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Commentary on the paper by Seear et al (see page898)
Although there is unanimity in the general public’s mind that childhood asthma is continuing to rise, evidence is accumulating that the prevalence has now plateaued, or may even be in gradual decline.1 Whether this is real or confounded by changes in diagnostic labelling remains unclear. Whatever the prevalence, the underlying causes remain elusive, and suggestions are as numerous as research groups, each with their own agendas to promote. It is possible to build cases for a number of different environmental factors including varying exposures to specific allergens,2 to bacterial and viral pathogens and their products (the hygiene hypothesis),3,4 to environmental air pollution,5 to diet,6 and to obesity,7 among a range of ever increasing suggestions. An important issue for the public and for many health professionals, particularly those not familiar with the extensive primary literature, is to distinguish between those factors that might be relevant to causation and those that are responsible for provoking episodes of airflow obstruction in children with pre-existing disease. The reasons for this frequent failure to distinguish causation from exacerbation is understandable as factors known to exacerbate existing disease such as environmental tobacco smoke and exercise may also act synergistically with putative causative factors in promoting exacerbations. Whatever the cause, or causes, of the current high prevalence in urbanised consumer societies, one of the major features of the disease is the propensity of affected individuals to become more breathless than their unaffected peers on exercise. The association of exercise with exacerbations of disease has been known for centuries, and among the early descriptions of this feature, Floyer in 1698 noted that “all violent exercise makes the asthmatics to breathe short”.8 The mechanisms underlying the association between exercise and excessive breathlessness due to airflow obstruction are now better understood than in Floyer’s time and appear to be due to airway cooling against a background of chronic airway inflammation.9,10
Whereas the levels of physical activity appear to be in decline in urbanised, consumer societies, exercise induced bronchospasm (EIB) continues to be a common complaint in children with asthma. EIB is also commonly reported by and diagnosed in elite athletes, although understandable concerns have been expressed that some of the high levels of reporting may not be due to asthma at all but rather due to the breathlessness associated with extreme exercise.9 In this context concerns have also been expressed that β2 agonists, purportedly used to control the symptom, may be abused and used to seek ergogenic advantage.9,11 β2 Agonists can, theoretically, promote muscle anabolism and increase metabolism of lipids and carbohydrate,12–14 although in short term studies and at conventional doses of inhaled β2 agonists, no such advantages have been shown.11
The general decline of physical activity in the general population alongside little change or marginal increases in energy input and the resultant increase in obesity is also relevant to any discussion about exercise and asthma, as it has been suggested that on one hand low levels of physical activity, reduced physical fitness, and associated obesity may contribute to the severity and persistence of asthma,7 while regular exercise, and the associated increased physical fitness, might reduce the risk of persistent disease.15
All these issues come together in the real and perceived associations between asthma and EIB. On the one hand, exercise is good for children, whereas on the other, it may provoke unpleasant symptoms of airflow obstruction in the presence of established asthma. Furthermore, in intensively exercising athletes the diagnosis has the potential of being used to justify the abuse of asthma medication, and β2 agonists in particular.
Set against these concerns it needs to be remembered that EIB may be a feature of poorly controlled disease requiring a greater intensity of prophylactic treatment including inhaled corticosteroids, long-acting β2 agonists, and/or leukotriene receptor antagonists.16 The study by Seear et al in the present issue17 confirms a previous study18 in children with apparently severe and refractory EIB and in whom the diagnosis could not be confirmed by formal testing in the controlled laboratory environment. Indeed EIB could only be confirmed in 15% of children tested. Final diagnostic categories included poor physical fitness, habit cough, vocal cord dysfunction, and a significant proportion (21%) for whom no diagnostic category could be assigned.17 Another perhaps surprising feature of the present report was the very low use of other forms of exercise challenge, including free-range running before referral to a tertiary specialist respiratory centre, despite the fact that these children were considered to have severe and refractory EIB.
What then should paediatricians and healthcare professional dealing with this problem do, and how can over-diagnosis of EIB, and by inference coexisting asthma, be avoided? In this context it has been suggested that the free range running test might be a useful screening test for identifying children with asthma in community settings,19,20 although its reliability has been questioned in other studies.21,22 However, the problems with this simple test need to be balanced against the relevance of exercise in the controlled laboratory environment to exercise in the real world where interaction with air pollution and other provoking agents in the child’s natural environment can occur. As the authors of the present report concede, it would have been possible to exclude true EIB in the majority of their subjects by a full and detailed history and medical examination without recourse to a formal exercise challenge.17
There is a clear need to educate ourselves and the public about the relevance of EIB and the distinction between the provocation of airflow obstruction as a cause of breathlessness and other common causes interpreted as EIB, such as poor physical fitness, habit cough, and laryngeal dysfunction, or in the case of athletes the high demands of exercise itself.
The emerging evidence that we may be over-diagnosing asthma invites a careful and comprehensive clinical assessment of every new presenting child in order to establish what is and what is not EIB, and by further inference what is and what is unlikely to be asthma.
Commentary on the paper by Seear et al (see page898)
Competing interests: none declared
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