Many people suffering from allergic respiratory diseases may be perplexed by their symptoms flaring with foul weather. They may not be aware that thunderstorms are a risk factor of asthma attacks. With global warming, there seems a rise in acute asthma attacks with thunderstorms in recent years. This issue is still under-recognized by the general public.
Thunderstorm asthma is an informal term, not a standard diagnosis, used to describe any observed increase in acute bronchospasm cases following the occurrence of thunderstorms in the local vicinity. There is reasonable evidence of a causal relationship between asthma attacks and thunderstorms in the patients suffering from pollen allergy. Associations between thunderstorms and asthma morbidity have also been identified in multiple locations around the world.
The link between thunderstorms and asthma outbreaks was noted for the first time in 1983. During the hours of a thunderstorm, 26 asthma cases were treated in the Emergency Department at the East Birmingham Hospital (UK) in a 36-h period. It was a remarkable increase in the number of asthma ED admissions, compared with a daily average of two or three cases in the days preceding the outbreak. Other asthma outbreaks during thunderstorms have since been reported in Australia, Europe, North America, and the Middle East.
The largest asthma outbreak ever recorded was in London on June 24, 1994. coinciding with a heavy thunderstorm. During a 30-h period, 640 patients with asthma or other airways disease (357 of whom were affected only by seasonal rhinitis) attended several EDs, nearly 10 times the expected number of 66 patients. In total, 104 patients were admitted, including 5 patients to an intensive care unit.
The most recent episode was an epidemic of thunderstorm asthma occurred in Melbourne. On November 21, 2016, Melbourne experienced the locally largest, most devastating epidemic of thunderstorm asthma with 2,332 ambulance calls, 3,365 excess respiratory-related ED presentations and 9 deaths possibly related to this thunderstorm event.
During these episodes, only a proportion of the patients had a history of a previous diagnosis of asthma. Many reported a history of grass pollen allergy and had probable undiagnosed asthma. Rhinitis was prevalent among them, with a reported high rate of 88%.
How Do Thunderstorms Result in Asthma Attacks?
The literature suggests epidemic thunderstorm asthma occurs due to a complex interaction of patient and environmental factors. Patient factors include previous aeroallergen sensitization and a previous history of allergic rhinitis. Environmental factors include high concentrations of respirable aeroallergens including small particles and airborne fungal spores in the atmosphere and thunderstorm outflow tracts that produce downdrafts containing these aeroallergens.
It is the airflow patterns in thunderstorms, not the electrical activity, thunder itself or rain, which trigger asthma epidemics. Generally, thunderstorm outflows include upward air currents (updrafts) and downward air currents (downdrafts). The downdrafts of cold air concentrate particles of pollens and mold spores and then sweep them into the high humidity of the air. The particles are broken down into small, respirable fragments, which are released by rain. Because these allergens are high concentrated, they can cause severe asthma attacks in patients who are sensitized to various allergens. Although grass-pollen-induced allergy is not a prerequisite for thunderstorm asthma, it acts as a motivating factor in patients with hay fever and mold allergy.
Thunderstorms can concentrate pollen grains at ground level, which may release allergenic particles of respirable size into the atmosphere after their rupture by osmotic shock. During the first half hour of a thunderstorm, patients suffering from pollen allergy may inhale a high concentration of the allergenic material that is dispersed into the atmosphere. This is due to dry updrafts that entrain whole pollens into the high humidity at the cloud base where they may rupture, followed by cold downdrafts that carry pollen fragments to ground level where outflows distribute them. Because of strong electric fields that develop during thunderstorms, positive ions are released from the ground and could attach to particles, while electric charge may enhance pollen rupture, thus, enhancing bronchial hyper-responsiveness.
Some hypothesize that the updrafts, which drag air into thunderstorm clouds, collect pollen grains which rupture to release pollen fragments, and are then distributed outwards by downdrafts. In other words, pollen may be spread by entering rain droplets and then being released when the rain droplets evaporate. A study suggested that changes in the electrical charge on aeroallergen particles, which might occur during thunderstorms, could promote deposition of particles within the alveoli. This increases the probability of an allergic response.
The levels of allergens in ambient air, such as pollen grains and fungal spores, have been observed to fluctuate prior to or during thunderstorm asthma episodes. Studies have shown that the amount of grass pollen grains trapped in thunderstorm outflow were between 4-12 times higher than elsewhere, making them readily available for breathing. For examples, a study indicated that the 1994 episode in London had an increase in grass pollen to a 6 year high prior to the thunderstorm and increases in airborne fungal spores; another study conducted in Australia also identified that there was a 4-fold increase in closed pollen grains and a 7-fold increase in ruptured pollen grains during a thunderstorm compared with the previous hour, for excess asthma days.
Much of evidence indicates that asthma epidemics related to thunderstorms are limited to the seasons when there are high concentrations of airborne allergenic pollens. They usually occur in spring and summer, and are particularly common in late July. Winds and rain showers provide suitable conditions for hydration of pollen capsules, release of pollens into the air and transportation of airborne pollens to regions far and near, creating a nurturing environment for thunderstorm-related asthma attacks.
Over the last 50 years, global temperature has markedly risen. Changes are occurring in the amount, intensity, frequency and type of precipitation. There is also an increasing trend in extreme events such as droughts, floods, thunderstorms and hurricanes. Scientific studies have shown a positive correlation between climate change and allergic respiratory diseases. Global warming affects the onset, duration and intensity of the pollen season, since plants exhibit enhanced photosynthesis and reproductive effects and produce more pollen. Changes in production, dispersion and allergen content of pollen and spores have been confirmed in different regions and species. It seems that global warming is increasing the risk of acute onset of asthma following thunderstorm.
Thunderstorm asthma as sudden surges in acute respiratory illness not only increases the patients’ sufferings, but also have the potential to increase pressures on acute health services, and deplete available resources. Several strategies may be helpful for reducing the risk of asthma attacks related to thunderstorms:
a. All patients affected by pollen allergy should be alerted to the danger of being outdoors during a thunderstorm in the pollen season as such events may cause severe exacerbation.
b. Individuals with a history of grass pollen allergy should avoid outdoor activities within 24 hours after a thunderstorm or rain shower as pollens and mold spores are in the air.
c. Wearing a mask prior to and within 24 hours after a thunderstorm or rain shower may be helpful for reducing the incidence of asthma attacks.
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3. Rangamuwa KB, Young AC, Thien F. An epidemic of thunderstorm asthma in Melbourne 2016: asthma, rhinitis, and other previous allergies. Asia Pac Allergy. 2017 Oct;7(4):193-198.
4. Thien F, Beggs PJ, Csutoros D, et al. The Melbourne epidemic thunderstorm asthma event 2016: an investigation of environmental triggers, effect on health services, and patient risk factors. Lancet Planet Health. 2018 Jun;2(6):e255-e263.