Intended for healthcare professionals

Editorials

Asthma associated with thunderstorms

BMJ 1996; 312 doi: https://doi.org/10.1136/bmj.312.7031.590 (Published 09 March 1996) Cite this as: BMJ 1996;312:590
  1. Adrian Bauman
  1. Associate professor Epidemiology Unit, Liverpool Hospital, Liverpool, NSW 2170, Australia

    Grass pollen and the fall in temperature seem to be to blame

    Despite its increasing prevalence, the aetiology of asthma remains mysterious. However, a panoply of factors continues to be associated with acute episodes of asthma. In recent years, environmental epidemiologists have conducted numerous studies investigating the relations between indoor and outdoor air pollutants and asthma, particularly focusing on exposures to ozone, sulphur dioxide, nitrogen dioxide, and particulate matter of respirable diameter. Researchers have found it difficult to standardise measures of exposure, and most have used an ecological design, searching for associations between exposures measured in environments and outcomes measured in individuals (typically asthma attacks or health care utilisation). Despite the large amount of research, the evidence that air pollution causes asthma remains controversial.1

    Research into the causes of chronic diseases, such as asthma, seldom produces the immediate gratification of the epidemic curve seen in acute infectious disease, which can then be followed sleuth-like, by searches for causal agents. However, asthma has recently obliged with several epidemics linked to environmental factors. Some reports suggest a point source of an environmental causative agent, as in the Barcelona asthma “epidemic,” which was linked to soya bean dust.2

    More complex environmental mechanisms have been proposed to explain “thunderstorm associated asthma,” described in two papers in this issue of the BMJ.3 4 This phenomenon was recognised over a decade ago in Britain5 and has been reported as a recurrent seasonal phenomenon in Australian studies.6 These studies have consistently suggested that this phenomenon occurs in late spring, is associated with thunderstorms or a drop in temperature, and is followed by a rapid increase in attendance with asthma at hospitals or in general practice. No unusual levels of air pollutants were noted at the time of these epidemics. Packe reported that increases in airborne fungal spores (Didymella and Sporabolomyces spp) might act as a trigger.5 Recent studies have shown strong associations with rye grass pollen and have described a mechanism whereby allergenic starch particles may be released from rye grass, triggered by the atmospheric changes preceding and during thunderstorms.6 7

    Celenza et al (p 604) report an epidemic of asthma related to a thunderstorm that occurred in London in June 1994.3 Earlier reports of this epidemic suggested that it occurred across southern England.8 9 10 Some observers speculated that this epidemic might be related to air pollution,9 although all previous studies that have measured air pollution during thunderstorm related epidemics of asthma have found it to be normal for the time of day and month of the year.5 6

    Celenza et al have conducted a detailed analysis that furthers our understanding of this phenomenon.3 By analysing asthma attendances and environmental factors during the epidemic period and the surrounding two months, they noted different patterns of association. The acute epidemic period of 48 hours showed a “classical” rise in attendances, associated with a preceding fall in temperature and substantial change in levels of airborne grass pollen, rising a few hours before the asthma attendance peaked and falling within nine hours. Asthma attendances outside the period of the epidemic were associated with a complex and different set of environmental variables, suggesting that the epidemic itself had a unique aetiology.

    The hypothesis that grass pollen was to blame gains further support from the paper by Wallis et al (p 601).4 The observation that 44% of the patients had never previously had asthma strengthens the possibility that there is a group of atopic individuals who are sensitive to grass pollen4 6 and who react acutely to this seasonal but infrequent interaction of biological and meteorological conditions. Young adults seem to be most affected, a group who are not usually the most frequent attenders at emergency departments.

    Doctors should be aware of this phenomenon, but it may not merit the “asthma weather alerts” seen on television in Melbourne, Austrialia, last November. Sensationalist portrayals of asthma are a favourite of the mass media,11 but fuelling the tabloid press is counterproductive to developing a wider understanding of asthma and its prevention. This group of pollen sensitive asthmatic individuals might be further investigated from a clinical perspective, with a view to developing targeted approaches to primary or secondary prevention.

    References

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    View Abstract