| Survey Results of EPA and EPA-Sponsored Research on the Health Effects of Exposure to Indoor Mold |
| Ongoing Research as of October 1, 2007 |
| Project Title |
Project Description |
Agency Contact |
Telephone Number |
|---|---|---|---|
| Isolating and Characterizing IgE Reactive Proteins | To isolate, characterize, and identify allergenic proteins produced by molds. Steve Vesper supplies the starting material from which I purify the allergenic proteins. | Maura Donohue | 513-569-7634 |
| Mechanistic Indicators of Childhood Asthma (MICA) Study | The Mechanistic Indicators of Childhood Asthma (MICA) study uses air, biologic, and clinical measures as well as novel molecular biology, chemistry, and gene technologies to identify factors that affect individual susceptibility to asthmatic responses. EPA scientists are applying computational methods to analyze, characterize, and possibly quantify combined risk factors that relate to asthma severity in childhood. MICA addresses agency need to study the interplay of environmental and genetic factors to better understand adverse health effects associated with environmental exposures. The purpose of this study is not necessarily directed at mold-related issues, but the secondary data that we collect could address some of the interests that GAO is interested in. The study was not designed to directly address the research questions that a GAO survey intends to inventory. | Jane E. Gallagher | 919-966-0638 |
| El Paso Children's Health Study and The Detroit Children's Health Study | The El Paso Children's Health Study was conducted in El Paso, Texas, while the Detroit Children's Health study was conducted in Detroit and Dearborn, Michigan. Both studies were primarily focused on the role of residential proximity to roadways in the development of childhood asthma. As part of this data collection activity, we have also collected questionnaire data on indoor exposures, including home dampness and the presence of visible molds. In the future, we plan to examine the relationship between home dampness and the prevalence of asthma symptoms and the levels of pulmonary function and exhaled nitric oxide. | Lucas Neas | 919-966-9961 |
| Study on Asthma and Environmental Factors, Which Included an Application of the ERMI Index | Historically indoor mold exposures had been assessed with short-term air samples (usually 3 to 5 minutes), which were then evaluated by microscopic counting or culturing, followed by microscopic observations. The results were then compared to short-term outside air samples. In both types of samples, the molds are usually only identified to the genus level, and in some critical cases, unrelated genera are lumped together. Interpreting the meaning of the analytical results was left to the individual receiving them. No scientific method was established to standardize the interpretation. The result has been confusion created by the following specific problems. First, short air samples only provide a "snap-shot" of mold conditions. In reality, the mold in the air changes from hour to hour, day to day, morning to afternoon, and season to season. Second, human identification of molds is highly dependent on the skill and expertise of the analyst. In many cases, the species of molds cannot be determined by microscopic observation of spores. The toxin profiles for each genus is also dramatically different. Third, culture-based results depend on the media used to culture the sample. Some molds grow well on one medium and not another. So you inherently have a mold selection process depending on which medium is used for the culturing. In other cases, a fast growing mold will overwhelm a slow growing mold, and the slow growing mold will be under counted. Fourth, comparison of indoor samples to outdoor samples makes no sense because the species outdoors are different from those indoors. What was needed was an objective method of mold analysis that removed the subjective human element from the process. Ten years ago we set out to develop a DNA-based method of mold analysis. DNA is highly stable and highly specific. But to do this, the relevant DNA of the indoor molds needed to be sequenced. This effort culminated in a new technology called mold-specific quantitative PCR (MSQPCR), which was patented by the U.S. EPA (PTO# 6,387,652). Many commercial laboratories have now been licensed by EPA to perform this analysis (see http://www.epa.gov/nerlcwww/moldtech.htm.), and it is freely available to researchers to use. Next, a standard protocol for sampling the indoor environment and interpreting the MSQPCR results was needed. In conjunction with HUD, we developed a standard sampling and analytical process for dust samples (Vesper et al., Journal of Occupational and Environmental Medicine, 2007; 49:829-833). Dust represents the long-term accumulation of the daily exposures of the person living in the particular environment. By the application of the MSQPCR technology to dust samples in a representative selection of homes across the U.S., we were able to develop the Environmental Relative Moldiness Index, or ERMI, scale for U.S. homes. The ERMI scale can be used to describe the mold burden in any newly sampled home on the basis of its relative position compared to the entire U.S. housing stock. This provides a simple, objective evaluation of the mold burden in a home. We are now using the ERMI scale in epidemiological studies in the U.S. to try to determine if the ERMI values can be used to understand the risk of asthma or related respiratory symptoms. To that end, we have performed and are continuing to perform various studies to try to determine if there is an association. To date we have completed studies in Cleveland, Cincinnati, Chapel Hill, and Detroit, and we are working on studies in Baltimore and New Orleans. In summary, higher ERMI values have been associated with increased risk of asthma or asthma-related symptoms. In the Cleveland study, we were able to show that remediating the water and mold problem in the homes of asthmatic children improved the health of the asthmatic children living in those homes (Kerscmar et al., Environmental Health Perspectives, 2006; 114:1574-1580). However, as with all epidemiological studies, the results demonstrate an association, not cause and effect. | Stephen Vesper | 513-569-7367 |
| Cross-Reactivity among Mold Extracts | Immunological cross-reactivity among mold extracts complicates the analysis of health effects of any particular mold. The cross-reactivity may result from sequence homology between different mold species proteins, or it may result from glycosylations of the proteins. We are studying both aspects. In vivo studies are looking at the functionality of the cross-reactivity. Do the IgE antibodies raised against one mold extract and binding to another mold extract result in triggering of an allergic or asthmatic event? Western blot analysis is being used to address the question of glycosylation. Does deglycosylation of the proteins change the IgE-reactivity profile when cross-reactivity has been previously observed? | Marsha D. W. Ward | 919-541-1193 |
| Detection of Mold-Specific Immunoglobulin in Human Sera and Comparison to Immunoglobulin in Mouse Sera | Asthma is a significant public health problem that has been on the increase for the past 30 years in Western societies, especially among children. It has been estimated that up to 90 percent of asthmatics are atopic and have an allergy trigger for their asthmatic episodes. Although indoor mold contamination is known to exacerbate symptoms in asthmatics, its role in the induction of allergic asthma is unclear. Immunoglobulin E (IgE) is an important antibody in Type I allergy and often mediates asthmatic events. Both total and allergen-specific IgE have been used in verifying the allergic status of patients. We have acquired sera from 12 adults (Yeatts et al., 2007) and 22 children (Vesper et al., Journal of Environmental Monitoring, 2007; 9:826-830) with persistent asthma (ranging from mild to severe disease), living within a 30-mile radius of Chapel Hill, North Carolina (NC ACES/PACES), and 100 asthmatic and 100 nonasthmatic children from the Mechanistic Indicators of Childhood Asthma (MICA) study, a nested study under the Detroit Children's Health Study. The purpose of our study is 1) to gain insight into the prevalence of human asthmatic's IgE-reactivity with selected molds and house dust mite (HDM) extracts and 2) to compare the serum IgE-reactive protein profiles of humans and immunized mice. If human and mouse immune systems process the same proteins as allergens, then the animal model provides a valid and strong tool for evaluating human risk from mold exposures. Hypothesis: 1) mold-induced immune responses (the production of mold-specific IgE and IgG) in an animal model can be used to predict human risk regarding exposure to molds and 2) Human and mouse IgE will react with the same mold proteins. Data has been collected and is currently being analyzed. | Marsha D. W. Ward | 919-541-1193 |
| Early Biomarkers of Allergy Induction | Asthma is a significant public health problem that has been on the increase for the past 30 years in Western societies, especially among children. It has been estimated that up to 90 percent of asthmatics are atopic and have an allergy trigger for their asthmatic episodes. Although indoor mold contamination is known to exacerbate symptoms in asthmatics, its role in the induction of allergic asthma is unclear. The induction of an adaptive immune response, such as an allergy, requires multiple exposures and time. Additionally, due to the complex nature of immune responses evaluating new agents requires in vivo studies. The development of an in vitro method to screen for the allergic potential of molds or other agents would allow a quicker assessment of indoor environments. However, such a method requires distinguishing inflammatory or irritant responses from those leading to allergy. Our study will evaluate the patterns of gene expression in lung tissue following a single acute exposure to mold extracts and a nonallergenic or low allergenic protein (e.g. bovine serum albumin) to distinguish allergic responses from more generalized inflammatory or nonallergic immune responses. The goal is to identify a set of "candidate" biomarker genes from lung tissue mRNA samples by expression microarray analysis and quantitative reverse-transcriptase polymerase chain reaction (quantitative RT-PCR). These biomarker genes may be part of biochemical pathways, or indicators of innate or early adaptive immune responsiveness. A long-term goal of this project is to use the panel or panels of biomarkers identified from these studies to guide the development of an in vitro screening protocol to further refine the system for allergy or asthma hazard identification. Data has been generated and is currently being analyzed. | Marsha D. W. Ward | 919-541-1193 |
| Identification and Characterization of Mold Allergens | The identification and characterization of mold or fungal allergens will provide insight into the classes of mold proteins that induce allergic responses. Additionally, due to immunological cross-reactivity among mold extracts, it is possible that certain mold proteins may be common mold allergens. Once identified these mold allergens may allow the determination of unhealthy indoor environments. Furthermore, human IgE against these proteins would be indicative of mold exposure potentially allowing thresholds of exposure to be evaluated. In our studies, mouse sera raised against specific mold extracts is used to perform immunoblots to detect IgE reactive proteins in mold extracts followed by mass spectrometric analysis to determine peptide sequence. The sequence data is used to probe protein databases for homologous proteins. When possible a strategy is then developed to confirm the functional identity of the IgE-reactive protein. A manuscript describing the study will soon be submitted to a peer-reviewed journal. Other mold extracts are currently under study. | Marsha D. W. Ward | 919-541-1193 |
| Relative Potency of Mold Extraction in a Mouse Model | Asthma is a significant public health problem that has been on the increase for the past 30 years in Western societies, especially among children. It has been estimated that up to 90 percent of asthmatics are atopic and have an allergy trigger for their asthmatic episodes. Although indoor mold contamination is known to exacerbate symptoms in asthmatics, its role in the induction of allergic asthma is unclear. It is not only important to identify indoor mold allergens but to assess the potency they have to induce allergic or asthmatic responses in comparison to a well characterized indoor allergen, such as house dust mite. We have compared the capacity of fungal extracts (Stachybotrys chartarum [SCE] and Metarhizium anisopliae [MACA]) and house dust mite extract (HDM) to induce allergic responses in BALB/c mice. Stachybotrys chartarum is found in water damaged homes and Metarhizium anisopliae is licensed for use as an indoor biopesticide. The extracts were administered in doubling doses from 2.5 - 80 µg total protein. A manuscript describing the study will soon be submitted to a peer-reviewed journal. | Marsha D. W. Ward | 919-541-1193 |
| Study of Putative Asthmagenic Molds | Asthma is a significant public health problem that has been on the increase for the past 30 years in Western societies, especially among children. It has been estimated that up to 90 percent of asthmatics are atopic and have an allergy trigger for their asthmatic episodes. Although indoor mold contamination is known to exacerbate symptoms in asthmatics, its role in the induction of allergic asthma is unclear. Vesper et al. (Vesper et al., Journal Occupational and Environmental Medicine, 2006; 48:852-858) categorized molds statistically more common in water-damaged Cleveland area homes as Group I molds and those found in every home as Group II molds. Remediation of water-damaged homes of asthmatics resulted in a significant reduction in symptoms. However, removal and remediation of water-damage would affect many things in the home besides mold concentrations. Therefore, there is a need to assess the relative allergenic potency of these molds using our mold allergy animal model. Preliminary data suggests that not all Group I molds induce allergic asthma-like responses in the mouse model but some of the nonallergenic molds appear to exacerbate airway responses. | Marsha D. W. Ward | 919-541-1193 |
| The Effect of Gestational Exposure to Mold on Allergy Induction in a Mouse Model | Asthma is a significant public health problem that has been on the increase for the past 30 years in Western societies, especially among children. It has been estimated that up to 90 percent of asthmatics are atopic and have an allergy trigger for their asthmatic episodes. Although indoor mold contamination is known to exacerbate symptoms in asthmatics, its role in the induction of allergic asthma is unclear. There is little understanding of the effect aeroallergens may have on the developing immune system. Determination of whether these effects increase or decrease susceptibility to allergic asthma induction would lead to strategies to protect children, particularly in the genetically predisposed atopic population. It appears that early in life the immune system is biased to promote allergic or asthmatic responses to certain antigens. Some of these allergens have been studied extensively (e.g. dust mite and cockroach), and specific antigens responsible for sensitization have been characterized. However, few of the mold allergens have been characterized, despite their widespread distribution and potential importance in the induction and exacerbation of asthma. This project focuses on gestational exposures to mold extracts and the effect this exposure has on the development of allergy or asthma in adult life using a mouse model of allergic asthma. In the initial studies, the mouse dams will be exposed to mold extract previously shown to induce allergic asthma responses in a mouse model. Control group dams will be exposed to vehicle. The offspring will be subdivided into three groups for adult exposure to the homologous mold extract, a heterologous allergen (house dust mite), and vehicle to evaluate any changes in allergic responses. Later studies will evaluate other mold extracts or other protein allergens as the homologous allergen to extend and confirm the findings. The impact on the other immune functions and windows of developmental vulnerability will also be assessed. Samples have been collected and the resulting data is currently being analyzed. | Marsha D. W. Ward | 919-541-1193 |
| U.S. EPA Environmental Technology Verification Program: Environmental and Sustainable Technology Evaluations (ESTE): Verification of Microbial Resistant Building Materials— Gypsum Wallboard | Approximately 90 percent of the interior finished surfaces of buildings are covered with gypsum products. The United States produces an estimated 30 million tons of gypsum board annually. Demand for gypsum products in the United States, Canada, and Mexico will continue to grow, reaching 46.8 million metric tons in 2007. Currently, each year, 3 million to 5 million tons of gypsum board ends up as scrap material and disposed of in landfills, with much of this scrap the result of moisture and mold problems. Mold, being ubiquitous, can be found in any nonsterile environment, while upwards of 40 percent of all homes in North America contain fungal growth with gypsum wallboard being a primary growth material. The goal of this project is the generation of a product evaluation system that will establish the performance of mold resistant building products. This evaluation system can then be used to test building products, the first of which is gypsum wallboard. This verification is intended to be used by building professionals and the consumer public, enabling them to make informed decisions regarding the use of different building products while simultaneously lowering the amount of gypsum scrap material that needs to be landfilled. The objective of this verification project is to evaluate the different types of microbial resistant gypsum products that are currently being marketed. Different manufacturers have come up with separate methods of controlling or eliminating microbial growth on gypsum products including removing microbial growth substrates and adding different antimicrobial compounds to the products. The evaluation of gypsum wallboard would test the following;
• Ability of gypsum products to support fungal (mold) growth • Resistance to moisture uptake • Volatile Organic Compound (VOC) emissions • Sustainability Criteria |
Timothy R. Dean | 919-541-2304 |
| Relationship of Gypsum Wallboard, Moisture, and Moisture Meters | Uncertainties continue to exist in the relationship of gypsum wallboard, moisture content, and moisture meters. Moisture meters designed to support the wood industry have become a mainstay in the indoor remediation area. Confusion surrounding safe or acceptable levels of moisture in gypsum wallboard is complicated by the varied results obtained by differing detection methods and instrumentation. This research effort is focusing on understanding the response of moisture meters to moisture within gypsum wallboard under varied conditions such as moisture loading, wall construction, temperature and humidity, etc. The initial research focused on a moisture meter routinely used in the field to determine the moisture content in gypsum wallboard. The meter readings are often used qualitatively (higher or lower moisture relative to a reference location) to determine the amount of wallboard to remediate. Because meters vary in their technology and method of detection, it is necessary to establish test procedures to ensure their usefulness and dependability as an aid in wallboard moisture detection and remediation. A method was developed to create a series of gypsum-wallboard-moisture-content-reference standards by exposing wallboard sample sections to static moisture content levels. Gravimetric analysis revealed good accuracy and precision of the reference standards to their theoretical values. The moisture meter was then compared against these reference standards to determine its accuracy and precision. | Dale Greenwell | 919-541-2828 |
| Laboratory and Field Research on the Efficacy of Chlorine Dioxide for the Remediation of Mold Contaminated Buildings | The goal of this research is to evaluate the efficacy of chlorine dioxide for inactivating a variety of viable mold and mold spores and neutralizing allergens and mycotoxins found in mold-contaminated structures. An underlying objective of the effort is to compare the efficacy of chlorine dioxide fumigation to conventional remediation methods by measuring the presence of viable mold vegetative cells and spores or detectable mycotoxins before and after remediation. The research activity is divided into two phases: Phase 1 is the field research, and Phase 2 is the laboratory research. | Blair Martin | 919-541-7504 |
| Mold Prevention and Decontamination of Air Conveyance Systems | The presence of moisture on HVAC system cooling coils and drip pans from condensate flow establishes conditions favorable for microbial growth. The established microbial growth can then be responsible for releasing gases (microbial volatile organic compounds, or MVOCs) or particles (BioPM) into the conditioned air stream. In addition, mold, bacteria, and virus containing aerosols in the indoor environment are distributed throughout the building by HVAC operation. Indoor building materials contaminated by mold and bacteria, emit allergenic and pathogenic particles that are distributed throughout the building interior by HVAC system operation. In addition, the presence of a microbial film on the cooling coils results in loss of heat transfer efficiency, overall component operation and the possible cause of condensate blow-by into the supply airduct. This research involves concurrent laboratory and field demonstrations that measure biological contaminants and heat transfer efficiency before and after treatment with UV with and without hydrogen peroxide. Hydrogen peroxide in combination with UV may greatly improve the antimicrobial reaction to quickly eliminate biofilm. Results contribute to the characterization of fungal organisms and their byproducts (MVOC's and BioPM) and will help building owners, building occupants, and building remediators deal with this problem. | Marc Y. Menetrez | 919-541-7981 |