On Nov 21, 2016, Melbourne (VIC, Australia) was experiencing the peak of an unprecedented spring heatwave. Temperatures that day climbed to 35°C, the hottest recording since March that year, and the pollen count was extremely high, with airborne ryegrass pollen concentrations of more than 100 grains per m3 of air. Around 1400 h, the Australian Bureau of Meteorology issued warnings across most of the state for severe thunderstorms with damaging winds. Between 1700 h and 1830 h, the temperature suddenly dropped from 35°C to the low 20s and thunderstorms started to erupt, sending severe gust front winds over Melbourne's metropolitan area. Within an hour, in a nightmarish scenario, the emergency medical services started to receive hundreds of calls for acute respiratory distress and breathing difficulties throughout the state. By midnight they had received calls for 1326 cases, a caseload so extreme that they ran out of ambulances after attending to 500. The call volume remained above normal levels until 0700 h the next day. Within 30 h of the storm breaking, there were 3365 excess respiratory-related presentations to emergency departments (ie, 672% above the average), and 476 excess asthma-related admissions to hospital (992% above the average). Additionally, there was a substantially increased number of out-of-hospital cardiac arrests and prehospital deaths. In total, around 10 000 people needed treatment in hospital emergency departments for asthma attacks within a short time of the thunderstorm and ten people died, six within a week of the storm. A representative of Ambulance Employees Australia commented to a newspaper that Nov 21 “would have been a traumatising night…an event equivalent to a terrorist attack where people are critically injured”. The 2016 Melbourne event was the largest and most catastrophic occurrence of epidemic thunderstorm asthma, defined as multiple presentations of acute asthma attacks or bronchospasms immediately after a thunderstorm. The event was not unique; although rare, there have been 26 epidemic thunderstorm asthma events reported globally since 1983. 11 of these events have happened in Australia, mostly in the Melbourne area, but thunderstorm asthma events have also been documented in Saudi Arabia, North America, Iran, China, UK, and Italy, with epidemic events noted in 1994 in London (UK), in 2013 in Ahvaz (Iran), and in 2016 in Kuwait. The most recent thunderstorm asthma event was recorded in Yulin (China) in 2018. Because thunderstorm asthma events have occurred most frequently in the state of Victoria (Australia), policymakers there (and in other regions with a history of thunderstorm asthma) have taken proactive measures to manage the harmful outcomes of epidemic thunderstorm asthma, including creating a website that forecasts the risk of an event occurring within the next 3 days and issuing news alerts warning of the imminent possibility of epidemic thunderstorm asthma. The forecasts are based on a risk matrix identifying the meteorological and environmental conditions involved in thunderstorm asthma (such as high concentrations of an aeroallergen), combined with identification of biological risk factors and susceptible individuals, according to those most affected in previous events. The Victoria risk forecast website deems the highest risk of an epidemic thunderstorm asthma event occurring between Oct 1 and Dec 31 (the ryegrass pollen season) on days when there is a high pollen forecast and severe thunderstorms with strong winds are likely to be present, and that people with current, past, or undiagnosed asthma or hay fever are most at risk, especially those with both conditions or poorly controlled asthma. This risk prediction is generally accurate regarding the basic data from the 2016 Melbourne event—a high pollen count coincided with a thunderstorm that day, and the 2018 inquest heard that all ten people who died had pre-existing asthma. However, the causes and risk factors underlying epidemic thunderstorm asthma are more complex than initially thought. High pollen counts and thunderstorms often occur together, but don't always trigger asthma events. Ryegrass pollen grains are normally too large to reach the lungs and usually get no further than the upper airways after inhalation. The role of thunderstorms was originally thought to centre around high humidity conditions causing pollen rupture and release of sub-pollen particles that are small enough to be easily inhaled deep into the lungs. However, the relative humidity during events such as the 2016 Melbourne event was very low with little rainfall, thus humidity-induced rupturing cannot explain the 2016 Melbourne event. A model hypothesised that alternative pollen rupture mechanisms, especially those caused by lightning strikes, might have generated the pattern of a large release of sub-pollen particles in the 2016 Melbourne event following the storm's path; however, the correlation between the lightning strikes and asthma attacks is not perfect and many other triggers of thunderstorm asthma will need to be uncovered in future studies. Ryegrass pollen might be the main allergen involved in thunderstorm asthma in Australia, but other allergens play a role in thunderstorm asthma events in other countries, such as Parietaria pollen in an event in Naples (Italy) in 2004 and mugwort pollen in the 2018 Yulin event. Concentrations of other allergens such as fungal spores are also hugely increased during thunderstorms. Identifying individuals who might be at risk of epidemic thunderstorm asthma is just as complicated. Although all ten individuals who died in the 2016 Melbourne event had a previous diagnosis of asthma, some reports suggest that current asthma was not a sufficient predictor of risk of a thunderstorm asthma attack during the 2016 Melbourne event, with only 28% of 2242 cases presenting to emergency departments having current doctor-diagnosed asthma. However, nearly all patients in this event and previous thunderstorm asthma events had clinical allergic rhinitis (ie, hay fever) with a ryegrass pollen allergy; therefore, managing control of allergic rhinitis and uptake of allergen immunotherapy in individuals with allergic rhinitis or seasonal asthma with a high level of sensitisation to grass pollen allergens could help to prevent epidemic thunderstorm asthma. Sensitisation to relevant allergens appears to confer baseline risk for epidemic thunderstorm asthma. Further studies of the 2016 Melbourne event showed that strong predictors of epidemic thunderstorm asthma symptoms were a history of allergic rhinitis (odds ratio [OR] 2·77, p<0·001), and being admitted to hospital for asthma in the preceding year (adjusted OR 3·16, 95% CI 1·63–6·12). In the 2013 Ahvaz epidemic thunderstorm asthma event, most of the 2000 individuals presenting to emergency departments with acute bronchospasm had no history of asthma, but nearly 40% had allergies. In the most recent thunderstorm asthma event in Yulin, of 51 children admitted to hospital with asthma symptoms, only 25% had a confirmed previous diagnosis of asthma, but 67% had a history of allergic rhinitis. An unexpected finding from studies of the 2016 Melbourne event was that thunderstorm asthma disproportionately affected individuals from Asian backgrounds. In one study, being of self-identified Asian or Indian ethnicity was the strongest predictor of epidemic asthma symptoms, even in individuals who had symptoms but did not seek medical help (OR 3·24, p<0·001). In a second study, the highest risk factor requiring admission to hospital during the event was being of Asian ethnicity but born in Australia (OR 5·42, 95% CI 1·56–18·83), suggesting that susceptibility to thunderstorm asthma might be due to interactions between genes and the environment. Additionally, of the ten individuals who died, six were of Asian or Indian ethnicity (relative risk 4·54, 95% CI 1·28–16·09; p=0·01). Francis Thien (Box Hill Hospital & Monash University, Box Hill, VIC, Australia) commented “Those of Asian or Indian ethnic descent were at increased risk in the Melbourne 2016 event, which may be related to [an] increased predisposition to allergy of Asian migrants to Australia and other western countries.” Some clinical tests can identify a risk of thunderstorm asthma occurring in some individuals; in one study of 228 people with seasonal allergic rhinitis during the 2016 Melbourne event, higher ryegrass pollen-specific IgE concentrations, eosinophil counts, and fractional exhaled nitric oxide concentrations were associated with thunderstorm asthma symptoms, therefore such tests could be used to inform patient-specific treatment recommendations. The high concentrations of eosinophils suggest that patients with epidemic thunderstorm asthma have a high degree of uncontrolled airway inflammation that predisposes to exacerbation during thunderstorm asthma events. Additionally, as shown in longitudinal studies of children, increases in serum IgE to the Lol p 5 allergen of ryegrass pollen coincided with progression to asthma; thus sensitisation to Lol p 5 allergen might underlie the immunological link between Lol p 5 and allergic inflammation in the lungs during epidemic thunderstorm asthma events. Therefore, risk stratification based on measuring an individual's IgE concentrations to key allergen components of ryegrass pollen could predict their symptom severity during epidemic thunderstorm asthma. Potential molecular pathways that are thought to be involved in the pathobiology of thunderstorm asthma include respiratory cells undergoing hypoxia in response to exposure to grass pollen protein extract, triggering a change in F-actin configuration. This prompts secretion of the pro-inflammatory cytokine IL-8 and release of the epithelial transmembrane protein E-cadherin from cell-to-cell junctions, resulting in a decrease in epithelial barrier integrity. The IL-4 cytokine pathway has also been shown to play a role in the aetiology of thunderstorm asthma. Management strategies for preventing thunderstorm asthma include forecasting risk and early warnings to reduce exposure to high pollen counts near the time of a thunderstorm. Allergen immunotherapy can prevent epidemic thunderstorm asthma and inhibition of the IL-4 pathway with targeted monoclonal antibody immunotherapy can effectively treat thunderstorm asthma, although these treatments are expensive and require repeated administration. In addition to immunotherapy, adhering to any prescribed inhaled corticosteroid therapy and taking preventive inhaled steroids before or during a thunderstorm is important for susceptible individuals. Gennaro D'Amato (Federico II University of Naples, Naples, Italy) commented: “It is important to use inhaled corticosteroids or oral corticosteroids in association with a beta2 bronchodilator. It is not sufficient to use only a short-acting beta2 agonist (eg, salbutamol) without corticosteroids.” He continued, “Masks should be worn outdoors when there is a risk of thunderstorms in pollen season.” The risk of epidemic thunderstorm asthma events is likely to increase in the future, as climate change increases erratic weather patterns such as thunderstorms, and wet and dry seasons increase pollen production and aeroallergen concentrations, posing challenges for the health of at-risk populations. D'Amato commented “Considering climate change with increasing prevalence of thunderstorms and increasing atmospheric concentrations of pollen grains due to global warming, it is possible that in future there will be an increasing frequency of thunderstorm asthma. It is important to focus the attention of clinicians on these events, which are frequently still underestimated.”
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