Summary
Background
Asthma epidemics associated with thunderstorms have had catastrophic effects on people and emergency services. Seasonal allergic rhinitis ( SAR) is present in the vast majority of people who develop thunderstorm asthma (TA), but there is little evidence regarding risk factors for thunderstorm asthma (TA) among the rhinitis population. seasonal allergy (SAR).
Aim
We sought to identify risk factors for a history of AT and hospital presentation in a cohort of people with SAR.
Methods
This multicenter study recruited adults from Melbourne, Australia, with a prior self-reported diagnosis of TA and/or SAR.
Clinical information, spirometry results, white blood cell count, rye grass pollen-specific IgE concentration (RGP-sp), and fraction of exhaled nitric oxide were measured to identify risk factors for a history of TA in people with SAR.
Results
Of a total of 228 people with seasonal allergic rhinitis (SAR), 35% (80 of 228) reported only SAR (the I-SAR group), 37% (84 of 228) reported thunderstorm asthma symptoms (TA ) but had not attended hospital for treatment (the O-TA group ), and 28% (64 of 228) had presented to hospital for TA (the H-TA group ).
All patients in the H-TA group reported a previous diagnosis of asthma.
Logistic regression analysis of factors associated with O-TA and H-TA indicated that lower FEV 1 and an Asthma Control Questionnaire score greater than 1.5 were associated with H-TA.
Higher blood rye grass pollen-specific IgE (RGP-sp IgE), eosinophil count, and fractional level of exhaled nitric oxide were significantly associated with both O-TA and H-TA.
Receiver operating curve analysis showed that an RGP-sp IgE concentration greater than 10.1 kU/l and a prebronchodilator FEV 1 value of 90% or less were biomarkers of increased risk for H-TA.
Conclusion
Clinical testing can identify the risk of a history of AT in people with SAR and therefore inform patient-specific treatment recommendations.
Comments
"Thunderstorm asthma" is thought to be triggered by the combination of wind, humidity and lightning, which break down grass pollen and mold spores and break them down into aerosol-like particles. Such particles could cause asthma symptoms and exacerbations. After a 2016 thunderstorm in Melbourne, Australia, there were 3,400 excess emergency department visits for asthma and 10 asthma deaths.
Researchers in Australia studied 228 patients with self-reported allergic rhinitis and thunderstorm asthma. Sensitivity to rye grass pollen , lower lung function, peripheral eosinophilia >300/µL, high fractional levels of exhaled nitric oxide, and worse asthma control scores were associated with thunderstorm asthma.
Grass pollen allergy and forced expiratory volume in 1 second <90% predicted were most strongly associated with excess risk of hospitalization.
Australia appears to be the epicenter of thunderstorm asthma, but there are patients in the US who complain of increased asthma symptoms with late spring and early summer storms. AND
The take-home message seems to be that the more allergic inflammation you have, the higher your risk of thunderstorm asthma. And conversely, the better controlled your asthma is, the less likely you are to have an exacerbation related to a thunderstorm or any other trigger.
