© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Indoor Air 2014; 24: 221–222 wileyonlinelibrary.com/journal/ina Printed in Singapore. All rights reserved
INDOOR AIR doi:10.1111/ina.12075
Letter to the Editor Fungi in homes – how do we measure? In a recent study in Indoor Air, no relation was found between domestic fungal exposure and asthma, rhinitis, and eczema (Choi et al., 2013). Although some early reviews did not ﬁnd such a relationship (Institute of medicine, 2004), several later studies have conﬁrmed a relationship between fungal exposure at home and airways inﬂammation and general symptoms (Lignell et al., 2005; M€ uller et al., 2002; Park and Cox-Ganser, 2011; Weinmayr et al., 2013). Particularly important are studies where an improvement in symptomatology and inﬂammatory cytokine status has been found after intervention against fungi (Roponen et al., 2013). The lack of a relationship in the study might be due to inadequate exposure determinations. The range of exposure variables might have been too small to detect eﬀects according to the authors’ comment regarding ergosterol levels. Culturable fungi are a poor predictor of the exposure dose (Garrett et al., 1998). This descriptor does not account for dead cells or fractions of cells, which are not viable but retain their biological eﬀect through diﬀerent cell wall agents. Airborne fractions are particularly important as they may comprise a large proportion of the total cell biomass and easily penetrate into the lungs (Adhikari et al., 2011). Measurements of cell wall agents in terms of different glucans were taken using an immunoassay.
Unfortunately, the authors do not cite an extensive methodological study, where diﬀerent methods to analyze glucan were compared (Iossifova et al., 2008). There were no correlations between the immune assay and a Limulus-based assay in ﬂoor dust by weight, and only a low correlation if the amount was expressed per surface area. The Limulus test had a higher sensitivity and speciﬁcity and was more accurate in measuring glucan standards. The sensitivity of the immune assay was too low to detect airborne samples, which from an inhalation point of view are more relevant. Furthermore, the authors do not cite any of the articles where a relation has been found between airway symptoms and fungi using the Limulus-based assay (e.g., Rylander et al., 1998; Yee et al., 2010). In view of these shortcomings, the study presents only a very weak evidence for the absence of a relation between fungal exposure and the studied diseases. R. Rylander BioFact Environmental Health Research Centre, Lerum, Sweden E-mail: [email protected]
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