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ASSESSING THE ALLERGIC POTENTIAL OF INDOOR AIR FUNGAL CONTAMINANTS
Citation:
Ward, MDW, M. E. Viana, Y. Chung, N. H. HaykalCoates, L B. Copeland, S H. Gavett, AND MJK Selgrade. ASSESSING THE ALLERGIC POTENTIAL OF INDOOR AIR FUNGAL CONTAMINANTS. Presented at Fifth International Conf. on Bioaerosols Fungi, Bacteria, Mycotoxins and Human Health, Saratoga Springs, NY, September 10-12, 2003.
Description:
Assessing the Allergic Potential of Indoor Air Fungal Contaminants
Marsha D W Ward1, Michael E Viana2, Yonjoo Chung3, Najwa Haykal-Coates1, Lisa B Copeland1, Steven H Gavett1, and MaryJane K Selgrade1. 1US EPA, ORD, NHEERL, RTP, NC, USA. 2NCSU, CVM, Raleigh, NC, USA, 3 UNC, SPH, Chapel Hill, NC, USA.
The indoor environment has increased in importance to children's health with children now spending more than 90% of their time indoors. However, the health effects caused by childhood exposures to indoor molds are complex. Molds are an important component of this environment and have been associated with exacerbation of asthma. Their contribution to the induction of allergic asthma is less certain.
We have assessed the allergic potential of three fungal extracts in a female BALB/c mouse model: 1) the biopesticide Metarhizium anisopliae (MACA) and 2) Stachybotrys chartarum (SCE-1) and 3) Penicillium chrysogenum (PC). The latter two fungi have been associated both water damaged buildings and sick building syndrome. In a series of studies mice were subjected to 4 aspiration (ASP) exposures to 10 g of MACA or SCE-1, bovine serum albumin (BSA) (negative control), and HBSS (vehicle control) over a 4-week period. Additional mice were ASP exposed 3X to HBSS with a final MACA or SCE-1 exposure as inflammatory controls. Serum and bronchoalveolar lavage fluid (BALF) were collected before (D0), and at 1 (D1) and 3 (D3) days following the final ASP exposure. Additionally, whole-body plethysmography (Buxco) was used to assess pulmonary resistance and bronchoconstriction. Mice were assessed for immediate responses (10 minute baseline and 1 hour following each aspiration exposure) and airway hyperresponsiveness to methacholine (D1 and D3). In other similarly designed experiments, mice were exposed by ASP to as high a dose as 100 ?g of PC.
Exposure to both MACA and SCE-1 extracts caused increased BALF total protein, LDH, and IL-5 levels (D1). BALF total cell counts as well as neutrophil (D1), eosinophil and lymphocyte (D1-3) counts were elevated. As was serum total IgE. Furthermore, these extracts caused significant increases in Buxco measures compared to both HBSS and BSA. Additionally, 4 IgE-inducing proteins have been identified in MACA. Current data indicates that only the mice exposed to 100 ?g of PC demonstrate levels of BALF total protein, LDH, and total and differential cell counts comparable to or higher than those levels in mice exposed to 10 ?g of MACA.
Available data indicates that PC extract may not be as potent at inducing allergic responses as are MACA and SCE-1. Respiratory exposure to either MACA or SCE-1 causes responses similar to those observed in human allergic lung disease suggesting that these two molds, at least, may have a role in the induction of asthma.
(Supported by NCSU/EPA Cooperative Training Agreement CT826512010 and UNC/EPA Cooperative Training Agreement CT829471.) (This abstract does not reflect EPA policy.)