The spectre of indoor moulds as a contributor to respiratory disease keeps raising its fruiting body and just won’t go away. Numerous studies support a circumstantial and temporal link between high mould exposure and worse symptoms in susceptible individuals. However, it seems that the majority of respiratory physicians (at least in Europe) are at best non-believers. They are reluctant to consider moulds as important in patients with respiratory symptoms, rarely make specific enquiry, and almost never make attempts to reduce mould exposure. This contrasts with enthusiasm bordering on evangelism from some experts in the USA where huge litigation raises the stakes, with over 10 000 cases pending and multi-million settlements already routine.¹ In the past we have been hindered by profound ignorance of the biology of these important environmental contaminants. What do we know about indoor moulds, and how are they implicated in respiratory diseases, and specifically asthma? Should we be trying to reduce mould exposure for specific patients or the whole population and, if so, how?

Evidence for outdoor mould exposure and exacerbations of asthma is strong. For example, Alternaria is the dominant allergen in the mid west USA with strong temporal relationships between exposure and asthma severity. There are huge airborne spore counts (1000 times grass pollen counts) on peak days, associated with immediate worsening in sensitised subjects^2–5 and increased asthma deaths.⁶

However, assessing indoor mould exposure and relating exposure to worse respiratory disease is a much more complex issue. A range of mould species is undoubtedly associated with serious respiratory disease including infection (sinus and pulmonary) and allergy (allergic bronchopulmonary aspergillosis). In addition, there is strong evidence for a link between severe asthma and indoor mould sensitisation.⁷ But it has been unclear …