Latest news on relationship between thunderstorms and respiratory allergy, severe asthma, and deaths for asthma

Thunderstorm asthma (TA) refers to the sudden increase in acute bronchospasm following a storm during pollen seasons, necessitating primary care facilities by general practitioner (GP) visits, emergency department (ED) admissions, and hospitalizations, sometimes also endotracheal intubation for severe asthma and near-fatal asthma (NFA). In the scientific literature, there are descriptions of epidemics of TA in various geographical areas of the world1-8 and climate change scenarios indicate there will be an increase in the intensity and frequency of heavy rainfall episodes, including thunderstorms, in all the world.6 On November 21, 2016, at 18:00, a dreadful storm with a gust front crossing Melbourne (Victoria, Australia) plunging suddenly temperatures of 10°C in one hour, raising humidity above 70% induced a catastrophic epidemic of TA with 10 deaths and about 9000 subjects in hospitals and ED rooms for severe asthma and NFA.4, 5 This event contributed to improve our knowledge on outbreaks of TA and on its etiopathogenetic aspects.2, 7, 8 In Melbourne, there was an extraordinary association of environmental factors with a very unusual weather occurrence with wind and torrential rain combined with a high pollen count (grass pollen airborne count of more than 100 pollens for cubic meter), sending high quantity of pollens and allergenic submicronic particles derived from pollens across the city. In Melbourne, ambulance and hospitals experienced high scale of involvement in such a reduced time period of a few hours on 21 November with grass allergens dispersed over a very large geographical area of Victoria. The rapid onset of the medical emergency and its consequences was unprecedented in the scale of the intensity in comparison with previous events, and it tested the capacity of Melbourne health system to be ready for this type of medical emergency. However, demand management strategies were insufficient to manage such a widespread and rapid onset event, with ambulance resources quickly depleted and using police officers to conduct welfare checks (Figure 1).4, 5 The event of Melbourne greatly surpassed the previous epidemic of London of June 19943 that was the largest documented outbreak before the Victoria epidemic. The other events in several areas (Birmingham, Nottingham, Cambridge (UK); Naples (Italy), Calgary (Canada); Wagga Wagga and previous epidemics of Melbourne (Australia); and several other cities of the World) were of reduced impact, and deaths were registered only in Victoria's event of 2016.4, 5 In the outbreaks in Naples, we observed a case of relapse of NFA improved only after endotracheal intubation in ED.7, 8 We treated the patient, pregnant at 5 months, intubated for 7 days in ED, with intravenous infusion of corticosteroids, theophylline, and Bronchodilators beta2-agonists, and obtained very good results with added infusion of magnesium sulfate.7, 8 The intravenous treatment with epinephrine is useful only in case of cardiac arrest and is insufficient for the treatment of asthma. After Melbourne's epidemics of TA, the number of publications on this topic has rapidly increased, with 22 manuscripts in PubMed in 19 months, from January 2017 to July 2018, reaching about the same number of papers published in 33 years since the first description of Packe and Ayres on 19852 to now. In their manuscript5 in this issue of allergy, Hew et al, in thunderstorm-affected patients in Melbourne (mean age of 32.0 years and a male predominance of 56%) interviewed by clinical telephone questionnaire, found that vulnerability factors for TA are the followings: allergic rhinitis; ryegrass pollen sensitization; pre-existing asthma; poor adherence to corticosteroid-based preventers; and outdoor location at the time of the storm. The same individual susceptibility factors with suboptimal disease control were observed by us in Naples outbreak of 2004, with the difference in Parietaria as trigger factor in Naples in side of grasses in Victoria and other areas.1, 7, 8 In the subjects affected by TA in the event of Melbourne, Australian authors found4, 5 the majority (more than 50%) did not have the previous diagnosis of asthma, although most of these had symptoms suggestive of latent asthma; rhinitis was prevalent in more than 80% of subjects with more than 70% of these being moderate to severe. There was ethnic predominance of Asian patients among ER presentations, hospital admission, and fatal cases. In their manuscript, Hew et al5 observe that odds for hospital admission were lower in Asian patients born overseas and higher in Asian patients born locally, than in non-Asian patients. They conclude that susceptibility to severe TA may be enhanced by gene-environment interactions. Regarding the mechanisms of TA, it is now clear that TA is characterized at the beginning of storm, by a rapid increase in visits for asthma in GP and ED for an allergic, IgE-mediated, airways’ response in atopic subjects to trigger factors such as allergenic microparticles quickly released by cytoplasm of pollens, in particular grasses in all the world and Parietaria in Mediterranean area and sometimes also the mold Alternaria.6-8 After water imbibition and rupture of pollens by osmotic shock, the cytoplasmatic content of pollen grains can circulate into the atmosphere as a bioaerosol of allergenic particles and due to its small size to penetrate deeply into lower bronchial airways inducing asthma attacks as a result of sudden severe allergic inflammation. However, considering the quick reduction in temperature that happened in Melbourne, it cannot be excluded a coadjuvant role of cold in increasing bronchial inflammation,9 while there is not a clear definition of the role of electric charges and thunderbolts.6-8 Fortunately, TA outbreaks are neither frequent nor responsible for a high amount of exacerbation of allergic respiratory diseases.5-7 However, the mechanisms involved in the release of allergens from pollens during thunderstorms and associated risk should be known by physicians, not only allergists but also GPs and pollen allergic patients, to help with prevention. Information about the risk of an asthma attack is relevant also in subjects affected only by seasonal allergic rhinitis (Table 1). In addition, the health consequences of TA may be prevented with adequate measures by meteorological forecast and pollen count and by correct use of adequate antiallergic and antiasthma therapy not only in asthma subjects but also in rhinitis.4, 5, 8 The authors declare that they have no conflict of interest.

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