Abstract
In their recent study on endotoxin exposure as a risk factor for asthma, Thorne and colleagues found a relation between floor dust endotoxin levels and diagnosed asthma, asthmamedication, and wheezing among adults (1). While I agree with the authors’ conclusion that the symptomatology reflects an inflammatory response that is more pronounced among those with an allergy, I would caution against any conclusions concerning causality. In house dust, endotoxin is only one of many microbial cell wall agents (MCWAs) with biological effects; other examples are mycobacterial lipoglycans, lipoteichoic acid, peptidoglycan, N-acetylmuramic acid, and lipoarabinomannan (2). Many MCWAs have inflammatory properties. Although the MCWA (1-3)-D-glucan is not inflammatory by itself (3), it reflects the presence of mold cells, which cause a neutrophilic inflammation akin to endotoxin. Previous reports have shown a significant correlation between levels of airborne endotoxin and (1-3)-D-glucan (4). So while we all would like to see a specific agent as the reason for effects found, the environment seldom provides this opportunity. From a practical point of view, however, endotoxin is useful as a marker for risk, and a reduction of these levels, particularly in occupational settings, will reduce the risk, whether this is related to endotoxin or some other covarying agent.
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