Comments on "bioaerosol lung damage in a worker with repeated exposure to fungi in a water-damaged building" - Correspondence

In their case report of a worker with lung damage associated with microbial exposure, Trout et al. (1) emphasized the need for further research on markers of exposure to bioaerosols, particularly fungi that produce mycotoxins. The authors presented an interesting pilot serologic investigation for IgG and IgM antibodies to roridin (a macrocyclic trichothecene mycotoxin produced by Stachybotrys chartarum) and found no elevation of antibodies in the index case, an individual with repeated exposure to a water-damaged building. The clinical evaluation of the index case did not reveal elevation of IgG or IgE responses to S. chartarum, although precipitating antibodies were reportedly positive "only to Thermoactinomyces vulgaris."

Although the environmental evaluation and subsequent discussion on bioaerosols focuses on fungi (particularly S. chartarum) and mycotoxins, Trout et al. (1) did not discuss the role that inhaled bacterial antigens may have played in this individual's illness. This is perplexing, as inhalation exposure to T. vulgaris is listed as one of the most frequent causes of hypersensitivity pneumonitis by Cormier (2), who was cited by Trout et al. (1). Similar to fungi, actinomycetes can grow on building materials in wet and warm places, and spread their spores into the air (3).

The pulmonary and immunologic effects of repeated exposure to T. vulgaris have been studied in animal models (4), and the clinical relevance of elevated and repeated serologic testing of IgG and IgA for T. vulgaris has been described after human exposures in agricultural settings (5). In a more recent EHP Grand Rounds article describing a case of hypersensitivity pneumonitis from residential exposure, the presence of another clinically significant thermophilic bacteria (Saccharopolyspora rectivirgula) was documented in a water-damaged home, and precipitating antibodies to this organism were present in the affected individual (6).

Although I acknowledge the importance of reducing or preventing exposure to bioaerosols in the indoor environment as well as the need for reliable biomarkers of exposure, limiting the extent of the reported investigation and discussion in this case to fungi and mycotoxins seems unjustified. It would be helpful if Trout et al. (1) could further discuss the results of the serologic testing with respect to T. vulgaris and if the environmental assessment of bioaerosol exposure included bacterial antigens.

Daniel L. Sudakin
Oregon State University
Corvallis, OR
E-mail: sudakind@ace.orst.edu

REFERENCES AND NOTES

(1.) Trout D, Bernstein J, Martinez K, Biagini R, Wallingford K. Bioaerosol lung damage in a worker with repeated exposure to fungi in a water-damaged building. Environ Health Perspect 109:641-644 (2001).

(2.) Cormier Y. Hypersensitivity pneumonitis. In: Environmental and Occupational Medicine (Rom E, ed). Philadelphia: Lippincott-Raven;1998;457-465.

(3.) Gazenko SV, Reponen TA, Grinshpun SA, Willeke K. Analysis of airborne actinomycete spores with fluorogenic substrates. Appl Environ Microbiol 64(11):4410-4415 (1998).

(4.) Jagerroos HJ, Seppa AV, Mantyjarvi RA. Pulmonary and immune responses to a Thermoactinomyces vulgaris antigen respiratory sensitization in C57BL/6J mice. Exp Pathol 29(2):95-102 (1986).

(5.) Ojanen T, Terho EO, Tukiainen H, Mantyjarvi RA. Class-specific antibodies during follow up of patients with farmer's lung. Eur Respir J 3(3):257-260 (1990).

(6.) Apostolakos M J, Rossmore H, Beckett WS. Hypersensitivity pneumonitis from ordinary residential exposures. Environ Health Perspect 109:979-981 (2001).

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