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Bioaerosol lung damage: trout's response. (Correspondence).

In his letter referring to our recent paper in EHP(1), Sudakin points out that hypersensitivity lung diseases have been shown to be associated with exposure to thermophilic actinomycetes such as Thermoactinomyces vulgaris. Exposures to these organisms related to lung disease have been reported in both outdoor settings (when handling materials such as compost or decomposing organic matter--the classic example being farmer's lung) and indoor settings (2). Regarding the indoor environment, reported exposures to thermophilic organisms that cause documented hypersensitivity lung disease have occurred in situations involving contamination of air-handling systems, primarily heating and/or humidification systems (3-7). Thermophilic fungi (thermophiles) grow optimally at temperatures between 35 [degrees] and 50 [degrees] C (95 [degrees]-122 [degrees] F) or hotter. In contrast, most fungi are considered mesophiles, growing optimally between 15 [degrees] and 30 [degrees] C (59 [degrees]-86 [degrees] F) (8).

Precipitating antibodies indicate exposure to a substance and may provide supporting evidence for a specific etiologic exposure; these tests do not independently prove or disprove a diagnosis of hypersensitivity lung disease (9). Although the presence of precipitating antibodies can provide justification for environmental evaluation of exposure to specific antigens (10), the results of precipitin testing must be interpreted with knowledge of potential occupational and/or environmental exposures experienced by the patient. One of the limitations of these antibody tests is that a single test that indicates the presence of precipitating antibodies does not provide any information concerning the source of the antigens to which the person was exposed.

The primary problem in the building of concern in our report around the time of the patient's illness (and our evaluation) was large-scale water incursion allowing for massive fungal contamination of building materials in multiple areas of the building. These types of environmental conditions are not conditions in which thermophiles would be expected to grow well. As is commonly found in hotels, each room of the building in question had a dedicated unit ventilator to condition the occupied space. Inspection of selected unit ventilators in the building at the time of our evaluation revealed no obvious reservoirs of microbial growth. In addition, our evaluation, and the illness experienced by the patient in our report, took place during the cooling season when heating units would not routinely be in use.

Given the above and the activities of the patient likely leading to aerosolization of the fungal contamination, there is no reason to believe exposure to thermophilic organisms played a role in this patient's building-related illness. It is unlikely that an environmental evaluation for thermophilic organisms in the areas that were grossly contaminated with fungi would have provided any useful information regarding the illness experienced by the patient discussed in our report. Additional discussion of the potential role of thermophilic organisms in the etiology of hypersensitivity lung diseases in general was beyond the scope of our paper.
Douglas B. Trout
National Institute for Occupational Safety
and Health
Cincinnati, Ohio
E-mail: dtrout@cdc.gov


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.) Stetzenbach LD. Introduction to aerobiology. In: Manual of Environmental Microbiology (Hurst CJ, Knudsen GR, McInerney MJ, Stetzenbach LD, Walter MV, eds). Washington, DC:ASM Press, 1997;619-628.

(3.) Banaszak EF, Barboriak J, Fink J, Scanlon G, Schlueter DP, Sosman A, Thiede W, Unger G. Epidemiologic studies relating thermophilic fungi and hypersensitivity lung syndromes. Am Rev Respir Dis 110:585-591 (1974).

(4.) Banaszak EF, Thiede WH, Fink JN. Hypersensitivity pneumonitis due to contamination of an air conditioner. N Engl d Med 283:271-276 (1970).

(5.) Fink JN, Banaszak EF, Thiede WH, Barboriak JJ. Interstitial pneumonitis due to hypersensitivity to an organism contaminating a heating system. Ann Int Med 74:80-83 (1971).

(6.) Sweet LC, Anderson JA, Callies QC, Coates EO Jr. Hypersensitivity pneumonitis related to a home furnace humidifier. J Allergy Clin Immunol 48:171-178 (1973).

(7.) Tourville DR, Weiss WI, Wertlake PT, Leudemann GM. Hypersensitivity pneumonitis due to contamination of a home humidifier. J Allergy Clin Immunol 49:245-251 (1972).

(8.) Burge HA, Otten JA. Fungi. In: Bioaerosols: Assessment and Control (Macher JM, Ammann H, Burge HA, Milton DK, Morey PR, eds). Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1999;19.1-19.13.

(9.) Rose CS. Antigens. In: Bioaerosols: Assessment and Control (Macher JM, Ammann H, Burge HA, Milton DK, Morey PR, eds). Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1999;25.1-25.11.

(10.) Reed CE, Swanson MC, Lopez M, Banaszak EF, Barboriak J, Fink J. Measurement of IgC antibody and airborne antigen to control an industrial outbreak of hypersensitivity pneumonitis. J Occup Med 25(3):207-210 (1983).
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Author:Trout, Douglas B.
Publication:Environmental Health Perspectives
Date:Nov 1, 2001
Words:787
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