Thunderstorm Asthma

Complex MONDO:0004784 Pathograph 7 Show in embeddings browser Asthma Allergic Disease Respiratory Disease

Thunderstorm asthma (epidemic thunderstorm asthma, ETSA) is an acute, often epidemic outbreak of severe asthma exacerbations occurring during thunderstorms in the pollen (or outdoor mold) season among individuals sensitized to grass pollen or fungal spores. It is not a separate nosological entity from allergic asthma but a distinctive trigger-defined presentation: a combination of meteorological conditions and individual atopic susceptibility produces a sudden, high respirable load of allergen-bearing paucimicronic particles that reach the lower airways and precipitate near-simultaneous asthma attacks across a population. Many affected individuals have no prior asthma diagnosis and present only with seasonal allergic rhinitis. The catastrophic Melbourne event of November 2016 remains the largest recorded outbreak.

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5
Pathophys.
7
Phenotypes
1
Hypotheses
7
Pathograph
4
Medical Actions
2
References
1
Deep Research
◈

Mechanistic Hypotheses

1
Pollen-rupture / respirable-allergen hypothesis
pollen_rupture_respirable_allergen CANONICAL
The leading mechanistic model holds that thunderstorm outflows concentrate pollen at ground level where osmotic rupture releases respirable allergen-bearing paucimicronic particles that penetrate the lower airways of sensitized individuals, triggering epidemic asthma. Contributory cofactors proposed include electrical fields enhancing pollen rupture and outdoor mold spores.
Show evidence (1 reference)
PMID:11799365 SUPPORT Other
"Here we provide the first direct observations of the release of grass pollen allergens as respirable aerosols."
First direct experimental demonstration of respirable grass-pollen allergen aerosol release, the cornerstone of the hypothesis.
⚙

Pathophysiology

5
Thunderstorm Concentration and Osmotic Rupture of Pollen Grains
During a thunderstorm in the pollen season, dry updrafts entrain whole pollen grains into the high humidity at the cloud base, where the grains imbibe water and rupture by osmotic shock; cold downdrafts and outflows then carry the fragments to ground level and concentrate them in a shallow band of air. This releases respirable allergenic particles (cytoplasmic starch granules and other paucimicronic components, ~0.5-2.5 µm) from grains that are themselves too large (>10 µm) to enter the lower airways.
response to osmotic stress (pollen grain rupture) GO:0006970 ↑ INCREASED
Downstream
Deep Airway Deposition of Paucimicronic Allergen Particles Rupture converts non-respirable pollen grains into respirable allergen-laden aerosols capable of penetrating the lower airways.
Show evidence (2 references)
PMID:26765082 SUPPORT Human Clinical
"thunderstorms can concentrate pollen grains at ground level which may then release allergenic particles of respirable size in the atmosphere after their rupture by osmotic shock"
Review of thunderstorm-asthma epidemics articulates the core mechanism: ground-level concentration of pollen followed by osmotic rupture releasing respirable allergen particles.
PMID:11799365 SUPPORT Other
"After a cycle of wetting and drying followed by wind disturbance, grasses flowering within a chamber produced an aerosol of particles that were collected in a cascade impactor. These particles consisted of fragmented pollen cytoplasm in the size range 0.12 to 4.67 microm; they were loaded..."
Controlled-chamber aerobiology demonstrated that a wet-dry cycle yields respirable allergen-bearing pollen-cytoplasm fragments, the proposed thunderstorm mechanism.
Deep Airway Deposition of Paucimicronic Allergen Particles
The respirable allergen-bearing particles released by ruptured pollen are small enough to bypass upper-airway filtration and deposit on the bronchial epithelium of the lower airways, delivering a sudden, high allergen dose directly to the asthmatic effector site. This explains why pollen — long linked to asthma despite grains being too large to reach the bronchi — can trigger lower-airway disease under thunderstorm conditions.
bronchial epithelial cell CL:0002328
Downstream
IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation In a sensitized airway, deposited allergen cross-links specific IgE on mucosal mast cells.
Show evidence (2 references)
PMID:11799365 SUPPORT Other
"Asthma incidence has long been linked to pollen, even though pollen grains are too large to penetrate into the airways where asthmatic responses originate. Pollen allergens found in small, respirable particles have been implicated in a number of asthma epidemics, particularly ones following..."
Establishes that whole pollen is too large for the lower airways and that small respirable allergen particles are the agents implicated in thunderstorm/rainfall asthma epidemics.
PMID:26765082 SUPPORT Human Clinical
"During the first 20-30 min of a thunderstorm, patients suffering from pollen allergies may inhale a high concentration of the allergenic material that is dispersed into the atmosphere, which in turn can induce asthmatic reactions, often severe."
Describes the brief, intense inhaled-allergen exposure that drives the acute lower-airway reaction in sensitized individuals.
Bronchial Epithelial Barrier Dysfunction Facilitating Allergen Access
Asthmatic and atopic airways exhibit a dysregulated epithelial barrier — disrupted tight and adherens junctions, loss of terminal differentiation, and impaired innate defense — that pre-dates and predisposes to allergic disease. Aeroallergens, many of which carry proteolytic activity, further degrade epithelial tight junctions, enhancing paracellular allergen penetration to antigen-presenting cells in the lamina propria. This "epithelial barrier" component helps explain heightened susceptibility of pollen-sensitized airways to the sudden allergen load of a thunderstorm.
bronchial epithelial cell CL:0002328
inflammatory response GO:0006954 ↑ INCREASED
Show evidence (3 references)
PMID:28583446 SUPPORT Human Clinical
"In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation."
Supports a causal role for bronchial epithelial barrier abnormalities in translating environmental (allergen) exposures into airway immune dysregulation and exacerbation.
PMID:28583447 SUPPORT Human Clinical
"Allergens can contain proteases and have been shown to disrupt epithelial tight junctions"
Allergen-associated proteases disrupt epithelial tight junctions, a mechanism increasing allergen access across the airway barrier.
PMID:28583447 SUPPORT Human Clinical
"epithelial dysfunction characterized by these traits appears to pre-date atopy and development of allergic disease"
Indicates epithelial barrier dysfunction precedes atopy, supporting it as a predisposing host factor rather than only a consequence.
IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation
In individuals sensitized to grass pollen (and/or Alternaria) allergens, the inhaled respirable allergen cross-links allergen-specific IgE bound to high-affinity receptors on airway mucosal mast cells, triggering degranulation and release of histamine, leukotrienes, and prostaglandins (type I immediate hypersensitivity). Recruitment of eosinophils and type 2 helper T cells amplifies the type 2 inflammatory response.
mast cell CL:0000097 eosinophil CL:0000771 T-helper 2 cell CL:0000546
type I hypersensitivity GO:0016068 ↑ INCREASED mast cell degranulation GO:0043303 ↑ INCREASED type 2 immune response GO:0042092 ↑ INCREASED
Downstream
Bronchoconstriction and Acute Airflow Obstruction Mast-cell mediators induce airway smooth muscle contraction, mucus secretion, and edema.
Show evidence (1 reference)
PMID:17624415 SUPPORT Human Clinical
"Twenty-three of 26 cases had IgE sensitization to Alternaria species."
Case-control data show IgE sensitization to a relevant aeroallergen in the great majority of thunderstorm-asthma cases, supporting an IgE-mediated mechanism.
Bronchoconstriction and Acute Airflow Obstruction
Mast-cell-derived mediators provoke airway smooth muscle contraction (bronchospasm), mucosal edema, and mucus hypersecretion, producing acute variable airflow obstruction. Because exposure is sudden and intense and affects many sensitized individuals simultaneously, the result is an epidemic of acute, sometimes near-fatal, asthma attacks within a short window.
goblet cell CL:0000160
airway smooth muscle contraction GO:0006939 ↑ INCREASED
Show evidence (1 reference)
PMID:32960102 SUPPORT Human Clinical
"Epidemic thunderstorm asthma (ETSA) is due to a complex interaction of environmental and individual susceptibility factors, with outbreaks reported globally over the last four decades."
Frames the outcome as an epidemic of asthma exacerbations arising from combined environmental and host susceptibility factors.
⬡

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Thunderstorm Asthma Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.
●

Phenotypes

7
Respiratory 3
Wheezing Wheezing HP:0030828
Show evidence (1 reference)
PMID:26765082 PARTIAL Human Clinical
"patients suffering from pollen allergies may inhale a high concentration of the allergenic material that is dispersed into the atmosphere, which in turn can induce asthmatic reactions, often severe"
The cited abstract supports acute asthmatic reactions following the inhaled allergen surge; wheeze is the characteristic clinical manifestation of those reactions but is not named in the snippet, so this is graded PARTIAL.
Dyspnea Dyspnea HP:0002094
Temporal: ACUTE
Show evidence (1 reference)
PMID:32960102 PARTIAL Human Clinical
"Assessment of the clinical and immunological data highlights risk factors for ETSA presentation, hospital admission, and intensive care admission."
Severe presentations requiring hospital and intensive care admission reflect acute, severe breathlessness; cited as indirect support.
Cough Cough HP:0012735
Show evidence (1 reference)
PMID:11799365 PARTIAL Other
"This could explain asthmatic responses associated with grass pollination, particularly after moist weather conditions."
Respirable grass-pollen allergen aerosols explain the asthmatic respiratory responses (including cough) seen after moist weather.
Other 4
Acute Asthma Exacerbation Asthma HP:0002099
Temporal: ACUTE
Show evidence (1 reference)
PMID:11359963 SUPPORT Human Clinical
"Thunderstorm outflows were detected on 33% of epidemic days and only 3% of control days (odds ratio 15.0, 95% confidence interval 6.0 to 37.6)."
Strong epidemiological association between thunderstorm outflows and epidemic asthma exacerbation days.
Allergic Rhinitis VERY_FREQUENT Allergic rhinitis HP:0003193
Show evidence (1 reference)
PMID:29229087 SUPPORT Human Clinical
"allergic rhinitis during the grass pollen season was almost universal (99%), as were ryegrass pollen sensitization (100%) and exposure to the outdoor environment during the thunderstorm (94%)"
Allergic rhinitis was present in 99% of assessed thunderstorm-asthma patients, supporting VERY_FREQUENT.
Airway Obstruction Airway obstruction HP:0006536
Temporal: ACUTE
Show evidence (1 reference)
PMID:11359963 SUPPORT Human Clinical
"high concentrations of allergenic particles produced by an outflow of colder air, associated with the downdraught from a thunderstorm"
The allergen surge drives the acute asthmatic airflow obstruction that defines epidemic days.
Near-Fatal Respiratory Failure VERY_RARE Respiratory failure requiring assisted ventilation HP:0004887
Show evidence (1 reference)
PMID:32960102 SUPPORT Human Clinical
"Risk factors associated with ETSA deaths are evaluated."
The literature explicitly addresses ETSA deaths and intensive-care admission, supporting a rare near-fatal/fatal outcome.
💊

Medical Actions

4
Inhaled Short-Acting Beta-2 Agonist (Bronchodilator)
Action: Pharmacotherapy NCIT:C15986
Agent: salbutamol (albuterol) CHEBI:2549
First-line rescue therapy for acute bronchospasm during a thunderstorm asthma attack; inhaled SABAs (e.g., salbutamol/albuterol) relax airway smooth muscle. Patients with pollen allergy, including those with only seasonal rhinitis, should have access to reliever therapy and be warned about exposure during thunderstorms in the pollen season.
Mechanism Target:
Bronchoconstriction and Acute Airflow Obstruction
Show evidence (1 reference)
PMID:32960102 PARTIAL Human Clinical
"pharmacological and immunological management approaches to reduce individual susceptibility and prevent ETSA are discussed"
The overview discusses pharmacological management to reduce susceptibility to and treat ETSA; bronchodilators are standard acute care.
Corticosteroid Therapy
Action: Pharmacotherapy NCIT:C15986
Agent: corticosteroid CHEBI:50858
Inhaled corticosteroids for control and systemic corticosteroids for acute severe exacerbations reduce airway inflammation. Preventive inhaled corticosteroid use in at-risk pollen-allergic patients is part of risk reduction strategies.
Mechanism Target:
IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation
Show evidence (1 reference)
PMID:32960102 PARTIAL Human Clinical
"to improve uptake of pharmacological and immunological risk reduction and preventive strategies"
Pharmacological preventive strategies (including inhaled corticosteroids) are part of recommended ETSA risk reduction.
Allergen Immunotherapy
Action: immunotherapy procedure MAXO:0001002
Allergen-specific immunotherapy (e.g., to ryegrass pollen) is an immunological strategy to reduce individual susceptibility in sensitized patients at risk of thunderstorm asthma.
Mechanism Target:
IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation
Show evidence (1 reference)
PMID:32960102 PARTIAL Human Clinical
"pharmacological and immunological management approaches to reduce individual susceptibility and prevent ETSA are discussed"
Immunological management (allergen immunotherapy) is discussed as a strategy to reduce individual ETSA susceptibility.
Exposure Avoidance and Public Health Warning
Action: therapeutic avoidance of environmental exposure MAXO:0000053
Forecasting of thunderstorms and high pollen, public alerts, and advice to pollen-sensitive individuals to remain indoors during thunderstorms in the pollen season are central preventive measures (therapeutic avoidance of the triggering environmental exposure).
Show evidence (1 reference)
PMID:32960102 SUPPORT Human Clinical
"Public awareness and education are required to reduce exposure, and to improve uptake of pharmacological and immunological risk reduction and preventive strategies."
The literature explicitly recommends public awareness/education and exposure reduction as preventive strategies for ETSA.
🌍

Environmental Factors

3
Thunderstorm During Pollen Season
The defining trigger: a thunderstorm (specifically its cold outflow) in the grass-pollen or outdoor-mold season. Outbreaks are tightly, temporally linked to thunderstorm activity and do not occur outside pollen/spore seasons.
Show evidence (1 reference)
PMID:11359963 SUPPORT Human Clinical
"Thunderstorm outflows were detected on 33% of epidemic days and only 3% of control days (odds ratio 15.0, 95% confidence interval 6.0 to 37.6). The association was strongest in late spring and summer."
Quantifies the thunderstorm-outflow association with epidemic asthma days and its seasonal (pollen-season) confinement.
Grass (Ryegrass) Pollen Sensitization and Exposure
Sensitization to grass pollen — ryegrass (Lolium perenne) in particular — together with acute outdoor exposure during the storm is a core risk factor. In the Melbourne cohort, ryegrass pollen sensitization was present in 100% of assessed patients.
Show evidence (1 reference)
PMID:29229087 SUPPORT Human Clinical
"We conclude that ryegrass pollen sensitization, clinical allergic rhinitis, and acute allergen exposure constitute a risk-factor 'trifecta' for thunderstorm asthma."
Identifies the ryegrass-sensitization / allergic-rhinitis / acute-exposure "trifecta" as the susceptibility profile for thunderstorm asthma.
Outdoor Mold (Alternaria/Cladosporium) Sensitization
Sensitization to outdoor fungal spores, especially Alternaria alternata (and Cladosporium), is an additional and in some settings dominant risk factor; spore counts rise during thunderstorms.
Show evidence (1 reference)
PMID:17624415 SUPPORT Human Clinical
"Alternaria alternata sensitivity is a compelling predictor of epidemic asthma in patients with seasonal asthma and grass pollen allergy and is likely to be the important factor in thunderstorm-related asthma."
Case-control evidence that Alternaria sensitization strongly predicts epidemic thunderstorm-related asthma.
{ }

Source YAML

click to show 
name: Thunderstorm Asthma
creation_date: "2026-06-30T00:00:00Z"
category: Complex
disease_term:
  preferred_term: thunderstorm-related (epidemic) asthma
  term:
    id: MONDO:0004784
    label: allergic asthma
parents:
- Asthma
- Allergic Disease
- Respiratory Disease
description: >-
  Thunderstorm asthma (epidemic thunderstorm asthma, ETSA) is an acute,
  often epidemic outbreak of severe asthma exacerbations occurring during
  thunderstorms in the pollen (or outdoor mold) season among individuals
  sensitized to grass pollen or fungal spores. It is not a separate
  nosological entity from allergic asthma but a distinctive trigger-defined
  presentation: a combination of meteorological conditions and individual
  atopic susceptibility produces a sudden, high respirable load of
  allergen-bearing paucimicronic particles that reach the lower airways and
  precipitate near-simultaneous asthma attacks across a population. Many
  affected individuals have no prior asthma diagnosis and present only with
  seasonal allergic rhinitis. The catastrophic Melbourne event of November
  2016 remains the largest recorded outbreak.

pathophysiology:
- name: Thunderstorm Concentration and Osmotic Rupture of Pollen Grains
  description: >-
    During a thunderstorm in the pollen season, dry updrafts entrain whole
    pollen grains into the high humidity at the cloud base, where the grains
    imbibe water and rupture by osmotic shock; cold downdrafts and outflows
    then carry the fragments to ground level and concentrate them in a
    shallow band of air. This releases respirable allergenic particles
    (cytoplasmic starch granules and other paucimicronic components,
    ~0.5-2.5 µm) from grains that are themselves too large (>10 µm) to enter
    the lower airways.
  biological_processes:
  - preferred_term: response to osmotic stress (pollen grain rupture)
    term:
      id: GO:0006970
      label: response to osmotic stress
    modifier: INCREASED
  triggers:
  - preferred_term: thunderstorm outflow during pollen season
  - preferred_term: high ambient grass pollen concentration
  downstream:
  - target: Deep Airway Deposition of Paucimicronic Allergen Particles
    description: >-
      Rupture converts non-respirable pollen grains into respirable
      allergen-laden aerosols capable of penetrating the lower airways.
    causal_link_type: DIRECT
  evidence:
  - reference: PMID:26765082
    reference_title: "Thunderstorm-related asthma: what happens and why."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "thunderstorms can concentrate pollen grains at ground level which may then release allergenic particles of respirable size in the atmosphere after their rupture by osmotic shock"
    explanation: >-
      Review of thunderstorm-asthma epidemics articulates the core mechanism:
      ground-level concentration of pollen followed by osmotic rupture
      releasing respirable allergen particles.
  - reference: PMID:11799365
    reference_title: "Release of allergens as respirable aerosols: A link between grass pollen and asthma."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "After a cycle of wetting and drying followed by wind disturbance, grasses \nflowering within a chamber produced an aerosol of particles that were collected \nin a cascade impactor. These particles consisted of fragmented pollen cytoplasm \nin the size range 0.12 to 4.67 microm; they were loaded with group 1 allergens."
    explanation: >-
      Controlled-chamber aerobiology demonstrated that a wet-dry cycle yields
      respirable allergen-bearing pollen-cytoplasm fragments, the proposed
      thunderstorm mechanism.

- name: Deep Airway Deposition of Paucimicronic Allergen Particles
  description: >-
    The respirable allergen-bearing particles released by ruptured pollen
    are small enough to bypass upper-airway filtration and deposit on the
    bronchial epithelium of the lower airways, delivering a sudden, high
    allergen dose directly to the asthmatic effector site. This explains why
    pollen — long linked to asthma despite grains being too large to reach
    the bronchi — can trigger lower-airway disease under thunderstorm
    conditions.
  cell_types:
  - preferred_term: bronchial epithelial cell
    term:
      id: CL:0002328
      label: bronchial epithelial cell
  downstream:
  - target: IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation
    description: >-
      In a sensitized airway, deposited allergen cross-links specific IgE on
      mucosal mast cells.
    causal_link_type: DIRECT
  evidence:
  - reference: PMID:11799365
    reference_title: "Release of allergens as respirable aerosols: A link between grass pollen and asthma."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Asthma \nincidence has long been linked to pollen, even though pollen \ngrains are too large to penetrate into the airways where asthmatic responses \noriginate. Pollen allergens found in small, respirable particles have been \nimplicated in a number of asthma epidemics, particularly ones following rainfall \nor thunderstorms."
    explanation: >-
      Establishes that whole pollen is too large for the lower airways and
      that small respirable allergen particles are the agents implicated in
      thunderstorm/rainfall asthma epidemics.
  - reference: PMID:26765082
    reference_title: "Thunderstorm-related asthma: what happens and why."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "During the first 20-30 min of a thunderstorm, patients suffering from \npollen allergies may inhale a high concentration of the allergenic material that \nis dispersed into the atmosphere, which in turn can induce asthmatic reactions, \noften severe."
    explanation: >-
      Describes the brief, intense inhaled-allergen exposure that drives the
      acute lower-airway reaction in sensitized individuals.

- name: Bronchial Epithelial Barrier Dysfunction Facilitating Allergen Access
  conforms_to: "epithelial_barrier_dysfunction#Increased Transepithelial Allergen Penetration and Innate Immune Activation"
  description: >-
    Asthmatic and atopic airways exhibit a dysregulated epithelial barrier —
    disrupted tight and adherens junctions, loss of terminal differentiation,
    and impaired innate defense — that pre-dates and predisposes to allergic
    disease. Aeroallergens, many of which carry proteolytic activity, further
    degrade epithelial tight junctions, enhancing paracellular allergen
    penetration to antigen-presenting cells in the lamina propria. This
    "epithelial barrier" component helps explain heightened susceptibility of
    pollen-sensitized airways to the sudden allergen load of a thunderstorm.
  cell_types:
  - preferred_term: bronchial epithelial cell
    term:
      id: CL:0002328
      label: bronchial epithelial cell
  biological_processes:
  - preferred_term: inflammatory response
    term:
      id: GO:0006954
      label: inflammatory response
    modifier: INCREASED
  evidence:
  - reference: PMID:28583446
    reference_title: "Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "In asthmatic \npatients abnormalities in many aspects of epithelial \nbarrier function have been identified. We postulate that such \nabnormalities play a causal role in immune dysregulation in the \nairways by translating \ngene-environment interactions that underpin disease pathogenesis and \nexacerbation."
    explanation: >-
      Supports a causal role for bronchial epithelial barrier abnormalities
      in translating environmental (allergen) exposures into airway immune
      dysregulation and exacerbation.
  - reference: PMID:28583447
    reference_title: "Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Allergens can contain proteases and have been shown to disrupt epithelial tight junctions"
    explanation: >-
      Allergen-associated proteases disrupt epithelial tight junctions,
      a mechanism increasing allergen access across the airway barrier.
  - reference: PMID:28583447
    reference_title: "Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "epithelial dysfunction characterized by these traits appears to \npre-date atopy and development of allergic disease"
    explanation: >-
      Indicates epithelial barrier dysfunction precedes atopy, supporting it
      as a predisposing host factor rather than only a consequence.

- name: IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation
  description: >-
    In individuals sensitized to grass pollen (and/or Alternaria) allergens,
    the inhaled respirable allergen cross-links allergen-specific IgE bound to
    high-affinity receptors on airway mucosal mast cells, triggering
    degranulation and release of histamine, leukotrienes, and prostaglandins
    (type I immediate hypersensitivity). Recruitment of eosinophils and
    type 2 helper T cells amplifies the type 2 inflammatory response.
  cell_types:
  - preferred_term: mast cell
    term:
      id: CL:0000097
      label: mast cell
  - preferred_term: eosinophil
    term:
      id: CL:0000771
      label: eosinophil
  - preferred_term: T-helper 2 cell
    term:
      id: CL:0000546
      label: T-helper 2 cell
  biological_processes:
  - preferred_term: type I hypersensitivity
    term:
      id: GO:0016068
      label: type I hypersensitivity
    modifier: INCREASED
  - preferred_term: mast cell degranulation
    term:
      id: GO:0043303
      label: mast cell degranulation
    modifier: INCREASED
  - preferred_term: type 2 immune response
    term:
      id: GO:0042092
      label: type 2 immune response
    modifier: INCREASED
  downstream:
  - target: Bronchoconstriction and Acute Airflow Obstruction
    description: >-
      Mast-cell mediators induce airway smooth muscle contraction, mucus
      secretion, and edema.
    causal_link_type: DIRECT
  evidence:
  - reference: PMID:17624415
    reference_title: "Epidemic asthma and the role of the fungal mold Alternaria alternata."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Twenty-three of 26 cases had IgE sensitization to Alternaria species."
    explanation: >-
      Case-control data show IgE sensitization to a relevant aeroallergen in
      the great majority of thunderstorm-asthma cases, supporting an
      IgE-mediated mechanism.

- name: Bronchoconstriction and Acute Airflow Obstruction
  description: >-
    Mast-cell-derived mediators provoke airway smooth muscle contraction
    (bronchospasm), mucosal edema, and mucus hypersecretion, producing acute
    variable airflow obstruction. Because exposure is sudden and intense and
    affects many sensitized individuals simultaneously, the result is an
    epidemic of acute, sometimes near-fatal, asthma attacks within a short
    window.
  biological_processes:
  - preferred_term: airway smooth muscle contraction
    term:
      id: GO:0006939
      label: smooth muscle contraction
    modifier: INCREASED
  cell_types:
  - preferred_term: goblet cell
    term:
      id: CL:0000160
      label: goblet cell
  notes: >-
    Goblet cells are annotated here as the source of the mucus
    hypersecretion component of acute airflow obstruction (a generic feature
    of asthmatic bronchoconstriction); the cited evidence on this node
    documents the epidemic outcome rather than goblet-cell biology specifically.
  evidence:
  - reference: PMID:32960102
    reference_title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Epidemic thunderstorm asthma (ETSA) is due to a complex \ninteraction of environmental and individual susceptibility factors, with \noutbreaks reported globally over the last four decades."
    explanation: >-
      Frames the outcome as an epidemic of asthma exacerbations arising from
      combined environmental and host susceptibility factors.

phenotypes:
- category: Respiratory
  name: Acute Asthma Exacerbation
  description: >-
    Sudden onset of asthma symptoms, frequently severe, during or shortly
    after a thunderstorm in the pollen season.
  phenotype_term:
    preferred_term: Asthma
    term:
      id: HP:0002099
      label: Asthma
    temporality: ACUTE
  evidence:
  - reference: PMID:11359963
    reference_title: "Thunderstorm outflows preceding epidemics of asthma during spring and summer."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Thunderstorm outflows were detected on 33% of epidemic days and only 3% \nof control days (odds ratio 15.0, 95% confidence interval 6.0 to 37.6)."
    explanation: >-
      Strong epidemiological association between thunderstorm outflows and
      epidemic asthma exacerbation days.
- category: Respiratory
  name: Wheezing
  description: Audible expiratory wheeze from airflow obstruction.
  phenotype_term:
    preferred_term: Wheezing
    term:
      id: HP:0030828
      label: Wheezing
  evidence:
  - reference: PMID:26765082
    reference_title: "Thunderstorm-related asthma: what happens and why."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: "patients suffering from \npollen allergies may inhale a high concentration of the allergenic material that \nis dispersed into the atmosphere, which in turn can induce asthmatic reactions, \noften severe"
    explanation: >-
      The cited abstract supports acute asthmatic reactions following the
      inhaled allergen surge; wheeze is the characteristic clinical
      manifestation of those reactions but is not named in the snippet, so
      this is graded PARTIAL.
- category: Respiratory
  name: Dyspnea
  description: Breathlessness, often acute and severe.
  phenotype_term:
    preferred_term: Dyspnea
    term:
      id: HP:0002094
      label: Dyspnea
    temporality: ACUTE
  evidence:
  - reference: PMID:32960102
    reference_title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: "Assessment of the \nclinical and immunological data highlights risk factors for ETSA presentation, \nhospital admission, and intensive care admission."
    explanation: >-
      Severe presentations requiring hospital and intensive care admission
      reflect acute, severe breathlessness; cited as indirect support.
- category: Respiratory
  name: Cough
  description: Cough accompanying acute bronchospasm.
  phenotype_term:
    preferred_term: Cough
    term:
      id: HP:0012735
      label: Cough
  evidence:
  - reference: PMID:11799365
    reference_title: "Release of allergens as respirable aerosols: A link between grass pollen and asthma."
    supports: PARTIAL
    evidence_source: OTHER
    snippet: "This could explain asthmatic responses \nassociated with grass pollination, particularly after moist weather conditions."
    explanation: >-
      Respirable grass-pollen allergen aerosols explain the asthmatic
      respiratory responses (including cough) seen after moist weather.
- category: Respiratory
  name: Allergic Rhinitis
  description: >-
    Seasonal allergic rhinitis is nearly universal among thunderstorm-asthma
    patients and is frequently the only prior allergic diagnosis, often
    without a previous asthma diagnosis.
  phenotype_term:
    preferred_term: Allergic rhinitis
    term:
      id: HP:0003193
      label: Allergic rhinitis
  frequency: VERY_FREQUENT
  evidence:
  - reference: PMID:29229087
    reference_title: "Who's at risk of thunderstorm asthma? The ryegrass pollen trifecta and lessons learnt from the Melbourne thunderstorm epidemic."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "allergic rhinitis during the grass pollen season was almost universal (99%), as were ryegrass pollen sensitization (100%) and exposure to the outdoor environment during the thunderstorm (94%)"
    explanation: >-
      Allergic rhinitis was present in 99% of assessed thunderstorm-asthma
      patients, supporting VERY_FREQUENT.
- category: Respiratory
  name: Airway Obstruction
  description: Acute variable airflow obstruction from bronchospasm, edema, and mucus.
  phenotype_term:
    preferred_term: Airway obstruction
    term:
      id: HP:0006536
      label: Airway obstruction
    temporality: ACUTE
  evidence:
  - reference: PMID:11359963
    reference_title: "Thunderstorm outflows preceding epidemics of asthma during spring and summer."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "high concentrations of allergenic particles produced by an outflow of colder air, associated with the \ndowndraught from a thunderstorm"
    explanation: >-
      The allergen surge drives the acute asthmatic airflow obstruction that
      defines epidemic days.
- category: Respiratory
  name: Near-Fatal Respiratory Failure
  description: >-
    A minority of patients develop life-threatening or near-fatal asthma
    requiring intensive care and assisted ventilation; the Melbourne 2016
    outbreak caused multiple deaths.
  phenotype_term:
    preferred_term: Respiratory failure requiring assisted ventilation
    term:
      id: HP:0004887
      label: Respiratory failure requiring assisted ventilation
  frequency: VERY_RARE
  evidence:
  - reference: PMID:32960102
    reference_title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Risk factors associated with \nETSA deaths are evaluated."
    explanation: >-
      The literature explicitly addresses ETSA deaths and intensive-care
      admission, supporting a rare near-fatal/fatal outcome.

environmental:
- name: Thunderstorm During Pollen Season
  description: >-
    The defining trigger: a thunderstorm (specifically its cold outflow) in
    the grass-pollen or outdoor-mold season. Outbreaks are tightly,
    temporally linked to thunderstorm activity and do not occur outside
    pollen/spore seasons.
  presence: PRESENT
  effect: HARMFUL
  evidence:
  - reference: PMID:11359963
    reference_title: "Thunderstorm outflows preceding epidemics of asthma during spring and summer."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Thunderstorm outflows were detected on 33% of epidemic days and only 3% \nof control days (odds ratio 15.0, 95% confidence interval 6.0 to 37.6). \nThe association was strongest in late spring and summer."
    explanation: >-
      Quantifies the thunderstorm-outflow association with epidemic asthma
      days and its seasonal (pollen-season) confinement.
- name: Grass (Ryegrass) Pollen Sensitization and Exposure
  description: >-
    Sensitization to grass pollen — ryegrass (Lolium perenne) in particular —
    together with acute outdoor exposure during the storm is a core risk
    factor. In the Melbourne cohort, ryegrass pollen sensitization was present
    in 100% of assessed patients.
  presence: PRESENT
  effect: HARMFUL
  evidence:
  - reference: PMID:29229087
    reference_title: "Who's at risk of thunderstorm asthma? The ryegrass pollen trifecta and lessons learnt from the Melbourne thunderstorm epidemic."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "We conclude that ryegrass pollen sensitization, clinical allergic rhinitis, and \nacute allergen exposure constitute a risk-factor 'trifecta' for thunderstorm \nasthma."
    explanation: >-
      Identifies the ryegrass-sensitization / allergic-rhinitis / acute-exposure
      "trifecta" as the susceptibility profile for thunderstorm asthma.
- name: Outdoor Mold (Alternaria/Cladosporium) Sensitization
  description: >-
    Sensitization to outdoor fungal spores, especially Alternaria alternata
    (and Cladosporium), is an additional and in some settings dominant risk
    factor; spore counts rise during thunderstorms.
  presence: PRESENT
  effect: HARMFUL
  evidence:
  - reference: PMID:17624415
    reference_title: "Epidemic asthma and the role of the fungal mold Alternaria alternata."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Alternaria alternata \nsensitivity is a compelling predictor of \nepidemic asthma in patients with seasonal asthma and grass pollen allergy and is \nlikely to be the important factor in thunderstorm-related asthma."
    explanation: >-
      Case-control evidence that Alternaria sensitization strongly predicts
      epidemic thunderstorm-related asthma.

treatments:
- name: Inhaled Short-Acting Beta-2 Agonist (Bronchodilator)
  description: >-
    First-line rescue therapy for acute bronchospasm during a thunderstorm
    asthma attack; inhaled SABAs (e.g., salbutamol/albuterol) relax airway
    smooth muscle. Patients with pollen allergy, including those with only
    seasonal rhinitis, should have access to reliever therapy and be warned
    about exposure during thunderstorms in the pollen season.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: salbutamol (albuterol)
      term:
        id: CHEBI:2549
        label: albuterol
  target_mechanisms:
  - target: Bronchoconstriction and Acute Airflow Obstruction
  evidence:
  - reference: PMID:32960102
    reference_title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: "pharmacological and immunological management approaches to reduce individual susceptibility and \nprevent ETSA are discussed"
    explanation: >-
      The overview discusses pharmacological management to reduce
      susceptibility to and treat ETSA; bronchodilators are standard acute care.
- name: Corticosteroid Therapy
  description: >-
    Inhaled corticosteroids for control and systemic corticosteroids for
    acute severe exacerbations reduce airway inflammation. Preventive inhaled
    corticosteroid use in at-risk pollen-allergic patients is part of risk
    reduction strategies.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: corticosteroid
      term:
        id: CHEBI:50858
        label: corticosteroid
  target_mechanisms:
  - target: IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation
  evidence:
  - reference: PMID:32960102
    reference_title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: "to improve uptake of pharmacological and immunological risk reduction and preventive strategies"
    explanation: >-
      Pharmacological preventive strategies (including inhaled corticosteroids)
      are part of recommended ETSA risk reduction.
- name: Allergen Immunotherapy
  description: >-
    Allergen-specific immunotherapy (e.g., to ryegrass pollen) is an
    immunological strategy to reduce individual susceptibility in sensitized
    patients at risk of thunderstorm asthma.
  treatment_term:
    preferred_term: immunotherapy procedure
    term:
      id: MAXO:0001002
      label: immunotherapy procedure
  target_mechanisms:
  - target: IgE-Mediated Mast Cell Activation and Type 2 Airway Inflammation
  evidence:
  - reference: PMID:32960102
    reference_title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: "pharmacological and immunological management approaches to reduce individual susceptibility and \nprevent ETSA are discussed"
    explanation: >-
      Immunological management (allergen immunotherapy) is discussed as a
      strategy to reduce individual ETSA susceptibility.
- name: Exposure Avoidance and Public Health Warning
  description: >-
    Forecasting of thunderstorms and high pollen, public alerts, and advice
    to pollen-sensitive individuals to remain indoors during thunderstorms in
    the pollen season are central preventive measures (therapeutic avoidance
    of the triggering environmental exposure).
  treatment_term:
    preferred_term: therapeutic avoidance of environmental exposure
    term:
      id: MAXO:0000053
      label: therapeutic avoidance of environmental exposure
  evidence:
  - reference: PMID:32960102
    reference_title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Public awareness and education are \nrequired to reduce exposure, and to improve uptake of pharmacological and \nimmunological risk reduction and preventive strategies."
    explanation: >-
      The literature explicitly recommends public awareness/education and
      exposure reduction as preventive strategies for ETSA.

mechanistic_hypotheses:
- hypothesis_group_id: pollen_rupture_respirable_allergen
  hypothesis_label: Pollen-rupture / respirable-allergen hypothesis
  status: CANONICAL
  description: >-
    The leading mechanistic model holds that thunderstorm outflows concentrate
    pollen at ground level where osmotic rupture releases respirable
    allergen-bearing paucimicronic particles that penetrate the lower airways
    of sensitized individuals, triggering epidemic asthma. Contributory
    cofactors proposed include electrical fields enhancing pollen rupture and
    outdoor mold spores.
  evidence:
  - reference: PMID:11799365
    reference_title: "Release of allergens as respirable aerosols: A link between grass pollen and asthma."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Here we provide the first direct observations of the release of \ngrass pollen allergens as respirable aerosols."
    explanation: >-
      First direct experimental demonstration of respirable grass-pollen
      allergen aerosol release, the cornerstone of the hypothesis.

references:
- reference: PMID:28342913
  title: "Thunderstorm-related asthma attacks."
- reference: PMID:32960102
  title: "Thunderstorm asthma: an overview of mechanisms and management strategies."
📚

References & Deep Research

References

2
PMID:28342913
Thunderstorm-related asthma attacks.
No top-level findings curated for this source.
PMID:32960102
Thunderstorm asthma: an overview of mechanisms and management strategies.
No top-level findings curated for this source.

Deep Research

1
Falcon ▸
1. Disease Information
Edison Scientific Literature 17 citations 2026-06-30T04:32:02.439995

1. Disease Information

Overview

Thunderstorm asthma (TA) is defined as acute asthma attacks or bronchospasm occurring immediately after thunderstorms, characterized by sudden onset, large-scale outbreaks, and potentially fatal acute exacerbations (xiao2026triggeringmechanismsof pages 2-4, xiao2026triggeringmechanismsof pages 1-2). It represents a unique clinical entity at the intersection of meteorology, aerobiology, and allergic respiratory disease, in which specific atmospheric conditions during thunderstorms generate respirable bioaerosols that trigger mass asthma events in sensitized populations (xiao2026triggeringmechanismsof pages 1-2).

Key Identifiers

  • ICD-10/ICD-11: Coded under J45 (Asthma) with environmental trigger specification. MeSH terms include "Asthma" (D001249), "Rhinitis, Allergic, Seasonal" (D006255), and "Hypersensitivity" (D006967) (NCT07055542 chunk 1).
  • MONDO ID: No specific MONDO entry exists for thunderstorm asthma as a distinct disease entity; it is classified within the broader asthma spectrum.
  • Common synonyms: Epidemic thunderstorm asthma (ETSA), thunderstorm-related asthma, thunderstorm allergy and asthma, storm-associated asthma.

Information Source

The information in this report is derived from aggregated disease-level resources, including population-based epidemiological studies, case series from epidemic events, mechanistic research studies, and clinical trial registries.

2. Etiology

Disease Causal Factors

Thunderstorm asthma follows a tripartite pathophysiological framework involving: (1) environmental triggers, (2) epithelial barrier disruption, and (3) immune dysregulation (xiao2026triggeringmechanismsof pages 2-4). The primary causal mechanism involves pollen rupture during thunderstorms: dry updrafts entrain whole pollen grains (10–100 μm) into thunderstorm clouds where high humidity causes them to rupture via osmotic shock, releasing approximately 700 starch granules as sub-pollen particles (SPPs) smaller than 2.5 μm (damato2015meteorologicalconditionsclimate pages 9-10, cecchi2025polleninducedasthmaa pages 3-4). Cold downdrafts then carry these pollen fragments to ground level, where they penetrate lower airways and trigger asthma attacks in sensitized individuals (damato2015meteorologicalconditionsclimate pages 9-10).

Multiple concurrent meteorological factors contribute: strong convection, humidity shifts, electrical activity, sudden temperature drops, and strong winds that dramatically alter bioaerosol profiles and disperse allergens and microbes (xiao2026triggeringmechanismsof pages 7-9). The 2016 Melbourne event demonstrated a 250% increase in ruptured grass pollen particles during the storm (xiao2026triggeringmechanismsof pages 2-4).

Risk Factors

Environmental Risk Factors

  • Seasonal allergic rhinitis (SAR): The predominant risk factor—SAR patients constituted 87% of emergency presentations in Melbourne 2016 and 79.35% in Hohhot, China (xiao2026triggeringmechanismsof pages 2-4).
  • Pollen sensitization: 96% of affected individuals in one study had positive skin prick tests to ryegrass pollen, with an adjusted odds ratio of 23.0 compared to other asthma patients (damato2015meteorologicalconditionsclimate pages 9-10). In Melbourne, 90% of thunderstorm asthma cases reported recent hay fever symptoms compared with 69% of other asthma patients (damato2015meteorologicalconditionsclimate pages 9-10).
  • Outdoor exposure during thunderstorms: Critical exposure factor; individuals who remained indoors with closed windows were protected (damato2015meteorologicalconditionsclimate pages 9-10).
  • High atmospheric pollen concentrations: Epidemics occur only during seasons with high airborne allergenic pollen levels (damato2015meteorologicalconditionsclimate pages 9-10).
  • Urban residence: Urban areas show higher TA risk due to elevated pollution and airborne allergen concentrations (xiao2026triggeringmechanismsof pages 4-5).
  • Air pollutants: PM2.5, PM10, ozone, and NOx interact synergistically with fragmented pollen to compromise epithelial barriers and enhance allergen sensitization (xiao2026triggeringmechanismsof pages 4-5, xiao2026triggeringmechanismsof pages 15-16).

Genetic Risk Factors

  • 17q21 locus: Contains variants affecting GSDMB and ORMDL3 expression levels, influencing asthma risk. Specific SNPs (rs72163891 and rs7216389) alter mucosal GSDMB levels and IFN class responses (xiao2026triggeringmechanismsof pages 9-11).
  • TLR polymorphisms: TLR4 polymorphisms (e.g., D298G/N397I) amplify inflammatory responses to storm-dispersed allergens and Gram-negative bacteria. TLR5 and TLR7 expression is reduced by 40% and 60% respectively in severe asthma patients, decreasing clearance of inhaled pathogens (xiao2026triggeringmechanismsof pages 7-9).
  • Epithelial barrier genes: FLG (filaggrin) and SPINK5 gene variants affect barrier integrity and increase susceptibility (xiao2026triggeringmechanismsof pages 1-2).
  • Epigenetic modifications: DNA methylation and histone modifications dynamically regulate susceptibility genes (xiao2026triggeringmechanismsof pages 1-2).
  • Microbiome-host interactions: Airway microbial dysbiosis, including decreased microbial diversity and dysregulated short-chain fatty acid metabolism, interacts with environmental exposures to modulate susceptibility (xiao2026triggeringmechanismsof pages 1-2).

Other Risk Factors

  • Smoking, obesity, and glucocorticoid-resistant asthma increase susceptibility (xiao2026triggeringmechanismsof pages 9-11).
  • Suboptimal asthma treatment (damato2015meteorologicalconditionsclimate pages 9-10).
  • Asian/Indian ethnicity groups showed higher susceptibility in Melbourne (xiao2026triggeringmechanismsof pages 2-4).

Protective Factors

  • Staying indoors with closed windows during thunderstorms provides direct protection (damato2015meteorologicalconditionsclimate pages 9-10).
  • Regular inhaled corticosteroid use may be protective by reducing airway hyperresponsiveness (damato2015meteorologicalconditionsclimate pages 9-10).
  • Optimal asthma treatment reduces risk of severe exacerbations during thunderstorm events (damato2015meteorologicalconditionsclimate pages 9-10).

Gene-Environment Interactions

Gene-environment interactions are pivotal in determining individual susceptibility to TA. Genetic variations in innate immunity (particularly TLR polymorphisms) combine with thunderstorm-specific environmental dispersal of allergens and microbes to amplify inflammatory responses (xiao2026triggeringmechanismsof pages 7-9). The interaction of 17q21 genetic variants with environmental factors such as viruses and pollutants during thunderstorms increases acute asthma episode risk (xiao2026triggeringmechanismsof pages 9-11). Geographic variations in TLR polymorphisms further influence TA risk by interacting with region-specific environmental exposures and allergen profiles (xiao2026triggeringmechanismsof pages 7-9). The specific mechanisms of these gene-environment interactions remain an active area of research and have hindered construction of precise risk prediction models (xiao2026triggeringmechanismsof pages 1-2).

3. Phenotypes

Symptoms and Clinical Signs

Thunderstorm asthma presents as acute-onset asthma with the following features:

  • Acute bronchospasm: Sudden onset wheezing, chest tightness, shortness of breath occurring within minutes to hours of thunderstorm onset (xiao2026triggeringmechanismsof pages 2-4).
  • Severe dyspnea: Can rapidly progress to severe respiratory insufficiency requiring ICU admission (damato2015meteorologicalconditionsclimate pages 9-10).
  • Rhinitis symptoms: Nasal congestion, sneezing, rhinorrhea frequently accompany or precede bronchospasm. Suggested HPO: HP:0003193 (Allergic rhinitis).
  • Cough: Productive or non-productive cough. Suggested HPO: HP:0012735 (Cough).
  • Near-fatal/fatal asthma: In severe cases, acute respiratory failure requiring mechanical ventilation (damato2015meteorologicalconditionsclimate pages 9-10). Suggested HPO: HP:0002878 (Respiratory failure).

Phenotype Characteristics

  • Age of onset: Can affect any age, but thunderstorms increase children's hospital visit risk by 27% with precipitation increases; each 1°C temperature drop increases risk among adults under 65 by 1.4% (xiao2026triggeringmechanismsof pages 2-4).
  • Severity: Variable—ranges from mild bronchospasm to near-fatal or fatal asthma attacks (damato2015meteorologicalconditionsclimate pages 9-10).
  • Progression: Episodic—directly linked to thunderstorm events during pollen seasons. Onset is typically acute (within 20-30 minutes of thunderstorm) (xiao2026triggeringmechanismsof pages 1-2).
  • Frequency: Seasonal, dependent on co-occurrence of high pollen counts and thunderstorm activity.

Quality of Life Impact

Thunderstorm asthma episodes can cause acute, severe disruption of daily functioning, with mass emergency department presentations overwhelming healthcare systems. A 3-year longitudinal study documented persistent asthma symptoms following the 2016 Melbourne event, suggesting lasting impact on respiratory health in some individuals.

Suggested HPO Terms

  • HP:0002099 (Asthma)
  • HP:0003193 (Allergic rhinitis)
  • HP:0002094 (Dyspnea)
  • HP:0012735 (Cough)
  • HP:0002878 (Respiratory failure)
  • HP:0100785 (Wheezing)
  • HP:0002098 (Respiratory distress)

4. Genetic/Molecular Information

Susceptibility Genes (Not Causal in Mendelian Sense)

Thunderstorm asthma is a complex, multifactorial condition without single-gene causation. However, several genes modify susceptibility:

  • GSDMB (Gasdermin B, 17q21): Variants affect mucosal expression levels and IFN responses; SNP rs7216389 is strongly associated with asthma susceptibility (xiao2026triggeringmechanismsof pages 9-11).
  • ORMDL3 (ORMDL Sphingolipid Biosynthesis Regulator 3, 17q21): Altered expression levels influence asthma risk through the 17q21 genomic locus (xiao2026triggeringmechanismsof pages 9-11).
  • TLR4 (Toll-like receptor 4): Polymorphisms such as D298G/N397I amplify inflammatory responses to allergens and LPS from storm-dispersed Gram-negative bacteria (xiao2026triggeringmechanismsof pages 7-9).
  • TLR5 and TLR7: Reduced expression (40% and 60% reductions respectively in severe asthma) impairs clearance of inhaled pathogens, increasing airway inflammation during thunderstorm events (xiao2026triggeringmechanismsof pages 7-9).
  • FLG (Filaggrin): Epithelial barrier-related gene; variants compromise barrier integrity (xiao2026triggeringmechanismsof pages 1-2).
  • SPINK5 (Serine Peptidase Inhibitor Kazal Type 5): Epithelial barrier-related gene affecting susceptibility (xiao2026triggeringmechanismsof pages 1-2).

Epigenetic Information

Dynamic changes in DNA methylation and histone modifications contribute to thunderstorm asthma susceptibility (xiao2026triggeringmechanismsof pages 1-2). These epigenetic modifications can be influenced by environmental exposures and may explain why some sensitized individuals are more vulnerable than others during identical thunderstorm events.

5. Environmental Information

Environmental Factors

  • Pollen: Ryegrass (Lolium perenne) pollen is the primary trigger in temperate zones (particularly Australia and Europe), while Parietaria, olive, and Artemisia pollen are implicated in other regions (cecchi2025polleninducedasthmaa pages 4-6, damato2015meteorologicalconditionsclimate pages 9-10). Pollen grains rupture via osmotic pressure to release sub-pollen particles (SPPs) of 0.5–2.5 μm diameter (cecchi2025polleninducedasthmaa pages 3-4).
  • Air pollution: PM2.5, PM10, ozone, and NOx show positive correlations with asthma hospital visits and interact synergistically with fragmented pollen (xiao2026triggeringmechanismsof pages 2-4, xiao2026triggeringmechanismsof pages 15-16).
  • Fungal spores: Alternaria alternata and other fungal molds dispersed during thunderstorms contribute to the bioaerosol mixture (xiao2026triggeringmechanismsof pages 17-18).
  • Meteorological conditions: Sudden temperature drops, humidity increases, strong winds, heavy rainfall, and electrical discharge from lightning all contribute to pollen rupture and bioaerosol dispersal (xiao2026triggeringmechanismsof pages 2-4, xiao2026triggeringmechanismsof pages 4-5).

Climate Change Impact

Climate change is driving significant increases in thunderstorm asthma frequency: 8 major TA events were documented from 1983–1999 compared to 17 events from 2000–2024, paralleling climate change-driven increases in extreme convective weather, extended pollen seasons, and enhanced pollen allergenicity (xiao2026triggeringmechanismsof pages 2-4). Warming temperatures extend pollen seasons and increase pollen levels globally, while thunderstorms are becoming more likely to coincide with elevated pollen counts (xiao2026triggeringmechanismsof pages 15-16). Rising CO2 levels enhance plant photosynthesis and reproductive capacity, resulting in increased pollen production (damato2015meteorologicalconditionsclimate pages 1-2).

6. Mechanism / Pathophysiology

Causal Chain

The pathophysiology follows an "environmental trigger → epithelial barrier disruption → immune dysregulation" framework (xiao2026triggeringmechanismsof pages 1-2):

Step 1 – Environmental Trigger (Upstream): Thunderstorms create unique atmospheric conditions. Dry updrafts entrain whole pollen grains into cloud bases where osmotic shock from high humidity causes rupture, releasing approximately 700 starch granules per grain as sub-pollen particles (SPPs) < 2.5 μm. Cold downdrafts distribute these to ground level alongside PM2.5, ozone, and fungal spores, forming complex bioaerosols (damato2015meteorologicalconditionsclimate pages 9-10, xiao2026triggeringmechanismsof pages 5-7).

Step 2 – Epithelial Barrier Disruption (Intermediate): SPPs and associated bioaerosols cause tight junction disruption, with pollen proteases cleaving occludin, claudins, E-cadherin, and ZO-1 proteins (xiao2026triggeringmechanismsof pages 4-5). This leads to impaired mucociliary clearance and increased epithelial permeability. Damaged epithelial cells release alarmins—IL-25, IL-33, and TSLP—which serve as the pathological hub linking environmental triggers to immune activation (xiao2026triggeringmechanismsof pages 1-2, xiao2026triggeringmechanismsof pages 5-7).

Step 3 – Immune Dysregulation (Downstream): - Type 2 pathway (ILC2/Th2 axis): Alarmins activate ILC2 cells and dendritic cells, promoting Th2 differentiation. IL-4, IL-5, and IL-13 production drives IgE upregulation, eosinophil activation and infiltration, and increased mucus production (xiao2026triggeringmechanismsof pages 5-7). - IgE-mediated responses: Elevated allergen-specific IgE binds to high-affinity FcεRI receptors on mast cells and basophils, causing histamine and inflammatory mediator release (xiao2026triggeringmechanismsof pages 5-7). - Non-type 2 pathway (Th17/neutrophilic): IL-6/IL-17-mediated neutrophilic inflammation contributes, particularly in severe or steroid-resistant cases (xiao2026triggeringmechanismsof pages 15-16). - TLR-mediated innate immunity: TLRs recognize storm-generated microbial components, activating NF-κB signaling and releasing TNF-α, IL-1β, and IL-6 (xiao2026triggeringmechanismsof pages 7-9). - Aryl hydrocarbon receptor: Activated by pollutant-pollen aggregates in airway epithelial cells (xiao2026triggeringmechanismsof pages 7-9).

Step 4 – Clinical Manifestation: Cascading immune and environmental insults cause severe epithelial damage, goblet cell hyperplasia, mucus overproduction, and airway smooth muscle contraction, culminating in acute bronchospasm and severe asthma attacks (xiao2026triggeringmechanismsof pages 7-9).

Molecular Pathways

  • NF-κB signaling pathway (inflammatory cytokine production)
  • IgE-FcεRI signaling (mast cell degranulation)
  • IL-4/IL-13 JAK-STAT6 pathway (Th2 polarization)
  • IL-5 signaling (eosinophil recruitment)
  • IL-17 pathway (neutrophilic inflammation)
  • Aryl hydrocarbon receptor pathway

Suggested GO Terms

  • GO:0006955 (Immune response)
  • GO:0006954 (Inflammatory response)
  • GO:0002377 (Immunoglobulin production)
  • GO:0045576 (Mast cell activation)
  • GO:0030595 (Leukocyte chemotaxis)
  • GO:0043312 (Neutrophil degranulation)

Suggested CL Terms (Cell Types)

  • CL:0000236 (B cell)
  • CL:0000545 (T-helper 2 cell)
  • CL:0000897 (CD4-positive, alpha-beta memory T cell)
  • CL:0000771 (Eosinophil)
  • CL:0000097 (Mast cell)
  • CL:0000623 (Natural killer cell)
  • CL:0001065 (ILC2 cell)
  • CL:0002063 (Type II pneumocyte)
  • CL:0000082 (Epithelial cell of lung)

7. Anatomical Structures Affected

Organ Level

  • Primary: Lungs (lower airways, bronchi, bronchioles) — UBERON:0002048 (lung)
  • Secondary: Upper airways (nasal mucosa, sinuses) — UBERON:0001707 (nasal cavity); conjunctivae

Tissue and Cell Level

  • Airway epithelium: Bronchial and bronchiolar epithelial cells with tight junction disruption (xiao2026triggeringmechanismsof pages 4-5)
  • Smooth muscle: Airway smooth muscle contraction (xiao2026triggeringmechanismsof pages 7-9)
  • Mucosa: Goblet cell hyperplasia and mucus overproduction (xiao2026triggeringmechanismsof pages 7-9)
  • Immune cells: Eosinophils, mast cells, ILC2 cells, Th2 cells, neutrophils

Body Systems

  • Respiratory system (primary)
  • Immune system (secondary — allergic/inflammatory cascade)

8. Temporal Development

Onset

  • Age of onset: Any age; affects both children and adults. Children show increased hospital visit risk with precipitation (27% increase), while adults under 65 show 1.4% increased risk per 1°C temperature drop (xiao2026triggeringmechanismsof pages 2-4).
  • Onset pattern: Acute — symptoms develop within 20–30 minutes to hours of thunderstorm onset during pollen season (xiao2026triggeringmechanismsof pages 1-2).

Progression

  • Disease course: Episodic — directly linked to thunderstorm events during high pollen seasons
  • Duration: Self-limited in most cases, though some patients may develop persistent asthma symptoms
  • Critical period: The first 30 hours after a thunderstorm event during pollen season represent the critical vulnerability window (xiao2026triggeringmechanismsof pages 1-2)

Patterns

  • Seasonal clustering during spring/summer pollen seasons
  • Increasing frequency over time: 8 major events in 1983–1999 vs. 17 events in 2000–2024 (xiao2026triggeringmechanismsof pages 2-4)

9. Inheritance and Population

Epidemiology

Thunderstorm asthma is not a continuous-prevalence disease but rather an episodic, epidemic phenomenon. Its frequency is increasing globally due to climate change (xiao2026triggeringmechanismsof pages 2-4).

Population Demographics

  • Geographic distribution: Documented across multiple continents including Australia, Europe (Italy, UK), Middle East (Kuwait, Iran), Asia (China—Hohhot, Yulin), North America (USA, Canada), New Zealand, and Israel (xiao2026triggeringmechanismsof pages 17-18, xiao2026triggeringmechanismsof pages 2-4).
  • Affected populations: Individuals with seasonal allergic rhinitis and pollen sensitization are predominantly affected. Geographic clustering reveals higher susceptibility among Asian/Indian ethnicity groups in Melbourne (xiao2026triggeringmechanismsof pages 2-4).
  • Climate zones: Temperate zones are linked to grass pollen and type 2 inflammation; arid zones show mixed phenotypes with drought-tolerant pollens like Artemisia and Salsola (xiao2026triggeringmechanismsof pages 2-4).

The following table summarizes major documented thunderstorm asthma events worldwide:

Location Year Key allergen(s) / trigger profile Affected individuals / scale Outcomes / notable findings Evidence
Melbourne, Victoria, Australia 2016 Grass pollen, especially ryegrass; thunderstorm-associated ruptured pollen particles 3,365 emergency presentations for breathing problems within 30 hours; 476 additional asthma admissions; 672% increase in ED visits; 992% increase in admissions 10 deaths; described as the most severe documented epidemic thunderstorm asthma event; 87% of emergency presentations had seasonal allergic rhinitis (xiao2026triggeringmechanismsof pages 1-2, xiao2026triggeringmechanismsof pages 2-4)
Wagga Wagga, New South Wales, Australia not stated in retrieved evidence Ryegrass pollen during thunderstorm conditions 215 asthmatic subjects attended emergency department 41 hospital admissions; 96% had positive skin tests to ryegrass pollen (damato2015meteorologicalconditionsclimate pages 9-10)
Naples, Italy 2004 Parietaria pollen during thunderstorm conditions 7 patients with severe asthma attacks 1 near-fatal case requiring ICU admission for severe bronchial obstruction and acute respiratory insufficiency; all 7 sensitized to Parietaria pollen (damato2015meteorologicalconditionsclimate pages 9-10)
Hohhot, China not stated in retrieved evidence Arid-zone pollen profile, including drought-tolerant pollens such as Artemisia/Salsola Exact event count not provided in retrieved evidence 79.35% of cases had seasonal allergic rhinitis; cited as a major recent outbreak in an arid region (xiao2026triggeringmechanismsof pages 2-4)
Ahvaz, Iran (southwest region) not stated in retrieved evidence Thunderstorm-linked aeroallergen outbreak; specific allergen not detailed in retrieved evidence Exact event count not provided in retrieved evidence Cited as a major outbreak region in global epidemiology summaries (xiao2026triggeringmechanismsof pages 17-18, xiao2026triggeringmechanismsof pages 2-4)
Kuwait not stated in retrieved evidence Thunderstorm-linked aeroallergen outbreak in desert climate; specific allergen not detailed in retrieved evidence Exact event count not provided in retrieved evidence Fatal and near-fatal cases reported in a desert-country setting (xiao2026triggeringmechanismsof pages 17-18)
New Zealand not stated in retrieved evidence Thunderstorm-related aeroallergen exposure; specific allergen not detailed in retrieved evidence Case/event numbers not provided in retrieved evidence Confirms thunderstorm-related asthma can occur outside Australia in comparable pollen seasons (xiao2026triggeringmechanismsof pages 17-18)
Canada not stated in retrieved evidence Thunderstorm-linked aeroallergen exposure; specific allergen not detailed in retrieved evidence Case/event numbers not provided in retrieved evidence Listed among documented countries with thunderstorm asthma reports (xiao2026triggeringmechanismsof pages 17-18)
Israel not stated in retrieved evidence Thunderstorm-linked aeroallergen exposure; specific allergen not detailed in retrieved evidence Case/event numbers not provided in retrieved evidence Listed among documented countries with thunderstorm asthma reports (xiao2026triggeringmechanismsof pages 17-18)
United Kingdom not stated in retrieved evidence Thunderstorm-linked pollen sensitization; specific allergen not detailed in retrieved evidence Case/event numbers not provided in retrieved evidence Referenced in global summaries as part of documented thunderstorm asthma literature (xiao2026triggeringmechanismsof pages 17-18)

Table: This table summarizes major documented thunderstorm asthma outbreaks and reports worldwide, highlighting geography, likely allergens, scale, and clinical outcomes. It is useful for comparing recurrent epidemiologic patterns across temperate and arid settings.

10. Diagnostics

Clinical Diagnosis

Thunderstorm asthma is primarily a clinical-epidemiological diagnosis based on: - Acute asthma presentation temporally associated with a thunderstorm event - Occurrence during high pollen season - Evidence of pollen sensitization (skin prick testing, serum specific IgE)

Biomarkers

  • Serum specific IgE (sp-IgE) to ryegrass pollen and allergen sub-components (Lol p 1, Lol p 5, Phl p 2, Phl p 5) — the CARISTA study is investigating sp-IgE thresholds as key predictive biomarkers (NCT07055542 chunk 1).
  • Blood eosinophil levels — inflammatory cell marker assessed in the CARISTA study (NCT07055542 chunk 1).
  • Skin prick testing to grass pollen — 96% positivity to ryegrass in affected populations (damato2015meteorologicalconditionsclimate pages 9-10).

Functional Tests

  • Spirometry (FEV1): Lung function testing to assess baseline airway obstruction and asthma severity (NCT07055542 chunk 1).
  • Peak expiratory flow: For monitoring acute bronchospasm.

Differential Diagnosis

  • Conventional asthma exacerbation (non-thunderstorm related)
  • Anaphylaxis
  • Acute bronchitis
  • Hyperventilation syndrome
  • Pulmonary embolism
  • Foreign body aspiration

Screening

The CARISTA study (NCT07055542) is developing a biomarker-based risk assessment tool to identify individuals at high risk of seasonal allergic and thunderstorm asthma, using sp-IgE thresholds, lung function, eosinophil levels, and allergen component sensitization profiles (NCT07055542 chunk 1).

11. Outcome/Prognosis

Mortality

The 2016 Melbourne event—the most severe documented epidemic thunderstorm asthma event—resulted in 10 deaths within 30 hours (xiao2026triggeringmechanismsof pages 1-2). Near-fatal cases requiring ICU admission have been documented in Naples and other locations (damato2015meteorologicalconditionsclimate pages 9-10). One case report documented a relapse in a pregnant woman who experienced near-fatal asthma 7 years after an initial thunderstorm episode (damato2015meteorologicalconditionsclimate pages 9-10).

Morbidity

During the 2016 Melbourne event, emergency departments experienced a 672% increase in visits for breathing problems (3,365 total visits) with 476 additional asthma admissions representing a 992% increase (xiao2026triggeringmechanismsof pages 1-2). Healthcare system surge capacity was severely strained.

Disease Course

Most cases are self-limited with appropriate acute treatment. However, longitudinal studies suggest some patients develop persistent asthma symptoms following severe thunderstorm asthma episodes.

12. Treatment

Acute Management

  • Inhaled bronchodilators (SABA): First-line for acute bronchospasm relief (xiao2026triggeringmechanismsof pages 13-15). Suggested MAXO: MAXO:0000381 (Bronchodilator therapy).
  • Oxygen therapy: For severe hypoxemic cases (damato2015meteorologicalconditionsclimate pages 9-10).
  • Systemic corticosteroids: Intravenous methylprednisolone for severe attacks (damato2015meteorologicalconditionsclimate pages 9-10). Suggested MAXO: MAXO:0000647 (Corticosteroid therapy).

Chronic/Preventive Management

  • Inhaled corticosteroids (ICS): Stabilize epithelial barrier function and reduce airway inflammation with consistent use; may be protective against thunderstorm-induced attacks (xiao2026triggeringmechanismsof pages 13-15, damato2015meteorologicalconditionsclimate pages 9-10). Suggested MAXO: MAXO:0001001 (Inhaled corticosteroid therapy).
  • Triple therapy (ICS/LABA/LAMA): For patients with inadequately controlled type 2 inflammation (xiao2026triggeringmechanismsof pages 13-15).
  • Allergen immunotherapy (AIT): Disease-modifying treatment for long-term management, administered subcutaneously, sublingually, or orally (xiao2026triggeringmechanismsof pages 13-15). Suggested MAXO: MAXO:0001189 (Allergen immunotherapy).
  • Biologic agents: Anti-IgE (omalizumab), anti-IL-5, and anti-IL-4R biologics for severe cases with persistent type 2 inflammation (xiao2026triggeringmechanismsof pages 13-15). Suggested MAXO: MAXO:0001195 (Biologic therapy).

Active Clinical Trial

The CARISTA Study (NCT07055542, University of Melbourne, recruiting since August 2025, estimated completion 2030) is enrolling 530 adults with seasonal allergic rhinitis to develop a biomarker-based risk assessment tool for predicting and preventing seasonal allergic and thunderstorm asthma exacerbations (NCT07055542 chunk 1, NCT07055542 chunk 2).

13. Prevention

Primary Prevention

  • Avoidance of outdoor exposure during thunderstorms: The most effective prevention; remaining indoors with closed windows during thunderstorm events in pollen season is protective (damato2015meteorologicalconditionsclimate pages 9-10).
  • Early warning systems: Integrating meteorological data with allergen concentration tracking to generate timely TA risk alerts. Machine learning models enhance detection of severe weather events coinciding with high pollen levels, enabling patients to receive alerts to stay indoors (xiao2026triggeringmechanismsof pages 15-16, xiao2026triggeringmechanismsof pages 12-13).
  • Public health education: Targeted health education for vulnerable populations (asthma/allergic rhinitis patients) to enhance self-protection skills and emergency response capabilities (xiao2026triggeringmechanismsof pages 12-13).
  • Air quality interventions: Strengthening air quality standards to reduce pollutants (PM2.5, O3, NO2) and implementing urban greening to mitigate airborne allergen concentrations (xiao2026triggeringmechanismsof pages 12-13).

Secondary Prevention

  • Pollen monitoring systems: Real-time monitoring and funding for pollen monitoring to provide accurate data for treatment decisions and allergen avoidance (xiao2026triggeringmechanismsof pages 15-16).
  • Wearable sensors and digital health: Personal health parameter monitoring through wearable devices and smart health management systems (xiao2026triggeringmechanismsof pages 13-15, xiao2026triggeringmechanismsof pages 12-13).
  • Cross-departmental collaboration: Coordination among meteorological, public health, and medical institutions for rapid response (xiao2026triggeringmechanismsof pages 12-13).

Tertiary Prevention

  • Individualized treatment pathways: Based on risk assessment including symptom management, exacerbation risk, type 2 inflammatory markers, allergic conditions, and comorbidities (xiao2026triggeringmechanismsof pages 15-16).
  • Collaborative multidisciplinary care: Involving pulmonologists, allergists, and otolaryngologists (xiao2026triggeringmechanismsof pages 15-16).
  • Targeted interventions for disadvantaged communities: Addressing socioeconomic factors affecting susceptibility (xiao2026triggeringmechanismsof pages 12-13).

14. Other Species / Natural Disease

Veterinary Relevance

Thunderstorm asthma is primarily a human condition linked to allergic sensitization. While horses can develop recurrent airway obstruction (equine asthma) triggered by environmental allergens, specific thunderstorm-triggered asthma epidemics in animals have not been well documented. Grass pollen affects multiple mammalian species, and companion animals (dogs, cats) can develop pollen-allergic conditions, though thunderstorm-specific triggering has not been systematically studied.

15. Model Organisms

Model Systems

No specific animal models have been developed exclusively for thunderstorm asthma. However, relevant model systems include: - Murine models of pollen-induced asthma: Ovalbumin-sensitized and pollen-challenged mouse models recapitulate aspects of IgE-mediated airway inflammation. - Sub-pollen particle exposure models: In vitro studies using osmotically ruptured pollen particles to study allergenicity at the component level. - Airway epithelial cell cultures: Human bronchial epithelial cells exposed to pollen extracts and particulate matter to study tight junction disruption, alarmin release, and barrier function.

Limitations

Current models do not fully recapitulate the mass-exposure, acute-onset nature of thunderstorm asthma or the complex bioaerosol mixtures (pollen fragments + pollutants + fungal spores) encountered during real thunderstorm events.

Summary and Future Directions

Thunderstorm asthma is an increasingly recognized, climate-sensitive public health emergency characterized by mass acute asthma events triggered by the confluence of thunderstorm meteorology and high allergenic pollen concentrations. The pathophysiology involves a cascade from environmental trigger (pollen rupture to sub-pollen particles) through epithelial barrier disruption to immune dysregulation via both type 2 (ILC2/Th2/IgE) and non-type 2 (Th17/neutrophilic) pathways (xiao2026triggeringmechanismsof pages 1-2, xiao2026triggeringmechanismsof pages 15-16). Climate change is amplifying the risk by extending pollen seasons, increasing pollen concentrations, and generating more frequent severe thunderstorms (xiao2026triggeringmechanismsof pages 2-4, xiao2026triggeringmechanismsof pages 15-16). Future research priorities include development of validated early warning systems using machine learning, identification of predictive biomarkers through studies like CARISTA (NCT07055542 chunk 1), elucidation of gene-environment interactions governing individual susceptibility (xiao2026triggeringmechanismsof pages 1-2), and implementation of integrated public health response frameworks across meteorological and healthcare systems (xiao2026triggeringmechanismsof pages 12-13).

References

  1. (xiao2026triggeringmechanismsof pages 2-4): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  2. (xiao2026triggeringmechanismsof pages 1-2): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  3. (NCT07055542 chunk 1): Creating A Risk Assessment Tool for Thunderstorm Asthma: the CARISTA Study. University of Melbourne. 2025. ClinicalTrials.gov Identifier: NCT07055542

  4. (damato2015meteorologicalconditionsclimate pages 9-10): G. D'Amato, S. Holgate, R. Pawankar, D. Ledford, L. Cecchi, M. Al‐Ahmad, Fatma Al-Enezi, S. Al‐Muhsen, I. Ansotegui, C. Baena-Cagnani, David J. Baker, H. Bayram, K. Bergmann, L. Boulet, J. Buters, M. D’Amato, Sofia Dorsano, J. Douwes, S. E. Finlay, D. Garrasi, Maximiliano Gómez, T. Haahtela, R. Halwani, Youssouf Hassani, B. Mahboub, G. Marks, P. Michelozzi, M. Montagni, C. Nunes, J. J. Oh, Todor A Popov, J. Portnoy, E. Ridolo, N. Rosário, M. Rottem, M. Sánchez-Borges, Elopy Sibanda, J. Sienra-Monge, C. Vitale, and I. Annesi-Maesano. Meteorological conditions, climate change, new emerging factors, and asthma and related allergic disorders. a statement of the world allergy organization. The World Allergy Organization Journal, Jul 2015. URL: https://doi.org/10.1186/s40413-015-0073-0, doi:10.1186/s40413-015-0073-0. This article has 764 citations and is from a peer-reviewed journal.

  5. (cecchi2025polleninducedasthmaa pages 3-4): L. Cecchi, M. Martini, K. Jaubashi, A.M. Marra, A. Musarra, F. Papia, A. Vaghi, G. Valenti, B. Yang, and M.B. Bilò. Pollen-induced asthma: a specific pheno-endotype of disease? European Annals of Allergy and Clinical Immunology, 57:197, Sep 2025. URL: https://doi.org/10.23822/eurannaci.1764-1489.403, doi:10.23822/eurannaci.1764-1489.403. This article has 3 citations and is from a peer-reviewed journal.

  6. (xiao2026triggeringmechanismsof pages 7-9): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  7. (xiao2026triggeringmechanismsof pages 4-5): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  8. (xiao2026triggeringmechanismsof pages 15-16): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  9. (xiao2026triggeringmechanismsof pages 9-11): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  10. (cecchi2025polleninducedasthmaa pages 4-6): L. Cecchi, M. Martini, K. Jaubashi, A.M. Marra, A. Musarra, F. Papia, A. Vaghi, G. Valenti, B. Yang, and M.B. Bilò. Pollen-induced asthma: a specific pheno-endotype of disease? European Annals of Allergy and Clinical Immunology, 57:197, Sep 2025. URL: https://doi.org/10.23822/eurannaci.1764-1489.403, doi:10.23822/eurannaci.1764-1489.403. This article has 3 citations and is from a peer-reviewed journal.

  11. (xiao2026triggeringmechanismsof pages 17-18): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  12. (damato2015meteorologicalconditionsclimate pages 1-2): G. D'Amato, S. Holgate, R. Pawankar, D. Ledford, L. Cecchi, M. Al‐Ahmad, Fatma Al-Enezi, S. Al‐Muhsen, I. Ansotegui, C. Baena-Cagnani, David J. Baker, H. Bayram, K. Bergmann, L. Boulet, J. Buters, M. D’Amato, Sofia Dorsano, J. Douwes, S. E. Finlay, D. Garrasi, Maximiliano Gómez, T. Haahtela, R. Halwani, Youssouf Hassani, B. Mahboub, G. Marks, P. Michelozzi, M. Montagni, C. Nunes, J. J. Oh, Todor A Popov, J. Portnoy, E. Ridolo, N. Rosário, M. Rottem, M. Sánchez-Borges, Elopy Sibanda, J. Sienra-Monge, C. Vitale, and I. Annesi-Maesano. Meteorological conditions, climate change, new emerging factors, and asthma and related allergic disorders. a statement of the world allergy organization. The World Allergy Organization Journal, Jul 2015. URL: https://doi.org/10.1186/s40413-015-0073-0, doi:10.1186/s40413-015-0073-0. This article has 764 citations and is from a peer-reviewed journal.

  13. (xiao2026triggeringmechanismsof pages 5-7): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  14. (xiao2026triggeringmechanismsof pages 13-15): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

  15. (NCT07055542 chunk 2): Creating A Risk Assessment Tool for Thunderstorm Asthma: the CARISTA Study. University of Melbourne. 2025. ClinicalTrials.gov Identifier: NCT07055542

  16. (xiao2026triggeringmechanismsof pages 12-13): Zhimin Xiao, Yilin Shi, Dongpeng Zhao, Ying Wang, and Yan Gu. Triggering mechanisms of acute thunderstorm asthma: epithelial barrier disruption and immune dysregulation. Respiratory Research, Feb 2026. URL: https://doi.org/10.1186/s12931-026-03532-6, doi:10.1186/s12931-026-03532-6. This article has 1 citations and is from a domain leading peer-reviewed journal.

Artifacts