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Thunderstorm Asthma

1. Disease Information

2026-06-30
Falcon MONDO:0004784 Model: Edison Scientific Literature 17 citations

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

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

Protective Factors

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:

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

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:

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

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

Suggested CL Terms (Cell Types)

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

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

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

The following table summarizes major documented thunderstorm asthma events worldwide:

Table (click to expand)
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

Chronic/Preventive Management

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

Secondary Prevention

Tertiary Prevention

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.

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