of
Medicine, Université de Sherbrooke,
Sherbrooke, QC, Canada
Abstract: Thunderstorm-triggered asthma (TA) is the occurrence of acute asthma attacks
immediately following a thunderstorm. Epidemics have occurred across the world during
pollen season and have the capacity to rapidly inundate a health care service, resulting in
potentially catastrophic outcomes for patients. TA occurs when specific meteorological and
aerobiological factors combine to affect predisposed patients. Thunderstorm outflows can
concentrate aeroallergens, most commonly grass pollen in TA, at ground level to release
respirable allergenic particles after rupture by osmotic shock related to humidity and rainfall.
Inhalation of high concentrations of these aeroallergens by sensitized individuals can induce
early asthmatic responses which are followed by a late inflammatory phase. Other environmental factors such as rapid temperature change and agricultural practices contribute to the
causation of TA. The most lethal TA event occurred in Melbourne, Australia, in 2016.
Studies on the affected individuals found TA to be associated with allergic rhinitis, ryegrass
pollen sensitization, pre-existing asthma, poor adherence to inhaled corticosteroid preventer
therapy, hospital admission for asthma in the previous year and outdoor location at the time
of the storm. Patients without a prior history of asthma were also affected. These factors are
important in extending our understanding of the etiology of TA and associated clinical
indicators as well as possible biomarkers which may aid in predicting those at risk and
thus those who should be targeted in prevention campaigns. Education on the importance of
recognizing asthma symptoms, adherence to asthma treatment and controlling seasonal
allergic rhinitis is vital in preventing TA. Consideration of allergen immunotherapy in
selected patients may also mitigate risk of future TA. Epidemic TA events are predicted to
increase in frequency and severity with climate change, and identifying susceptible patients
and preventing poor outcomes is a key research and public health policy priority.
Keywords: asthma, thunderstorm, rhinitis, ryegrass
Introduction
Correspondence: Nur-Shirin Harun
Department of Respiratory and Sleep
Disorders Medicine, The Royal
Melbourne Hospital, Grattan St, Parkville,
Melbourne, VIC, 3050, Australia
Tel +6 139 342 7708
Email
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http://doi.org/10.2147/JAA.S175155
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Thunderstorm-triggered asthma (TA) is the occurrence of acute asthma attacks immediately following a thunderstorm.1 TA epidemics are uncommon and are believed to occur
when specific meteorological and aerobiological conditions combine to affect predisposed patients. Symptoms such as breathlessness, cough or wheeze occur suddenly in
such patients due to bronchospasm and often require emergency medical treatment via
a general practitioner or emergency department (ED) presentation and/or hospitalization.
Episodes occur typically during storms in pollen season across the world.2
The largest and most devastating epidemic of TA occurred in Melbourne,
Australia, in November 2016 where more than 3,400 people sought emergency
medical attention and 10 deaths were reported.3–6 The unprecedented scale and
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Harun et al
severity of the attack and the unexpected nature of the
event saw emergency services rapidly overwhelmed.3,4 It
demanded an urgent and thorough investigation into the
phenomenon of TA via coronial inquiry and a rethink on
the likely attributable factors and what we can do to
prevent such tragic outcomes in the future.
Since the Melbourne 2016 event, there have been
a number of publications that have furthered our understanding of TA. In the absence of randomized trial data,
we rely on retrospective analyses for potential risk associations as well as data from some case-control studies.
Further research using larger cohorts and longer-term studies are required.
Epidemiology
Epidemics of TA have occurred throughout the world and
are characterized by a rapid increase in emergency visits for
asthma to general practices or hospital EDs following
a storm, above what would normally be expected for that
area.1,5 In Australia, community pharmacies can also be
overwhelmed, likely due to the over-the-counter availability
of short-acting β2-agonist (SABA) medications.3 These epidemics affect large numbers of people and can be potentially fatal, as the Melbourne 2016 epidemic uncovered.5
TA epidemics were first described over 30 years ago
and have occurred in the UK, North America, Southern
Europe and the Middle East during the late spring or early
summer pollen seasons (Table 1).4,5 Most frequently however, events have occurred in Australia – all during the
Spring season and most commonly in November – with at
least six discrete events in Melbourne alone since 1984
and elsewhere including rural New South Wales and
Canberra.3–5 Grass pollen is believed to have triggered
all Australian events as well as the majority of events
worldwide. Fungal spores and other types of pollen (such
as olive) have been implicated in some of the events in the
UK, Italy and Canada.4,7
While TA epidemics are considered relatively uncommon, asthma exacerbations following thunderstorms are
likely underreported. An observa (...truncated)