You are here:
Indoor Molds and Respiratory Hypersensitivity: A Comparison of Selected Molds and House Dust Mite Induced Responses in a Mouse Model
Citation:
WARD, M. D., Y. Chung, L. B. COPELAND, D. L. DOERFLER, AND C. M. PUCHEU-HASTON. Indoor Molds and Respiratory Hypersensitivity: A Comparison of Selected Molds and House Dust Mite Induced Responses in a Mouse Model. Presented at Bioaerosols Conference, Saratoga Springs, NY, September 06 - 09, 2011.
Impact/Purpose:
The objective was to compare the allergic responses induced by selected mold extracts to those of house dust mite extract (HDM), a known inducer of allergic asthma, in an allergic asthma mouse model. The selected molds are commonly found indoors, associated with water damaged buildings and/or sick building syndrome, or are biopesticides.
Description:
Introduction/Study Goal Molds are ubiquitous in the environment and exposures to molds contribute to various human diseases including allergic lung diseases. The Institute of Medicine reports and WHO gUidelines concluded that the role of molds in asthma induction is not clear but an association exists between damp bUildings, the presence of mold and asthma exacerbation. It has been estimated that 21% of current asthma in the US may be attributed to dampness and molds. The objective was to compare the allergic responses induced by selected mold extracts to those of house dust mite extract (HDM), a known inducer of allergic asthma, in an allergic asthma mouse model. The selected molds are commonly found indoors, associated with water damaged buildings and/or sick building syndrome, or are biopesticides. Methods In a series of studies female BALB/c mice were exposed to 2.5-80 I-Igof extract in HBSS (total volume of 50 1-11) by intratracheal aspiration (IA) 4 times over a four-week period. In some studies, whole-body plethysmography (Buxco) was used to assess airway hyperresponsiveness to methacholine (01). Serum and bronchoalveolar lavage fluid (BALF) were collected either 2 or 3 days (D2 or D3) after the final exposure. Results The relative allergenicity of the extracts was evaluated based on the lowest dose able to induce a significant response compared to control (0 I-Ig) and the robustness of the response. The endpoints examined included BALF total protein, LDH and both total and differential cell counts as well as serum total and antigen-specific IgE. The allergic impact of the mold extract exposures was different for each mold. Multiple exposures were required to induce increased BALF eosinophil counts and serum total and antigen-specific IgE. Conclusions These dose-response studies demonstrate the complex nature of molds and their differing capacities to induce allergy and by extension allergic asthma. Additionally, molds' differential capacities (potencies) to induce allergic/asthma-like responses were demonstrated by the comparison to HOM responses. Not all molds were able to induce allergic responses in the animal model but some of these molds may have components that exacerbate asthmatic responses. However, it must be stated that regardless of the allergenic potential of an agent, exposure levels and sensitization thresholds, critical factors in allergy development are unknown for humans for most allergens inclUding molds/fungi at this time. Our studies indicate that molds should be assessed individually for their allergy induction potential. Importantly, our data suggest a threshold dose for the induction of allergic responsiveness. (This abstract does not reflect EPA policy.)