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Mycotoxins and Building-Related Illness

Hodgson, Michael MD, MPH; Miller, David PhD; Jarvis, Bruce PhD; Storey, Eileen MD, MPH

Journal of Occupational & Environmental Medicine: September 1998 - Volume 40 - Issue 9 - p 763-764
Letters To The Editor
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Division of Occupational and Environmental Medicine; University of Connecticut Health Center; Farmington, Conn.

The Authors Reply: We appreciate the opportunity to respond to the comments of Drs Page and Trout about our recent outbreak investigation. We are relieved that they consider this a major public health issue, although we are unsure whether they mean moisture in the built environment, the potential adverse health effects of mycotoxin exposure in buildings, or something else. They do appear to recognize the constraints that physicians and epidemiologists encounter as they manage patients with disease in an environment that requires negotiations with employers for access, negotiations with employers and insurers for cost reimbursement, and negotiations with patients around disease, a very different situation from that encountered in NIOSH hazard evaluations.

There is ample evidence that moisture in buildings is associated with disease. One formal study attempt estimated that the etiologic fraction of asthma attributable to moisture in the home was at least 25%.1 For reasons outlined in the manuscript, many researchers believe a major portion of that problem is unrelated to type I allergy, at least in residential airways symptoms. The recent report on NIOSH investigations identified an association of moisture and respiratory symptoms2 in the workplace. Although it is tempting to implicate type I allergy, the few attempts to document an association have either failed3,4 or suggested that the explained fraction is trivially small.5 Over 25% of asthma reported to the occupational disease surveillance activities in Departments of Health in Massachusetts and Connecticut now represent building-related asthma. The problem is encountered by practicing physicians far more frequently than the peer-reviewed literature implies, where in a single outbreak,6 asthma was attributed to below-grade moisture incursion in a municipal building.

Most scientists recognize that case reports and outbreak investigations cannot provide generalizable knowledge, as the population to which they may be extrapolated is controversial. The purpose of such reports is generally to make the medical and scientific community aware of discussions, theories, and concerns they should be aware of, could keep their eyes open for, and perhaps recognize again if encountered elsewhere. The first systematic evidence on immunological effects of moisture will appear soon,7 although even that paper raises far more questions than it answers. The exciting work on airborne dust exposure, mycotoxins, and mechanistic implications in Dr Dearborne's laboratory in Cleveland is well known to scientists who follow the field and is likely to address some of Dr Trout's concerns. These provide exciting models of how scientists might investigate both outbreaks or clusters and exposure.

Our own investigation was conducted under severe constraints. Although we were initially invited in at the request of several judges, funding for the project (approximately $12,000) came from the administration and the workers' compensation carrier. Four phases were laid out as fairly standard approaches to epidemics, including interviews with suspected "index cases," a questionnaire survey, a clinical medical screening protocol, and a formal case-control study. As part of the work, we (the local physicians, the insurer, and the administration) agreed upon a set of management criteria for patients that were disseminated to employees and their physicians. On the basis of the initial medical interviews, the increased prevalence of symptoms in the questionnaire survey, and obvious physiologic abnormalities in the screening protocol, we were convinced that something was worth investigating. The insurance carrier was unwilling to fund a cross-sectional study using rhinometry before and after work or nasal smears for eosinophils. By the time our negotiations with the insurer, institutional review board clearance, and logistical constraints were resolved, many employees/patients were removed from work, three months after our first visit. As reported in the manuscript, at least one possible reason for the negative results in the case-control study may be that exposure had stopped for many of the subjects. Doing investigations such as this out of state poses some problems for clinicians.

We considered type I allergy an unlikely explanation for the lung function abnormalities because of the lack of association between immunoglobulin E (IgE) antibodies and either symptoms or physiologic changes. Lynch et al described an outbreak of hypersensitivity pneumonitis in which only 10% of subjects had abnormal chest x-rays, data of which we were unaware when we did this study and wrote the manuscript.8 We considered hypersensitivity pneumonitis an unlikely event because of the lack of association between IgG antibodies and either symptoms or physiologic changes. Don Milton has recently suggested that an endotoxin itself might be an explanation; we found no source of water aerosol and consider airborne endotoxins an unlikely phenomenon in this outbreak. Either of these are legitimate hypotheses, though with less evidence, in our view.

At present, NIOSH building investigations generally do not attempt to identify, as they have at least sometimes in the past, objective measures of disease, as at least markers of group differences, including physiologic testing such as spirometry or single-breath carbon-monoxide diffusing capacities9 or immunologic markers.10,11 Cooperation between the NIOSH Health Hazard Evaluation team, with greater field epidemiology flexibility and laboratory depth, and local practitioners, who may have access to patients with convincing evidence of poorly characterized disease and emerging syndromes, may lead us all to characterize occupational disease more effectively. This may require rethinking the specific roles we each play, identifying legal constraints that might impede information flow and sharing, and addressing issues of respect for the different strengths we bring to problems. Dr Trout has willingly recently participated in such a mixed investigational venture, with exciting productivity for both sides.

Michael Hodgson, MD, MPH

David Miller, PhD

Bruce Jarvis, PhD

Eileen Storey, MD, MPH

Division of Occupational and Environmental Medicine; University of Connecticut Health Center; Farmington, Conn.

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References

1. Cooper K, Demby S, Hodgson M. Moisture and lung disease. population-attributable risk calculations. In: J Woods, D Grimsrud, N Boschi, eds. Healthy Buildings 97/Indoor Air Quality 97, vol.1. 1997;213-218.
2. Sieber K, Stayner LT, Malkin R, et al. The NIOSH Indoor Environments Evaluation Experience: part three-associations between environmental factors and self-reported health conditions. Appl Occup Environ Hygiene. 1996;11:1387-1392.
3. Menzies R, Tamblyn R, Comtois P, et al. Case-control study of microenvironmental exposure to aero-allergens as a cause of respiratory symptoms-part of the SBS complex. Presented at: IAQ92: Environments for People, ASHRAE, Atlanta, 1992:201-210.
4. Apter A, Hodgson M, Lueng W-Y, Pichnarcik L. Nasal symptoms in the "Sick Building Syndrome." [Abstract]. Ann Allergy Asthma Immunol. 1997;78:152.
5. Menzies D, Nunes F, Comtois P, Hanley JA, Pasztor J. Aeroallergens and work-related respiratory symptoms among office workers. J Allergy Clin Immunol. 1998;101:38-44.
6. Hoffman RF, Wood RC, Kreiss K. Building-related asthma in Denver Office Workers. Am J Publ Health. 1993;843:89-93.
7. Dales R, Miller D, White J, Dulberg C, Lazarovits A. The influence of residential fungal contamination on peripheral blood lymphocyte populations in children. Arch Environ Health, in press.
8. Lynch DA, Way D, Rose CS, King TE Jr. Hypersensitivity pneumonitis: sensitivity of high-resolution CT in a population-based study. AJR Am J Roentgenol. 1992;159:469-472.
9. Hodgson MJ, Morey P, Attfield M, Fink JN, Sorensen W, Visvesvara G. Pulmonary disease in an office building: single-breath carbon-monoxide diffusing capacity as a cross-sectional field tool. Arch Environ Health. 1985;40:96-101.
10. Hodgson MJ, Morey PR, Simon J, Waters T, Fink JN. Acute and chronic hypersensitivity pneumonitis from the same source. Am J Epidemiol. 1987;125:631-638.
11. Johnanning E, Biagini R, Hull D, Morey P, Jarvis B, Landsbergis P. Health and immunology study following exposure to toxigenic fungi (Stachybotrys chartarum) in a water-damaged office environment. Int Arch Occup Environ Health. 1996;68:207-218.

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