19/09/2022
Thunderstorm Asthma!
Yes, it is a thing...
Read on for more information or phone if you think this is you, to discuss treatment options (even with concurrent GP medications)
https://pixabay.com/.../clouds-wheat-fields-fields.../
Thunderstorm Asthma
Individuals with hay fever (seasonal allergic rhinitis (SAR)) are at higher risk of thunderstorm asthma (TA), which is now recognised as an environmental health emergency. A new study indicates that in individuals with SAR, clinical tests can identify the risk of a history of TA and be used to inform patient-specific treatment recommendations (1).
Thunderstorm asthma refers to allergic asthma exacerbations that occur in the hours after a thunderstorm, especially storms occurring during pollen seasons. TA is thought to be triggered by the combination of wind, humidity, and lightning, which ruptures grass pollen and mould spores and breaks them into aerosolised particles (2).
Typically, intact pollen grains (35-40 µm diameter) are too large to pe*****te the lower airways, where inflammation commonly occurs in asthma (3). However, these pollen grains can rupture in the atmosphere when exposed to rainfall, high humidity, wind, and lightning activity, causing them to release extremely fine particles (≤2.5 µm diameter) that can pe*****te further into the lower airways compared with intact pollen (4,5,6). Each ruptured pollen grain releases hundreds of starch granules containing allergens that can induce asthma symptoms in susceptible individuals and respiratory distress in individuals with no history of diagnosed asthma (6,7).
Symptoms of TA include acute onset coughing, shortness of breath, wheezing, and respiratory distress within 20 – 30 minutes of a storm (😎. These symptoms occur due to an early allergic asthmatic response, where pollen particles initiate mast cell degranulation and bronchoconstriction. Mast cells release histamine and other inflammatory mediators that cause airway smooth muscle to contract, mucosal oedema (lining of the airway), and mucous production (mucus is produced to flush out the offending pollen/toxin) (9). The early asthmatic response is followed by an inflammatory phase, where an influx of inflammatory cells, including eosinophils, perpetuate bronchoconstriction, (airway narrowing and inflammation) (7,10,11). Although inhaled bronchodilators are often effective, hypoxia (lack of oxygen to the tissue) and respiratory failure can occur, with death a possible complication from the degree of inflammation (2).
TA epidemics have been reported worldwide. Most frequently, however, events have occurred in south-eastern Australia, during spring (12). Rye grass pollen is the primary trigger of all Australian events (13). However, fungal spores and other types of pollen have been implicated in events in the UK, Canada, and Italy (14,15,16,17,18).
Previous studies of Australian TA epidemics indicate that symptomatic hay fever (SAR) and the presence of allergen-specific IgE (blood test from your GP) to ryegrass pollen (RGP-spIgE) are almost universal in those who suffer from TA (12). Other risk factors include:
* exposure to the outdoor environment at the time of the storm
* age (20 -50 years) (comparable to the age distribution of allergic rhinitis)
* male s*x
* Asian or Indian ethnicity
* poor adherence to inhaled corticosteroid (ICS) preventer
* hospital admission for asthma in the previous year (8,19,20,21).
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