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Epidemic Thunderstorm Asthma: Lessons Learned from the Storm Down-Under

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Epidemic thunderstorm asthma (ETSA) is a global health problem that can strike without sufficient warning and can have catastrophic consequences. Because of climate change, future events are likely to become more common, more disastrous, and more unpredictable. To prevent loss of life and avoid surge events on health care infrastructure, identifying at-risk individuals and their potential biomarkers is the most prophylactic approach that can be taken to mitigate the deadly consequences of ETSA. In this review, we provide an update on the clinical mechanism, global prevalence, and characteristics of those patients moderately or severely at risk of ETSA. Identifying these patient characteristics will aid clinical professionals to provide suitable and personalized treatment plans and, in turn, avoid future loss of life.
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Clinical Commentary Review
Epidemic Thunderstorm Asthma: Lessons Learned
from the Storm Down-Under
Dwan Price, PhD
a,b,c
, Kira M. Hughes, BSc
b,c
, Francis Thien, MD, FRACP, FCCP
d
, and Cenk Suphioglu, PhD
a,b,c
Waurn
Ponds, Burwood, Box Hill, VIC, Australia
Epidemic thunderstorm asthma (ETSA) is a global health
problem that can strike without sufcient warning and can have
catastrophic consequences. Because of climate change, future
events are likely to become more common, more disastrous, and
more unpredictable. To prevent loss of life and avoid surge
events on health care infrastructure, identifying at-risk
individuals and their potential biomarkers is the most
prophylactic approach that can be taken to mitigate the deadly
consequences of ETSA. In this review, we provide an update on
the clinical mechanism, global prevalence, and characteristics of
those patients moderately or severely at risk of ETSA. Identifying
these patient characteristics will aid clinical professionals to
provide suitable and personalized treatment plans and, in turn,
avoid future loss of life. Ó2020 The Authors. Published by
Elsevier Inc. on behalf of the American Academy of Allergy,
Asthma & Immunology. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-
nc-nd/4.0/). (J Allergy Clin Immunol Pract 2020;-:---)
Key words: Epidemic thunderstorm asthma; Grass pollen; Al-
lergens; Allergic rhinitis; Sensitization; Allergen-specic IgE;
Melbourne; Risk factors; Biomarkers; Asthma treatment
Epidemic thunderstorm asthma is characterized by the
emergence of acute asthma presentations after a thunderstorm.
For example, on November 21, 2016, sensitized individuals in
Melbourne were impacted by the most signicant epidemic
thunderstorm asthma event in recorded history. Thousands were
hospitalized for severe respiratory presentations, a majority of
whom were found to suffer from allergic rhinitis or asthma, and
the death of 10 patients have been associated with the event.
Asthma-related hospital admissions rose by almost 1000% dur-
ing the 12-hour storm, an unprecedented number that the health
infrastructure was not prepared to handle.
1
Although multiple
epidemics have been observed across developing countries
worldwide, thunderstorm asthma events have occurred most
frequently in Melbourne, Australia, with at least 7 separate
epidemics recorded.
2
Events have been observed across other
states, but they are far less common and pose less of a risk to
public health compared with those in Melbourne.
CLINICAL MECHANISMS
The interactions between aeroallergens and meteorological
factors that occur during these epidemic thunderstorm asthma
(ETSA) events contribute to an increased severity of asthmatic
symptoms within sensitized populations.
3
The arrival of thun-
derstorms has been strongly linked with increased levels of
allergenic particles.
4
Thunderstorm outow concentrates
airborne allergens, such as pollen, near ground level,
5
increasing
the risk of exposure for predisposed individuals.
6
Pollen is well
documented to be present during ETSA events,
7
with grass
pollen identied as a major factor to trigger asthmatic
symptoms.
8
Other aeroallergens, such as fungal spores, have also
seen huge atmospheric increases during thunderstorms and may
also have an impact on respiratory health.
9,10
Intact pollen grains are too large to normally reach the lower
airways. However, pollen can naturally swell and rupture from
osmotic shock when exposed to high levels of moisture during
thunderstorms,
11
releasing hundreds of ne allergenic starch
granules of respirable size (Figure 1) into the atmosphere.
12,13
Recently, it has been shown that concentrations of pollen frag-
ments are at their highest, and remain high, during convective
thunderstorms.
14
These particulates can be small enough to
travel past the pharynx, reach the lower respiratory tract, and
trigger asthmatic symptoms.
15,16
Thunderstorm asthma epidemics usually occur during late
spring where pollen concentrations are highest. All 7 Melbourne
epidemics occurred in November, when ryegrass pollination was
at its peak.
17
The distribution of grass pollens is dependent on
the weather, and Melbournes high susceptibility to ETSA may
be inuenced by local weather patterns interacting with the
environment. Hot northern winds tend to push aeroallergens
from large grasslands down south toward a sensitized urban
population.
7
Thunderstorms aid in the dispersion of intact and
ruptured pollen grains, leading to sensitized individuals inhaling
a
NeuroAllergy Research Laboratory (NARL), School of Life and Environment al
Sciences, Faculty of Science, Engineering and Built Environment, Deakin Uni-
versity, Waurn Ponds, VIC, Australia
b
NeuroAllergy Research Laboratory (NARL), School of Life and Environmental
Sciences, Faculty of Science, Engineering and Built Environment, Deakin Uni-
versity, Burwood, VIC, Australia
c
Deakin AIRwatch Pollen and Spore Counting and Forecasting Facility, Deakin
University, Burwood and Waurn Ponds, VIC, Australia
d
Respiratory Medicine, Eastern Health, Box Hill Hospital and Monash University,
Box Hill, VIC, Australia
No funding was received for this work.
Conicts of interest: The authors declare that they have no relevant conicts of
interest.
Received for publication July 31, 2020; revised October 6, 2020; accepted for
publication October 18, 2020.
Available online --
Corresponding author: Cenk Suphioglu, PhD, School of Life and Environmental
Sciences, Faculty of Science, Engineering and Built Environment, Deakin Uni-
versity, 75 Pigdons Road, Waurn Ponds, VIC 3216, Australia. E-mail: cenk.
suphioglu@deakin.edu.au.
2213-2198
Ó2020 The Authors. Published by Elsevier Inc. on behalf of the American Academy
of Allergy, Asthma & Immunology. This is an open access article under the CC
BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
https://doi.org/10.1016/j.jaip.2020.10.022
1
Abbreviations used
ETSA- Epidemic thunderstorm asthma
FeNO- Fractional exhaled nitric oxide
ICS- Inhaled corticosteroids
INCS- Intranasal corticosteroids
RAST- Radioallergosorbent test
SLIT- Sublingual immunotherapy
high atmospheric levels of allergens within a short period of
time.
18
The climate in Australia experiences many spatial and
temporal variations that inuence weather parameters such as
temperature and rainfall. These changes can occur seasonally,
annually, or over long periods of time.
19
Abnormal weather
patterns have become more common due to climate change,
20
which may be responsible for the increased frequency and
severity of extreme weather health events
21
such as epidemic
thunderstorm asthma. The global impact of climate change has
been well studied in the Northern Hemisphere, with limited
long-term data on its projected ecological impact in the Southern
Hemisphere.
22
A POTENTIAL GLOBAL PROBLEM
ETSA events are not unique to Australia (see Figure 2).
Although infrequent, they are a global phenomenon, with 26
known events reported worldwide, and unlike ETSA events in
Australia, are rarely responsible for a large number of asthma
exacerbations. Exceptions include the 1994 London epidemic,
the 2013 Iran epidemic, and the 2016 Saudi Arabia epidemic.
Past ETSA events include those listed in Table I. The prevalence
of atopic conditions in populations from industrialized countries
has been associated with increased air pollutants.
47
Thunder-
storms occur more frequently in temperate climates, like Europe
or the Middle East, or subtropical environments, like
Australia.
48,49
All documented thunderstorm asthma events, as
shown in Table I and Figure 2, also coincided with their
respective countrys spring and summer pollen seasons.
50
A
combination of a susceptible population, extreme weather
patterns, and high aeroallergen concentration results in these
unique asthma epidemics. Thunderstorm-associated asthma
presentations have been observed in Mexico,
51
the USA,
52
and
Greece,
53
but no specic events have yet to be conrmed and
documented.
The allergenic triggers vary from country to country. ETSA
events are largely triggered by major community allergens. For
example, grass pollen is the dominant ETSA trigger in
Australia,
37,39-42,44
Conocarpus erectus is the suspected trigger
during ETSA events in Iran,
54
and Olea europaea and Parietaria
sp. in Italy.
33,34
WHO IS MOST AT RISK OF ETSA?
It is estimated that between 20% and 70% of individuals with
asthma are undiagnosed and are not receiving treatment.
55
This
is cause for concern, especially when attempting to identify the
subset of individuals who are at risk of ETSA. This is particularly
true for patients with ETSA, because these individuals may not
have previously suffered from asthma.
39,45
However, almost all
patients hospitalized suffered from allergic rhinitis or pollen
sensitization, and some patients presented signs of having
undiagnosed asthma.
45
Generally, all individuals who attended
emergency departments during the 2016 ETSA event in
Melbourne displayed the following characteristics.
Individuals with moderate risk
Asthmatic history. Compared with common asthma exac-
erbations, individuals who have been impacted by the 2016
Melbourne epidemic have experienced ongoing symptoms.
Approximately 80% of patients with ETSA were observed to
suffer from persistent asthmatic symptoms, 28% on a weekly
basis, with an inability to adequately self-manage.
56
This was
observed even among patients with a history of well-controlled
asthma, as individuals who were normally able to treat their
chronic condition were unable to ease their breathlessness. Also
of interest, 63% of patients with no prior history of asthma
reported developing symptoms during the months after exposure
to an epidemic thunderstorm event.
56
Ethnicity. Few studies had accounted for ethnicity when
investigating ETSA events. Independent from other risk factors,
Asian ethnicity has been found to considerably increase the risk
of susceptibility to thunderstorm asthma.
57
Atopic conditions are
FIGURE 1. Clinical mechanism of epidemic thunderstorm asthma
(ETSA). ETSA events largely coincide with peak pollen season.
High concentrations of aeroallergens (both pollen and fungal) are
swept via high winds toward a population of at-risk individuals.
Larger and intact pollen grains are trapped by the mucosal linings
of the upper airways (1). However, during an ETSA event, high
humidity levels cause the pollen to expand and rupture as a result
of osmotic shock. This releases an abundance of respirable
allergenic particles that are small enough to reach the lower
airways (2), triggering an asthmatic response.
J ALLERGY CLIN IMMUNOL PRACT
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more prevalent among Australians with Asian descent, with
allergic rhinitis twice as common compared with non-Asians.
Asthma severity was also shown to increase among Asian im-
migrants as their length of stay increased.
58
Interestingly during
the 2016 ETSA event in Melbourne, although patients of Asian
descent were less likely to be admitted to hospital compared with
their non-Asian counterparts, this trend reversed if those with
Asian heritage were born in Australia.
17
Critically, 25% of the
Melbourne population is of Asian descent; 6 of the 10 patients
who died after the 2016 Melbourne epidemic were of Asian
ethnicity.
7
Seasonal allergy. Patients most at risk of ETSA include
those with existing sensitivity to ryegrass,
59,60
a history of allergic
rhinitis, and are unlikely to be using inhaled asthma medica-
tions.
59
Sensitivity to ryegrass pollen was the leading contributor
to an individuals susceptibility to ETSA. Specically, a high
radioallergosorbent test (RAST) for grass pollen is a strong
indicator of heightened risk of ETSA in individuals with seasonal
allergies.
60
Of importance, some studies report ryegrass pollen
sensitization of all individuals presenting to emergency during
ETSA, further indicating the importance of ryegrass sensitization
as the leading contributor of susceptibility to ETSA.
61
Although
allergy to ryegrass appears to dominate among patients with
ETSA, many patients also had sensitivities to other seasonal grass
species including elevated IgE for Bermuda grass (94%), and
positive skin prick tests for Bahia grass (94%) and Timothy grass
(91%).
61
Medication use. During the 1997 Wagga Wagga epidemic,
the usage of inhaled corticosteroids (ICS) among patients with
asthma was low, but patients who had used ICS before the 1997
Wagga Wagga epidemic experienced less severe symptoms, high-
lighting the importance of prior asthma management to minimize
susceptibility during ETSA.
39
More recently, risk factors
associated with medication use included individuals taking beta-
blockers, but not those taking nonsteroidal anti-inammatory
drugs, which have been identied in patients with ETSA.
1
Individuals severely at risk
Of those individuals who attended emergency departments
during the 2016 ETSA event in Melbourne, a substantial
proportion reacted severely and required hospital admission.
These severely at-risk individuals displayed the following
characteristics.
Asthma. Not all individuals who suffered during ETSA had a
history of asthma. However, during an ETSA event, individuals
more likely to suffer severely and require hospital admission were
those who had a doctor-diagnosed history of their asthma,
59
were
aware of their asthma,
59
displayed asthmatic symptoms prior
to,
59
and importantly, if they were admitted to hospital in the
previous 12 months.
17
Of particular concern, 58% of asthmatic
patients with ETSA either lacked an asthma action plan or had
poorly controlled symptoms (55%), and in 68% of cases,
preventative corticosteroids were either underused or not
prescribed.
17
Many individuals experienced progressively
declining asthma control and persistent symptoms after an ETSA
event.
56
Allergen specific IgE. Of importance, individuals hospital-
ized during ETSA had elevated titers of IgE. Of particular
interest, 100% of hospitalized individuals had high levels of
ryegrass allergen specic IgE. These same individuals were also
allergic to Bermuda grass (96%), with some individuals
demonstrating some sensitivity toward common fungal allergens
from the genera Alternaria and Cladosporium.
59
More specif-
ically, in addition to overall elevated ryegrass pollen specic IgE,
patients with ETSA are also more likely to demonstrate serum
specic IgE to the major ryegrass allergen Lol p 5.
62
This is a
signicant observation as Lol p 5 is located within starch granules
inside pollen grains.
11,63
These granules are released into the air
on rupturing during certain atmospheric conditions, such as
ETSA.
11,13,64
Thus, detection of allergen specic IgE toward Lol
p 5 may add to the repertoire of biomarkers to assess an
individuals risk and vulnerability to future ETSA events.
FIGURE 2. Global prevalence of epidemic thunderstorm asthma (ETSA). Number of documented ETSA events, per country, since 1983.
An ETSA event is described as acute exacerbation of asthmatic symptoms in patients, often leading to an influx of presentations to the
emergency department, during or after a thunderstorm.
J ALLERGY CLIN IMMUNOL PRACT
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IDENTIFYING AND MANAGING THE PATIENT IN
ETSA
A comprehensive approach toward management and preven-
tion of ETSA includes: (i) environmental and public health
strategies, with forecasting and early warning to reduce exposure;
and (ii) reduction in individual susceptibility through primary
and secondary prevention.
In regions with thunderstorm asthma history and risk, thun-
derstorm forecasts together with pollen counts can be combined
in a risk matrix to issue public health warnings.
65,66
These
include taking proper precautions to remain indoors, take pre-
ventive inhaled steroids, and have ready access to bronchodilator
inhalers. This forecasting also enables health and emergency
service systems to be on alert and suitably prepared.
Thunderstorm asthma is characterized by airway inamma-
tion with IL-5-mediated sputum eosinophilia and eosinophil
degranulation.
40
ICS are rst-line medications for patients with
asthma that have been demonstrated to improve airway
responsiveness and inammation.
67
As already mentioned above,
a case control study after the Wagga Wagga episode in 1997
found a lower rate of ICS use in thunderstorm cases.
39
Most
reports of ETSA found that those affected were not on
ICS,
34,37,39,40,46
and this was a factor in ambulance calls,
68
emergency department presentations,
7,45,60,61
and admissions
to respiratory wards.
7,17
A number of factors may contribute to
this, including the following: (i) most ETSA-affected individuals
had predominantly allergic rhinitis with no prior diagnosis of
asthma or were not aware of asthma symptoms; (ii) they had less
severe or intermittent asthma for which regular ICS may not
have been indicated, or (iii) they were nonadherent to regular
ICS use despite having persistent asthma. Hence, the evidence
supports regular ICS use for those with diagnosed asthma, or a
history of thunderstorm asthma, throughout the susceptible grass
pollen season of spring and early summer months. The recent
change in Global Initiative in Asthma guidelines for a
combination of low-dose ICS with fast onset long-acting bron-
chodilator (formoterol) on an as neededbasis in step 1 of
therapy would be a suitable option for these patients with
intermittent or infrequent asthma symptoms.
1
As ETSA airway inammation is an archetypal type 2
inammation,
40
the measurement of the type 2 biomarker
fractional exhaled nitric oxide (FeNO) to guide therapy and dose
of inhaled steroids would be appropriate in these patients if
available. There are no prospective studies in ETSA to conrm
this, but elevated FeNO measurements in those who have
experienced ETSA
61
support this approach.
TABLE I. Global occurrences of thunderstorm asthma events: location, date, and number of individuals affected during the documented
ETSA event
Location Date No. of individuals affected Reference
Asia
Saudi Arabia November 2, 2002 No data
23
Ahvaz, Iran November 2, 2013 2000
24
Israel October 25, 2015 No data
25
Ahvaz, Iran October 28, 2015 33
26
Kuwait, Saudi Arabia December 1, 2016 844
27
Yulin, China September 11, 2018 391
12
Europe
Birmingham, England July 6, 1983 106
28
Nottingham, England June 20, 1984 19
29
UK July 22, 1989 32
30
London, England June 24, 1994 640þ
31
Cambridge, England July 29, 2002 57
32
Naples, Italy June 4, 2004 7
33
Puglia, Italy May 27, 2010 20
34
London July 23, 2013 40
35
Australia
Melbourne November 11, 1984 85
36
Melbourne November 8, 1987 154
37
Melbourne November 29, 1989 277
37
Tamworth November 1, 1990 110
38
Wagga Wagga October 30, 1997 215
39
Newcastle October 27, 1998 6
40
Melbourne November 19, 2003 70
41
Melbourne November 25, 2010 36
42
Melbourne November 8, 2011 30
43
Canberra October 27, 2014 15
44
Melbourne November 21, 2016 w10,000
45
North America
Canada July 31, 2000 157
46
ETSA, Epidemic thunderstorm asthma.
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As previously mentioned, almost all patients hospitalized with
ETSA suffered from allergic rhinitis and pollen allergy even if
there was no history of diagnosed asthma. Adequate control of
allergic rhinitis is recommended for control of asthma.
69-72
A
meta-analysis
73
and systematic review
74
of the role of intranasal
corticosteroids (INCS) in asthma demonstrated improved
asthma outcomes with the use of INCS compared with placebo,
despite a lack of further improvement with INCS as an addition
to ICS. Hence, identication of undiagnosed asthma symptoms
in those with allergic rhinitis and adequate treatment of allergic
rhinitis in those without a history of asthma are both important
factors in reducing the risk of ETSA.
Apart from the pharmacological approaches above, desensiti-
zation with specic allergen immunotherapy
75
induces long-term
immune tolerance to the responsible allergen. Sublingual
immunotherapy (SLIT) for grass pollen allergy has shown to ease
asthmatic symptoms for susceptible individuals who were
exposed to an ETSA event compared with individuals taking ICS
alone. Of those treated with SLIT (Oralair; manufactured by
Stallergenes, London, UK) before the 2016 ETSA event in
Melbourne, allergic individuals either had no asthma symptoms
(71%) or exacerbation of their asthma (0%), compared with
24% and 41%, respectively, of individuals who did not receive
preventative SLIT before the ETSA event.
75
Patients undergoing
SLIT before the pollen season have fewer allergic symptoms, and
even fewer again if repeat treatments are given over 2 consecutive
pollen seasons.
76
Patients with allergic rhinitis receiving SLIT
over 3 years demonstrate a decrease in airway inammation,
allergen specicT
reg
-cell proliferation, increased serum allergen
specic IgG, and lasting levels of IgG
4
þ
memory B cells, indi-
cating a persistent and lasting protective immune response
attributed to repeat SLIT of ryegrass pollen allergen.
76
This
suggests a primary and secondary role for allergen immuno-
therapy in reducing the risk of ETSA.
CONCLUSIONS
ETSA is a global health issue that will most likely become
more frequent and severe over the coming years due to climate
change. Australia, being the country hit hardest and most often
by these events, should prepare for future epidemics to avoid
burdening our current health infrastructure. It is crucial for
health professionals to identify potential biomarkers and risk
factors in affected individuals. These may include existing
sensitivity to seasonal allergenic grasses, prior history of allergic
rhinitis, overall elevated titers of IgE, elevated grass pollen
specic IgE, serum specic IgE to major grass allergens, such as
Lol p 5 from ryegrass and its cross-reactive analogues in other
grasses, and high RAST or positive skin prick tests to seasonal
allergens. Determining these factors will help patients receive
appropriate and effective treatment methods and reduce the
aftermath of the 2016 Melbourne epidemic from happening
again.
REFERENCES
1. Sultana RV, McKenzie DP, Fahey MT, Sutherland M, Nimorakiotakis V. Beta-
blocker use is an independent risk factor for thunderstorm asthma. Emerg Med
Australas 2019;31:955-60.
2. Campbell SL, Fox-Hughes PD, Jones PJ, Remenyi TA, Chappell K, White CJ,
et al. Evaluating the risk of epidemic thunderstorm asthma: lessons from
Australia. Int J Environ Res Public Health 2019;16:837.
3. Harun N-S, Lachapelle P, Douglass J. Thunderstorm-triggered asthma: what we
know so far. J Asthma Allergy 2019;12:101-8.
4. Darvall JN, Durie M, Pilcher D, Wigmore G, French C, Karalapillai D, et al.
Intensive care implications of epidemic thunderstorm asthma. Crit Care Resusc
2018;20:294.
5. Marks G, Colquhoun J, Girgis S, Koski MH, Treloar A, Hansen P, et al.
Thunderstorm outows preceding epidemics of asthma during spring and
summer. Thorax 2001;56:468-71.
6. DAmato G, Annesi-Maesano I, Cecchi L, DAmato M. Latest news on
relationship between thunderstorms and respiratory allergy, severe asthma, and
deaths for asthma. Allergy 2019;74:9-11.
7. Thien F, Beggs PJ, Csutoros D, Darvall J, Hew M, Davies JM, et al. The
Melbourne epidemic thunderstorm asthma event 2016: an investigation of
environmental triggers, effect on health services, and patient risk factors. Lancet
Planet Health 2018;2:e255-63.
8. Kailaivasan TH, Timbrell VL, Solley G, Smith WB, McLean-Tooke A, van
Nunen S, et al. Biogeographical variation in specic IgE recognition of
temperate and subtropical grass pollen allergens in allergic rhinitis patients. Clin
Transl Immunol 2020;9:e01103.
9. Idrose NS, Dharmage SC, Lowe AJ, Lambert KA, Lodge CJ, Abramson MJ,
et al. A systematic review of the role of grass pollen and fungi in thunderstor m
asthma. Environ Res 2020;181:108911.
10. Baxi SN, Sheehan WJ, Sordillo JE, Muilenberg ML, Rogers CA, Gafn JM,
et al. Association between fungal spore exposure in inner-city schools and
asthma morbidity. Ann Allerg Asthma Im 2019;122:610-615.e1.
11. Suphioglu C, Singh MB, Taylor P, Bellomo R, Holmes P, Puy R, et al.
Mechanism of grass-pollen-induced asthma. Lancet 1992;339:569-72.
12. Ali F, Behbehani N, Alomair N, Taher A. Fatal and near-fatal thunderstorm
asthma epidemic in a desert country. Ann Thorac Med 2019;14:155-60.
13. Taylor P, Staff I, Singh M, Knox R. Localization of the two major allergens in
rye-grass pollen using specic monoclonal antibodies and quantitative analysis
of immunogold labelling. Histochem J 1994;26:392-401.
14. Hughes DD, Mampage C, Jones L, Liu Z, Stone EA. Characterization of
atmospheric pollen fragments during springtime thunderstorms. Environ Sci
Technol Lett 2020;7:409-14.
15. Silver JD, Sutherland MF, Johnston FH, Lampugnani ER, McCarthy MA,
Jacobs SJ, et al. Seasonal asthma in Melbourne, Australia, and some
observations on the occurrence of thunderstorm asthma and its predictability.
PLoS One 2018;13:e0194929.
16. Dharmage SC, Perret JL, Custovic A. Epidemiology of asthma in children and
adults. Front Pediatr 2019;7:246.
17. Hew M, Lee J, Susanto NH, Prasad S, Bardin PG, Barnes S, et al. The 2016
Melbourne thunderstorm asthma epidemic: risk factors for severe attacks
requiring hospital admission. Allergy 2019;74:122-30.
18. DAmato G, Chong-Neto HJ, Monge Ortega OP, Vitale C, Ansotegui I,
Rosario N, et al. The effects of climate change on respiratory allergy and asthma
induced by pollen and mold allergens. Allergy 2020;75:2219-28.
19. Harris S, Lucas C. Understanding the variability of Australian re weather
between 1973 and 2017. PLoS One 2019;14:e0222328.
20. Joy A, Dunshea FR, Leury BJ, Clarke IJ, DiGiacomo K, Chauhan SS.
Resilience of small ruminants to climate change and increased environmental
temperature: a review. Animals (Basel) 2020;10:867.
21. Sisodiya SM, Fowler HJ, Lake I, Nanji RO, Gawel K, Esguerra CV, et al.
Climate change and epilepsy: time to take action. Epilepsia Open 2019;4:
524-36.
22. Prober SM, Raisbeck-Brown N, Porter NB, Williams KJ, Leviston Z,
Dickson F. Recent climate-driven ecological change across a continent as
perceived through local ecological knowledge. PLoS One 2019;14:
e0224625.
23. Al-Rubaish AM. Thunderstorm-associated bronchial asthma: a forgotten but
very present epidemic. J Fam Comm Med 2007;14:47.
24. Forouzan A, Masoumi K, Haddadzadeh Shoushtari M, Idani E, Tirandaz F,
Feli M, et al. An overview of thunderstorm-associated asthma outbreak in
southwest of Iran. J Environ Pub Health 2014;2014:504017.
25. Yair Y, Yair Y, Rubin B, Conno-Cohen R, Rosman Y, Shachar E, et al. First
reported case of thunderstorm asthma in Israel. Nat Hazards Earth Syst Sci
2019;19:2715-25.
26. Rabiee S, Mousavi H, Khafaie MA. Thunderstorm asthma outbreak, a rare
phenomenon in southwest Iran: patientsperspectives. Environ Sci Pollut Res
2018;25:36158-62.
27. Xu Y-Y, Xue T, Li H-R, Guan K. Retrospective analysis of epidemic
thunderstorm asthma in children in Yulin, northwest China [published online
ahead of print May 26, 2020]. Pediatr Res 2020. https://doi.org/10.1038/s41390-
020-0980-9.
28. Packe G, Ayres J. Asthma outbreak during a thunderstorm. Lancet 1985;326:
199-204.
J ALLERGY CLIN IMMUNOL PRACT
VOLUME -, NUMBER -
PRICE ET AL 5
29. Alderman P, Sloan J, Basran G. Asthma and thunderstorms. Arch Emerg Med
1986;3:260.
30. Allitt U, Stern MA. Asthma and Didymella ascospores following a thunder-
storm in Leicester (England). In: Agashe SN, editor. Aerobiology. New Delhi,
Calcutta: Oxford & IBH Publishing Co. PVT. Ltd.; 1997. p. 321-6.
31. Venables K, Allitt U, Collier C, Emberlin J, Greig J, Hardaker P, et al.
Thunderstorm-related asthmaethe epidemic of 24/25 June 1994. Clin Exp
Allergy 1997;27:725-36.
32. Pulimood TB, Corden JM, Bryden C, Sharples L, Nasser SM. Epidemic asthma
and the role of the fungal mold Alternaria alternata. J Allergy Clin Immunol
2007;120:610-7.
33. DAmato G, Cecchi L, Liccardi G. Thunderstorm-related asthma: not only grass
pollen and spores. J Allergy Clin Immunol 2008;121:537.
34. Losappio L, Hefer E, Contento F, Cannito C, Rolla G. Thunderstorm-related
asthma epidemic owing to Olea Europaea pollen sensitization. Allergy 2011;66:
1510.
35. Elliot A, Hughes H, Hughes T, Locker T, Brown R, Sarran C, et al. The impact
of thunderstorm asthma on emergency department attendances across London
during July 2013. Emerg Med J 2014;31:675-8.
36. Egan P. Weather or not. Med J Aust 1985;142:330.
37. Bellomo R, Gigliotti P, Treloar A, Holmes P, Suphioglu C, Singh MB, et al.
Two consecutive thunderstorm associated epidemics of asthma in the city of
Melbourne. The possible role of rye grass pollen. Med J Aust 1992;156:834-7.
38. Waters J, Corbett S, Gibson P, Hensley M, Wlodarczyk J. Epidemic asthma surveillance
in the New England Region 1990-1992. NSW Pub Health Bull 1993;4:100-1.
39. Girgis ST, Marks GB, Downs SH, Kolbe A, Car GN, Paton R. Thunderstorm-
associated asthma in an inland town in south-eastern Australia. Who is at risk?
Eur Respir J 2000;16:3-8.
40. Wark PAB, Simpson J, Hensley MJ, Gibson PG. Airway inammation in
thunderstorm asthma. Clin Exp Allergy 2002;32:1750-6.
41. Erbas B, Akram M, Dharmage SC, Tham R, Dennekamp M, Newbigin E, et al.
The role of seasonal grass pollen on childhood asthma emergency department
presentations. Clin Exp Allergy 2012;42:799-805.
42. Howden ML, McDonald CF, Sutherland MF. Thunderstorm asthmaa timely
reminder. Med J Aust 2011;195:512-3.
43. Davies JM, Erbas B, Simunovic M, Al Kouba J, Milic A, Fagan D. Literature
review on thunderstorm asthma and its implications for public health advice.
Brisbane, Australia: Queensland University of Technology; 2017.
44. Colley C. Canberra sneezes through worst hay fever season in years. The
Canberra Times. Available from: https://www.canberratimes.com.au/story/
6076295/canberra-sneezes-through-worst-hay-fever-season-in-years/. Accessed
November 4, 2020.
45. Rangamuwa KB, Young AC, Thien F. An epidemic of thunderstorm asthma in
Melbourne 2016: asthma, rhinitis, and other previous allergies. Asia Pac Allergy
2017;7:193-8.
46. Wardman A, Stefani D, MacDonald JC. Thunderstorm-associated asthma or
shortness of breath epidemic: a Canadian case report. Can Respir J 2002;9:
267-70.
47. DAmato G, Liccardi G, DAmato M, Holgate S. Environmental risk factors and
allergic bronchial asthma. Clin Exp Allergy 2005;35:1113-24.
48. DAmato G, Annesi-Maesano I, Vaghi A, Cecchi L, DAmato M. How do
storms affect asthma? Curr Allergy Asthma Rep 2018;18:24.
49. Lau ETC, Yung MMN, Karraker NE, Leung KMY. Is an assessment factor of
10 appropriate to account for the variation in chemical toxicity to freshwater
ectotherms under different thermal conditions? Environ Sci Pollut Res 2014;21:
95-104.
50. DAmato G, Vitale C, DAmato M, Cecchi L, Liccardi G, Molino A, et al.
Thunderstorm-related asthma: what happens and why. Clin Exp Allergy 2016;
46:390-6.
51. Rosas I, McCartney H, Payne R, Calderon C, Lacey J, Chapela R, et al.
Analysis of the relationships between environmental factors (aeroallergens, air
pollution, and weather) and asthma emergency admissions to a hospital in
Mexico City. Allergy 1998;53:394-401.
52. Grundstein A, Sarnat SE, Klein M, Shepherd M, Naeher L, Mote T, et al.
Thunderstorm associated asthma in Atlanta, Georgia. Thorax 2008;63:659-60.
53. Ilias I. Eight year retrospective study of thunderstorm-associated asthma attacks
in Athens Greece. Int J Environ Heal R 1998;8:335-7.
54. Rad HD, Assarehzadegan M-A, GoudarziG, Sorooshian A, Birgani YT, Maleki H,
et al. Do Conocarpus erectus airborne pollen grains exacerbate autumnal thunder-
storm asthma attacks in Ahvaz, Iran? Atmos Environ 2019;213:311-25.
55. Aaron SD, Boulet LP, Reddel HK, Gershon AS. Underdiagnosis and
overdiagnosis of asthma. Am J Respir Crit Care Med 2018;198:1012-20.
56. Foo CT, Yee EL, Young A, Denton E, Hew M, OHehir RE, et al. Continued
loss of asthma control following epidemic thunderstorm asthma. Asia Pac
Allergy 2019;9:e35.
57. Clayton-Chubb D, Con D, Rangamuwa K, Taylor D, Thien F, Wadhwa V.
Thunderstorm asthma: revealing a hidden at-risk population. Intern Med J 2019;
49:74-8.
58. Leung RC, Burdon JG, Carlin JB, Czarny D. Asthma, allergy and atopy in
Asian immigrants in Melbourne. Med J Aust 1994;161:418-25.
59. Harun N-S, Lachapelle P, Bowatte G, Lodge C, Braitberg G, Irving L, et al.
Thunderstorm-asthma epidemic in Melbourne, Australia: An analysis of patient
characteristics associated with hospitalization [published online ahead of print
March 12, 2020]. Can J Respir Crit Care Sl Med 2016. https://doi.org/10.1080/
24745332.2020.1727301.
60. Sutherland MF, Portelli EL, Collins AL, Rahman MA, McDonald CF. Patients
with thunderstorm asthma or severe asthma in Melbourne: a comparison. Med J
Aust 2017;207:434-5.
61. Lee J, Kronborg C, OHehir RE, Hew M. Whos at risk of thunderstorm
asthma? The ryegrass pollen trifecta and lessons learnt from the Melbourne
thunderstorm epidemic. Respir Med 2017;132:146-8.
62. Hew M, Lee J, Varese N, Aui PM, McKenzie CI, Wines BD, et al. Epidemic
thunderstorm asthma susceptibility from sensitization to ryegrass (Lolium
perenne) pollen and major allergen Lol p 5. Allergy 2020;75:2369-72.
63. Suphioglu C. Thunderstorm asthma due to grass pollen. Int Arch Allergy
Immunol 1998;116:253-60.
64. Buters J, Prank M, Soev M, Pusch G, Albertini R, Annesi-Maesano I, et al.
Variation of the group 5 grass pollen allergen content of airborne pollen in
relation to geographic location and time in season. J Allergy Clin Immunol
2015;136:87-95.e6.
65. Graham B. Charles Sturt is helping Wagga Wagga residents to breathe easier.
Charles Sturt University. Available from, https://news.csu.edu.au/in-brief/
charles-sturt-is-helping-wagga-wagga-residents-to-breathe-easier. Accessed
May 12, 2020.
66. Victoria State Government. Epidemic thunderstorm asthma forecast; 2019.
Available from, https://www2.health.vic.gov.au/public-health/environmental-
health/climate-weather-and-public-health/thunderstorm-asthma/forecasting.
Accessed May 12, 2020.
67. Chung LP, Upham JW, Bardin PG, Hew M. Rational oral corticosteroid use in
adult severe asthma: a narrative review. Respirology 2020;25:161-72.
68. Andrew E, Nehme Z, Bernard S, Abramson MJ, Newbigin E, Piper B, et al.
Stormy weather: a retrospective analysis of demand for emergency medical
services during epidemic thunderstorm asthma. BMJ 2017;359:j5636.
69. Bousquet J, Khaltaev N, Cruz AA, Denburg J, Fokkens WJ, Togias A, et al.
Allergic Rhinitis and its Impact on Asthma (ARIA) 2008 update (in
collaboration with the World Health Organization, GA(2)LEN and AllerGen).
Allergy 2008;63(Suppl 86):8-160.
70. Scadding GK, Durham SR, Mirakian R, Jones NS, Leech SC, Farooque S, et al.
BSACI guidelines for the management of allergic and non-allergic rhinit is. Clin
Exp Allergy 2008;38:19-42.
71. Bousquet J, Bedbrook A, Czarlewski W, Onorato GL, Arnavielhe S, Laune D,
et al. Guidance to 2018 good practice: ARIA digitally-enabled, integrated,
person-centred care for rhinitis and asthma. Clin Transl Allergy 2019;9:16.
72. Bousquet J, Schunemann HJ, Togias A, Bachert C, Erhola M, Hellings PW,
et al. Next-generation Allergic Rhinitis and Its Impact on Asthma (ARIA)
guidelines for allergic rhinitis based on Grading of Recommendations
Assessment, Development and Evaluation (GRADE) and real-world evidence.
J Allergy Clin Immunol 2020;145:70-80.e3.
73. Lohia S, Schlosser RJ, Soler ZM. Impact of intranasal corticosteroids on asthma
outcomes in allergic rhinitis: a meta-analysis. Allergy 2013;68:569-79.
74. Taramarcaz P, Gibson PG. Intranasal corticosteroids for asthma control in
people with coexisting asthma and rhinitis. Cochrane Database Syst Rev 2003;
4:CD003570.
75. OHehir RE, Varese NP, Deckert K, Zubrinich CM, Van Zelm MC,
Rolland JM, et al. Epidemic thunderstorm asthma protection with ve-grass
pollen tablet sublingual immunotherapy: a clinical trial. Am J Respir Crit
Care Med 2018;198:126-8.
76. Heeringa JJ, McKenzie CI, Varese N, Hew M, Bakx AT, Aui PM, et al.
Induction of IgG2 and IgG4 B-cell memory following sublingual
immunotherapy for ryegrass pollen allergy. Allergy 2020;75:1121-32.
J ALLERGY CLIN IMMUNOL PRACT
MONTH 2020
6PRICE ET AL
... Over the last few decades, incidences of respiratory admissions have risen due to the increased atmospheric concentration of airborne allergens. The fragmentation and dispersion of these allergens is aided by environmental factors like rainfall, temperature, and interactions with atmospheric aerosols [15]. Extreme weather parameters, which continue to become more frequent due to the impacts of climate change, have greatly fluctuated allergen concentrations and led to epidemic TA events which have left hundreds, if not thousands, struggling to breathe [5,9,[16][17][18]. ...
... The most prominent hypotheses for TA are linked with bioaerosols, and involve the role of rainwater in promoting the release of respirable particulate matter [15]. Pollen grains can be carried by thunderstorm at ground level, where pollen rupture would be increased with release of allergenic biological aerosols of paucimicronic size, derived from the cytoplasm and which can penetrate deep into lower airways. ...
... Pollen grains can be carried by thunderstorm at ground level, where pollen rupture would be increased with release of allergenic biological aerosols of paucimicronic size, derived from the cytoplasm and which can penetrate deep into lower airways. In other words, there is evidence that under wet conditions or during thunderstorms, pollen grains may, after rupture by osmotic shock, release into the atmosphere part of their content, including respirable, allergen-carrying cytoplasmic starch granules (0.5-2.5 µm) or other paucimicronic components that can reach lower airways inducing asthma reactions in pollinosis patients [15,17]. These allergens can likely penetrate deeper into the lung, provoking more severe symptoms. ...
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Thunderstorm-triggered asthma (TA) can be defined as the occurrence of acute asthma attacks immediately following a thunderstorm during pollen seasons. Outbreaks have occurred across the world during pollen season with the capacity to rapidly inundate a health care service, resulting in potentially catastrophic outcomes for allergicpatients. TA occurs when specific meteorological and aerobiological factors combine to affect predisposed atopic patients with IgE-mediated sentitization to pollen allergens. Thunderstorm outflows can concentrate aeroallergens, most commonly grass pollen but also other pollens such as Parietaria and moulds 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 can be followed by a late inflammatory phase. There is evidence that, during pollen season, thunderstorms can induce allergic asthma outbreaks, sometimes also severe asthma crisis and sometimes deaths in patients suffering from pollen allergy. It has been observed that changes in the weather such as rain or humidity may induce hydratation of pollen grains during pollen seasons and sometimes also their fragmentation which generates atmospheric biological aerosols carrying allergens. Asthma attacks are induced for the high concentration at ground level of pollen grains which may release allergenic particles of respirable size after rupture by osmotic shock. In other words, it is a global health problem observed in several cities and areas of the world that can strike without sufficient warning, inducing sometimes severe clinical consequences also with deaths of asthma patients. Due to constant climate change, future TA events are likely to become more common, more disastrous and more unpredictable, as a consequence it is important to have deep knowledge on this topic to prevent asthma attacks. Other environmental factors, such as rapid changes in temperature and agricultural practices, also contribute to causing TA.
... In general, the phenomenon of thunderstorm asthma is very poorly known in Sweden, both among the general public and medical caregivers. However, epidemic thunderstorm asthma is thought to be a global phenomenon, which can strike rather unexpectedly with catastrophic consequences, meaning it should be prepared for [42]. Furthermore, because of climate change, it is likely that the incidence of thunderstorm asthma will increase and have wide-reaching, negative consequences [42]. ...
... However, epidemic thunderstorm asthma is thought to be a global phenomenon, which can strike rather unexpectedly with catastrophic consequences, meaning it should be prepared for [42]. Furthermore, because of climate change, it is likely that the incidence of thunderstorm asthma will increase and have wide-reaching, negative consequences [42]. ...
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Full-text available
Background: Thunderstorm asthma is a term used to describe surges in acute respiratory illnesses following a thunderstorm and is often attributed to an intense exposure to aeroallergens. Several episodes of thunderstorm asthma have been observed worldwide; however, no such cases have been described in Sweden. In Sweden, the most prominent exposure to air-borne pollen occurs during the blooming of the birch. We aimed to explore the associations between respiratory health and the combined exposure to thunderstorms and birch pollen. Methods: We investigated the association between the daily numbers of outpatient visits due to respiratory cases and the combined exposure to thunderstorms and birch pollen during the period of 1 May-31 September in 2001-2017, in Stockholm County, Sweden, by using time series analysis with log linear models. Results: We detected noticeable increases in the number of outpatient visits on both the same day (max 26%; 95% CI 1.16-1.37) and the day after (max 50%; 95% CI 1.32-1.70) the occurrence of a thunderstorm, when the concentrations of birch pollen and the number of lightning discharges were within the highest categories. Conclusions: It is possible that co-exposure to heavy thunderstorms and high concentrations of birch pollen affects the respiratory health of the Stockholm population. To the best of our knowledge, this is the first study addressing the thunderstorm-related respiratory illnesses in Sweden and the effects of birch pollen. Our study may be important for future public health advice related to thunderstorm asthma.
... Twenty-six events have been reported worldwide since 1983. 70 Despite the low probability, Australia has recorded 11 separate events of thunderstorm asthma, 7 of which occurred in Melbourne (see Figure 4(a)). The pollen season varies across Australia due to the country's diverse climate and its impact on the distribution and production of airborne allergens (see Figure 4(b)). ...
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Full-text available
Australia is home to one of the highest rates of allergic rhinitis worldwide. Commonly known as ‘hay fever’, this chronic condition affects up to 30% of the population and is characterised by sensitisation to pollen and fungal spores. Exposure to these aeroallergens has been strongly associated with causing allergic reactions and worsening asthma symptoms. Over the last few decades, incidences of respiratory admissions have risen due to the increased atmospheric concentration of airborne allergens. The fragmentation and dispersion of these allergens is aided by environmental factors like rainfall, temperature and interactions with atmospheric aerosols. Extreme weather parameters, which continue to become more frequent due to the impacts of climate change, have greatly fluctuated allergen concentrations and led to epidemic thunderstorm asthma (ETSA) events that have left hundreds, if not thousands, struggling to breathe. While a link exists between airborne allergens, weather and respiratory admissions, the underlying factors that influence these epidemics remain unknown. It is important we understand the potential threat these events pose on our susceptible populations and ensure our health infrastructure is prepared for the next epidemic.
... This is important to assess because higheambient pollen exposure together with convergence line weather events can lead to catastrophic community-wide thunderstorm asthma events, such as the recent one in Melbourne, Australia, where people with no known overt asthma also proved susceptible. [7][8][9][10] Lung function can be a good marker of asthma exacerbation risk because exposure to ambient pollen may cause mild but acute measurable changes. However, the relationship between ambient pollen exposure and lung function is underinvestigated, especially within the community as evidenced by our own recent systematic review. ...
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Background Grass pollen exposure is a risk factor for childhood asthma hospital attendances. However, its short-term influence on lung function especially among those with other allergic conditions has been less well-studied. Objective To investigate this association in a population-based sample of children. Methods Within the HealthNuts cohort, 641 children performed spirometry during the grass pollen season. Grass pollen concentration was considered on the day of testing (lag 0), up to three days before (lag 1-lag 3) and cumulatively (lag 0-3). We used linear regression to assess the relevant associations, and examined potential interactions with current asthma, hay fever or eczema, and food allergy. Results Associations were observed only in children with allergic disease (p-value for interaction ≤ 0.1) . In children with food allergy, grass pollen concentration was associated with lower ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1/FVC) and lower mid-forced expiratory flows (FEF25-75%) at all lags (e.g. at lag-2, FEV1/FVC z-score = -0.50 [95% CI: -0.80, -0.20] and FEF25-75% z-score = -0.40 [-0.60, -0.04] per 20 grains/m³ pollen increase), and increased bronchodilator responsiveness (BDR) at lag-2 and lag-3 (e.g. at lag-2, BDR = (31 [-0.005, 62] ml). In children with current asthma, increasing grass pollen concentration was associated with lower FEF25-75% and increased BDR, while children with current hay fever or eczema had increased BDR only. Conclusion A proactive approach needs to be enforced to manage susceptible children, especially those with food allergy, before high grass pollen days.
... Later, when dealing with the pandemics, the government's response policies and medical insurance played significant roles (Mackowiak, 2021). However, emerging pandemics have become more frequent (Price, Hughes, Thien, & Suphioglu, 2021). Data from 2020 show that only in that year six pandemics have been found (World Health Organization-WHO, 2020a). ...
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Frequently emerging pandemics have caused participants’ low prevention cooperation. This paper studies a reward and punishment mechanism for a health system and individuals to enhance their prevention. In the traditional way of responding to the pandemic, health systems generally obtain full subsidies by government and pay attention to treatment. Meanwhile, individuals need to cooperate according to their treatment. However, emerging pandemics are increasing and spreading quickly. This has forced the government to change its full-subsidy treatment strategy to prevention incentive strategy. However, participants (individuals and the health system) appear to have a low motivation to do prevention. The aim of this paper is to give a new mechanism based on reward and punishment policies, which can be offered by the government to the participants to improve their prevention efficiency. We develop a game-theoretic model with three nonlinear programs (NLP) to identify the optimal policies, and obtain the factors that influence the optimal policies. Our findings show that under the proposed mechanism, all participants are willing to make decisions in accordance with the requirements of the government. Furthermore, we indicate that the designed mechanism has a positive network externality. We also prove that the given mechanism is effective regardless of whether the information of the individuals’ prevention efforts is available. A numerical example indicates that the proposed mechanism is more suitable for applications in areas with a large population.
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Epidemic asthma events represent a significant risk to emergency services as well as the wider community. In southeastern Australia, these events occur in conjunction with relatively high amounts of grass pollen during the late spring and early summer, which may become concentrated in populated areas through atmospheric convergence caused by a number of physical mechanisms including thunderstorm outflow. Thunderstorm forecasts are therefore important for identifying epidemic asthma risk factors. However, the representation of thunderstorm environments using regional numerical weather prediction models, which are a key aspect of the construction of these forecasts, have not yet been systematically evaluated in the context of epidemic asthma events. Here, we evaluate diagnostics of thunderstorm environments from historical simulations of weather conditions in the vicinity of Melbourne, Australia, in relation to the identification of epidemic asthma cases based on hospital data from a set of controls. Skillful identification of epidemic asthma cases is achieved using a thunderstorm diagnostic that describes near-surface water vapor mixing ratio. This diagnostic is then used to gain insights on the variability of meteorological environments related to epidemic asthma in this region, including diurnal variations, long-term trends, and the relationship with large-scale climate drivers. Results suggest that there has been a long-term increase in days with high water vapor mixing ratio during the grass pollen season, with large-scale climate drivers having a limited influence on these conditions. Significance Statement We investigate the atmospheric conditions associated with epidemic thunderstorm asthma events in Melbourne, Australia, using historical model simulations of the weather. Conditions appear to be associated with high atmospheric moisture content, which relates to environments favorable for severe thunderstorms, but also potentially pollen rupturing as suggested by previous studies. These conditions are shown to be just as important as the concentration of grass pollen for a set of epidemic thunderstorm asthma events in this region. This means that weather model simulations of thunderstorm conditions can be incorporated into the forecasting process for epidemic asthma in Melbourne, Australia. We also investigate long-term variability in atmospheric conditions associated with severe thunderstorms, including relationships with the large-scale climate and long-term trends.
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Pollen grains may contain allergens that exacerbate allergic respiratory diseases like asthma and rhinitis. In the presence of water, pollen grains (10–100 μm) can rupture to produce sub-pollen particles (SPP) with diameters <2.5 μm, which in comparison to intact pollen grains, have longer atmospheric lifetimes and greater penetration to the lower lung. The current study examines SPP, fungal spores, and bacteria in size-resolved atmospheric particulate matter (PM) using chemical and biological tracers. During springtime tree pollen season in Iowa City, Iowa, fine particle (PM2.5) concentrations of fructose (a pollen chemical tracer) increased on rainy sampling periods, especially during severe thunderstorms, and peaked when a tornado struck nearby. Submicron fluorescent particles, measured by single-particle fluorescence spectroscopy, were also enhanced during rain events, particularly thunderstorms in agreement with the chemical tracer measurements. PM2.5 sucrose (a pollen chemical tracer) concentrations were higher in early spring when nighttime temperatures were closer to freezing, while fructose concentrations were higher in late spring with warmer temperatures, consistent with chemical tracers being sensitive to seasonal temperature influences. The first co-located measurements of fructose and Bet v 1 (birch pollen allergen), indicated that SPP ranged in diameter from <0.25 to 2.5 μm during rainy sampling periods and that allergens and carbohydrates exhibited distinct size distributions. Meanwhile, mannitol (a fungal spore tracer) peaked on warm, dry days following rain and was primarily in supermicron particles (>1.0 μm), which is consistent with intact fungal spore diameters (1–30 μm). Bacterial endotoxins in PM also increased during extreme weather events, primarily in supermicron particles. While the concentrations of fructose, mannitol, and endotoxin all increased in PM2.5 μm during thunderstorms, the greatest relative increase in concentration was observed for fructose. Together, these observations suggest that SPP containing starch granules and allergens (Bet v 1) were released during rainy sampling periods. This study advances the use of chemical tracers to track SPP and other bioaerosols in the atmosphere, by providing new insight to their size distribution and response to extreme weather conditions.
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Purpose of review: The development and progression of chronic respiratory diseases are impacted by a complex interplay between genetic, microbial, and environmental factors. Here we specifically summarize the effects of environmental exposure on asthma, allergic rhinitis, and chronic rhinosinusitis. We furthermore discuss how digital health technology may aid in the assessment of the environmental exposure of patients and how it may be of added value for them. Recent findings: It is well established that one gets allergic symptoms if sensitized and exposed to the same allergen. Viruses, bacteria, pollutants, irritants, and lifestyle-related factors modify the risk of getting sensitized and develop symptoms or may induce symptoms themselves. Understanding these processes and how the various factors interact with each other and the human body require big data and advanced statistics. Mobile health technology enables integration of multiple sources of data of the patients' exposome and link these to patient outcomes. Such technologies may contribute to the increased understanding of the development of chronic respiratory disease. Summary: Implementation of digital technologies in clinical practice may in future guide the development of preventive strategies to tackle chronic respiratory diseases and eventually improve outcomes of the patient.
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The impact of climate change on the environment, biosphere and biodiversity has become more evident in the recent years. Human activities have increased atmospheric concentrations of carbon dioxide (CO2) and other greenhouse gases. Change in climate and the correlated global warming affects the quantity, intensity and frequency of precipitation type as well as the frequency of extreme events such as heat waves, droughts, thunderstorms, floods and hurricanes. Respiratory health can be particularly affected by climate change, which contributes to the development of allergic respiratory diseasesand asthma. Pollen and mold allergens are able to trigger the release of pro‐inflammatory and immunomodulatory mediators that accelerate the onset the IgE‐mediated sensitizationand of allergy. Allergy to pollen and pollen season at its beginning, in duration and intensity are altered by climatechange. Studies showed that plants exhibit enhanced photosynthesis and reproductive effects and produce more pollen as a response to high atmospheric levels of carbon dioxide (CO2).Molds which proliferation is increased by floods and rainy storms are responsible for severe asthma. Pollen and mold allergy is generally used to evaluate the interrelation between air pollution and allergic respiratory diseases, such as rhinitis and asthma. Thunderstorms during pollen seasons can cause exacerbation of respiratory allergy and asthma in patients with hay fever. A similar phenomenon is observed for molds.Measures to reduce greenhouse gas emissions can have positive health benefits.
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Climate change is a major global threat to the sustainability of livestock systems. Climatic factors such as ambient temperature, relative humidity, direct and indirect solar radiation and wind speed influence feed and water availability, fodder quality and disease occurrence, with production being most efficient in optimal environmental conditions. Among these climatic variables, ambient temperature fluctuations have the most impact on livestock production and animal welfare. Continuous exposure of the animals to heat stress compromises growth, milk and meat production and reproduction. The capacity of an animal to mitigate effects of increased environmental temperature, without progressing into stress response, differs within and between species. Comparatively, small ruminants are better adapted to hot environments than large ruminants and have better ability to survive, produce and reproduce in harsh climatic regions. Nevertheless, the physiological and behavioral changes in response to hot environments affect small ruminant production. It has been found that tropical breeds are more adaptive to hot climates than high-producing temperate breeds. The growing body of knowledge on the negative impact of heat stress on small ruminant production and welfare will assist in the development of suitable strategies to mitigate heat stress. Selection of thermotolerant breeds, through identification of genetic traits for adaption to extreme environmental conditions (high temperature, feed scarcity, water scarcity), is a viable strategy to combat climate change and minimize the impact on small ruminant production and welfare. This review highlights such adaption within and among different breeds of small ruminants challenged by heat stress.
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While falling rain washes pollen grains from the atmosphere, rain can also induce pollen rupturing into submicron pollen fragments. Compared to intact pollen, such fragments can penetrate deeper into the human respiratory system and persist longer in the atmosphere. Herein we provide the first online characterization of pollen fragments during thunderstorms and rain events. For the first time, we combine single-particle fluorescence spectroscopy with offline measurements of chemical tracers to provide direct evidence of atmospheric pollen fragments. We show a significant increase in pollen fragments with diameters 0.25-1.0 µm coincident with precipitation. Pollen fragment concentrations peak during convective thunderstorms with strong downdrafts, high rates of rainfall, and numerous lightning strikes, although lightning is not required for the fragments’ release. After storms, pollen fragments persist in the atmosphere for several hours. Our results show that while pollen grains decrease substantially during rain, peak concentrations of submicron pollen fragments occur during rain events and then persist for several hours. This study provides new information on the abundance, size-distribution, and meteorological drivers of pollen fragments in the atmosphere. Because pollen fragments potentially carry allergens and thunderstorms are predicted to increase in frequency and strength, understanding human exposures to pollen fragments is increasingly important.
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Thunderstorm asthma risk in geographic regions with temperate grasses is strongly correlated with the trifecta of ryegrass pollen (RGP) sensitization (serum RGP‐specific IgE), seasonal allergic rhinitis (SAR) and exposure to a thunderstorm during the pollen season.[1,2] Perennial ryegrass (Lolium perenne) is a wind‐pollinated pasture grass prevalent in southeastern Australia, North America and Southern Europe.
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Objective: Globally, grass pollens (GP) are major aeroallergen triggers of allergic rhinitis (AR) and asthma. However, patterns of allergic sensitisation to pollen of temperate (Pooideae: Lolium perenne) and subtropical (Chloridoideae: Cynodon dactylon and Panicoideae: Paspalum notatum) subfamilies in diverse climates remain unclear. This study aims to evaluate the level of allergic sensitisation and IgE specificity for major GP allergens representing the three subfamilies in biogeographically distinct regions. Methods: Participants (GP-allergic with AR, 330; non-atopic, 29; other allergies, 54) were recruited in subtropical: Queensland, and temperate: New South Wales, Western and South Australia, regions. Clinical history, skin prick test (SPT), total and specific IgE to GP and purified allergens (ImmunoCAP) were evaluated. Cross-inhibition of sIgE with Pas n 1, Cyn d 1 and Lol p 1 by GP extracts was investigated. Results: Queensland participants showed higher sensitisation to P. notatum and C. dactylon than L. perenne GP. sIgE was higher to Pas n 1 and Cyn d 1, and sIgE to Pas n 1 and Cyn d 1 was inhibited more by Panicoideae and Chloridoideae, respectively, than Pooideae GP. Conversely, participants from temperate regions showed highest sensitisation levels to L. perenne GP and Lol p 1, and sIgE to Lol p 1 was inhibited more by Pooideae than other GP. Conclusion: Levels and patterns of sensitisation to subtropical and temperate GP in AR patients depended on biogeography. Knowledge of the specificity of sensitisation to local allergens is important for optimal diagnosis and choice of allergen-specific immunotherapy to maximise benefit.
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We report on the first recorded case of thunderstorm asthma in Israel, which occurred during an exceptionally strong eastern Mediterranean multicell thunderstorm on 25 October 2015. The storms were accompanied by intensive lightning activity, severe hail, downbursts and strong winds followed by intense rain. It was the strongest lightning-producing storm ever recorded by the Israeli Lightning Detection Network (ILDN) since it began operations in 1997. After the passage of the gust front and the ensuing increase in particle concentrations, documented by air-quality sensors, the hospital emergency room (ER) presentation records from three hospitals – two in the direct route of the storm (Meir Medical Center in Kfar Saba and Ha'Emek in Afula) and the other just west of its ground track (Rambam Medical Center in Haifa) – showed that the amount of presentation of patients with respiratory problems in the hours immediately following the storm increased compared with the average numbers in the days before. This pattern is in line with that reported by Thien et al. (2018) for the massive thunderstorm asthma epidemic in Melbourne, Australia. The increase in patient presentations to the emergency rooms persisted for an additional 48–72 h before going back to normal values, indicating that it was likely related to the multi-cell outflow. We discuss how the likelihood of incidence of such public health events associated with thunderstorms will be affected by global trends in lightning occurrence.
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Documenting effects of climate change is an important step towards designing mitigation and adaptation responses. Impacts of climate change on terrestrial biodiversity and ecosystems have been well-documented in the Northern Hemisphere, but long-term data to detect change in the Southern Hemisphere are limited, and some types of change are generally difficult to measure. Here we present a novel approach using local ecological knowledge to facilitate a continent-scale view of climate change impacts on terrestrial biodiversity and ecosystems that people have perceived in Australia. We sought local knowledge using a national web-based survey, targeting respondents with close links to the environment (e.g. farmers, ecologists), and using a custom-built mapping tool to ask respondents to describe and attribute recent changes they had observed within an area they knew well. Results drawn from 326 respondents showed that people are already perceiving simple and complex climate change impacts on hundreds of species and ecosystems across Australia, significantly extending the detail previously reported for the continent. While most perceived trends and attributions remain unsubstantiated, >35 reported anecdotes concurred with examples in the literature, and >20 were reported more than once. More generally, anecdotes were compatible with expectations from global climate change impact frameworks, including examples across the spectrum from organisms (e.g. increased mortality in >75 species), populations (e.g. changes in recruitment or abundance in >100 species, phenological change in >50 species), and species (e.g. >80 species newly arriving or disappearing), to communities and landscapes (e.g. >50 examples of altered ecological interactions). The overarching pattern indicated by the anecdotes suggests that people are more often noticing climate change losers (typically native species) than winners in their local areas, but with observations of potential ‘adaptation in action’ via compositional and phenological change and through arrivals and range shifts (particularly for native birds and exotic plants). A high proportion of climate change-related anecdotes also involved cumulative or interactive effects of land use. We conclude that targeted elicitation of local ecological knowledge about climate change impacts can provide a valuable complement to data-derived knowledge, substantially extending the volume of explicit examples and offering a foundation for further investigation.
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An epidemic of thunderstorm asthma in pediatric patients occurred in Yulin, a northwest city of China, on 11 September 2018. We described the epidemic and retrospectively analyzed the demographic and clinical aspects of the involved children. The caseload data of patients were collected from the hospital information system in Yulin Pediatric Hospital. The detailed document of hospitalized children with thunderstorm asthma was sourced from the medical records. The mean number of daily visits to emergency/outpatient department and the daily admission to hospital were 2.7 and 16 times, respectively, than on the other days of September. A gender prominence of males was observed in both emergency/outpatient and inpatient department. Among the 51 hospitalized children with detailed medical records, 56% of them had never experienced or were diagnosed with asthma and 25% had confirmed diagnosis of asthma. Sixty-seven percent had a history of allergic rhinitis during August and September. Seventy-six percent of the hospitalized children presented as moderate asthma. Ninety-four percent of the pediatric patients had positive IgE against mugwort pollen and 78% were monosensitized to pollen. Thunderstorm asthma can affect children, especially who has allergic rhinitis or asthma without preventive management. Mugwort is also an aeroallergen in thunderstorm asthma attacks. Thunderstorm can induce asthma attacks in children with allergic rhinitis owing to mugwort and aggravate symptoms in children with confirmed diagnosis of asthma. Children with mugwort allergy are susceptible to thunderstorm asthma and a preponderance of boys was observed. Better identification of allergic children to mugwort, giving suitable protective measures during thunderstorm and standard therapy to existing allergic situation could be a benefit for children at risk of thunderstorm asthma.
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RATIONALE: On November 21, 2016 in Australia, a major thunderstorm-asthma epidemic struck Melbourne with an unprecedented number of emergency presentations, hospital admissions and fatalities. OBJECTIVES: We identified affected patients who presented to The Royal Melbourne Hospital, an adult tertiary center in North-West Melbourne. We aimed to characterize individual patient factors associated with hospital admission and identify biomarkers in patient subgroups that are at risk of being severely affected by thunderstorm-asthma. METHODS: Cross-sectional, retrospective analysis of demographics of 240 patients presenting to The Royal Melbourne Hospital on November 21 to 22, 2016 post thunderstorm-asthma event and clinical characteristics of 70 of those patients who subsequently attended an outpatient clinic review. RESULTS: Patients were generally young adults (mean age 35 years), with seasonal rhinitis (96%) and universally (100%) sensitized to ryegrass pollen. Forty-four patients (63%) had a known diagnosis of asthma while 20% reported no previous diagnosis but had symptoms consistent with asthma. Patient characteristics associated with hospitalization were: uncontrolled asthma symptoms in the month before the thunderstorm-asthma event, symptomatic allergic rhinitis, high blood eosinophilia and lower lung function. CONCLUSION: Thunderstorm-asthma affects people with seasonal rhinitis, ryegrass sensitization and can occur without prior history of asthma, with dramatic potential to inundate a healthcare system. Our data suggests that hospitalization, and thus a more severe thunderstorm-asthma exacerbation, was associated with a known history of asthma, prior uncontrolled asthma symptoms, allergic rhinitis, high eosinophil count and lower lung function. These factors may inform strategies to identify those most at risk of thunderstorm-asthma.
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Background: Thunderstorm asthma is defined as epidemics of asthma occurring shortly after a thunderstorm. While grass pollen has been implicated in thunderstorm asthma events, little is known about the role of fungi and studies have not been synthesised. Objective: This systematic review aims to evaluate whether grass pollen is necessary in thunderstorm asthma events and whether fungi also play a part in these associations. Methods: We conducted a systematic search using six electronic databases (i.e. CINAHL, Medline (Ovid), Web of Science, ProQuest Central, EMBASE and Google Scholar) and checked reference lists. The search terms used were pollen AND thunderstorm* AND asthma. The inclusion criteria were studies published in English with original human data relating to outdoor pollen and thunderstorm asthma. Results: Twenty of 2198 studies were eligible. Reported findings differed due to variation in methodological approaches and a meta-analysis was not possible. Nonetheless, of the 20 studies included, 15 demonstrated some relationship with nine demonstrating lagged effects up to four days for increasing grass pollen counts associated with increased risk of thunderstorm asthma. Of the 10 studies that examined fungi, nine demonstrated a positive relationship with thunderstorm asthma. The fungal taxa involved varied, depending on whether measurements were recorded before, during or after the thunderstorm. Nevertheless, none of the studies considered fungi as a potential effect modifier for the pollen-thunderstorm asthma association. Conclusion: We found evidence to suggest that grass pollen was a necessary factor for thunderstorm asthma but there are other as yet unrecognised environmental factors that may also be important. Further research is required to examine the role of fungi and other environmental factors such as air quality as potential effect modifiers of the association.