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2000 Progress Report: CECEHDPR - University of Michigan
EPA Grant Number: R826710Center: Michigan Center for the Environment and Children’s Health
Center Director: Israel, Barbara A.
Title: CECEHDPR - University of Michigan
Investigators: Israel, Barbara A. , Brown, Randall , Keeler, Gerald J. , Lin, Xihong , Parker, Edith , Philbert, Martin , Remick, Daniel , Robins, Thomas
Current Investigators: Israel, Barbara A.
Institution: University of Michigan - Ann Arbor
EPA Project Officer: Fields, Nigel
Project Period: September 1, 1998 through August 31, 2003 (Extended to August 31, 2005)
Project Period Covered by this Report: September 1, 1999 through August 31, 2000
Project Amount: $2,830,746
RFA: Centers for Children's Environmental Health and Disease Prevention Research (1998)
Research Category: Children's Health , Health Effects
Description:
Objective:Core 1: Community-Based Intervention to Reduce Environmental Triggers for Asthma Among Children. The first specific aim of this household and neighborhood level community-based intervention research project is to reduce exposure of children to environmental contaminants within their homes and neighborhoods that trigger asthma, thereby improving asthma-related health status and reducing asthma-related medical care utilization. Asthmatic children will be identified through elementary school screenings and their parents will be asked to enroll in a household intervention in which outreach workers will visit each household 12 times in 2 years (9 times in the intensive first year, and 3 times in the second year). Outreach workers will work with the family to reduce indoor household exposure factors identified as excerbating asthma, such as cockroach mites, cat dander, environmental tobacco smoke, and mold. Each household will also be supplied with educational materials and other resources to reduce indoor asthma triggers such as vacuum cleaners, bedding covers, cleaning kits, and mats. In the neighborhood component of the intervention, community organizers will work with neighborhood groups on asthma awareness and reduction of environmental threats to children's respiratory health. The second specific aim is to conduct a randomized, staggered design community-based intervention to test the following hypotheses: (1) The household level intervention will improve asthma-related health status (and other mental and physical health outcomes), and increase behaviors to reduce home environmental hazards; (2) A neighborhood level intervention when combined with a household level intervention will provide an enhanced effect on the outcomes at the household level; (3) A less intensive household intervention following an initial intensive intervention will maintain similar level effects; and (4) A long-term neighborhood intervention, when combined with a household-level intervention, will result in greater intervention effects than a household level intervention with a short-term neighborhood component. The third specific aim is to conduct a process and context evaluation in addition to the outcome evaluation of both components of the intervention.
Core 2: Indoor and Outdoor Air Contaminant Exposures. The prevalence of asthma has increased markedly over the past 15 years. It is the most common chronic disease of childhood in the developed world, affecting about 10 million U.S. children under the age of 16. Asthma is most common among urban and minority populations. The causes of these increases and the greater risk for urban, minority populations are not well understood. The causation, and aggravation, of childhood asthma is complex and involves many factors including genetic disposition, demographic variables, psychosocial stresses, and environmental exposures. Environmental exposures include both ambient (outdoor) exposures as well as indoor exposures within the home and at school. The first specific aim of the Asthma Exposure research project is to determine the prevalence of questionnaire-defined asthma among the elementary age school children in African-American and Latino populations in Detroit. Students and their families from 10 to 12 elementary schools (approximately 6000 students) in two areas in which the investigators have pre-existing strong community ties (i.e., southwest Detroit and the east side of Detroit) will be asked to complete a short, well validated asthma screening questionnaire. The second specific aim is to identify which components of the outdoor air, of indoor air contaminants, and family and neighborhood characteristics are associated with increased risk for asthma in this population. The third specific aim is to examine whether seasonal and daily changes in outdoor air pollution and indoor air contaminants explain fluctuations in the severity of asthma. The last specific aim is to provide ambient (community/neighborhood level), micro-environmental (inside schools and homes), and personal monitoring data to investigate the relationships between various exposure metrics and activity patterns of asthmatic children living in the southwest and east sides of Detroit. This approach will improve on the design of prior studies by collecting detailed multiple daily measures of ambient air contaminants together with comprehensive assessment of indoor air contaminants in households and schools and individual family and neighborhood measures of psychosocial factors, and assessing the association of these with a comprehensive set of health status measures, including lung function testing (FEV1), also collected on a daily basis.
Core 3: Chemokines in the Pathogenesis of Asthma. Asthma represents a serious health problem particularly for inner city children. Recent studies have identified that many of the asthmatic attacks are triggered by exposure to cockroaches. It is not exposure to the entire cockroach, but only small fragments or residue. These small fragments are responsible for the allergic response and they are called allergens. In the normal allergic, or asthmatic response, the body reacts to the allergens to start inflammation. This inflammation is initiated by having the cells of the body produce specific chemicals or mediators. With asthma, most of the mediators are produced directly in the lung. While many potential mediators have been examined previously, asthma still exacts a toll on children and adults. More specific, targeted therapy has the potential to improve the treatment of asthma by identifying those mediators directly responsible for the causing disease. This research project will test the hypothesis that asthma-like pulmonary injury is mediated by the local production of specific mediators, which are called chemokines. Chemokines are small molecular weight proteins which induce the movement and recruitment of inflammatory cells. The chemokines are powerful mediators with long lasting and potent biological activities. The first specific aim is to determine the acute and chronic pulmonary inflammation that develops after direct injection of the chemokines into the lung. The assessment of the injury will include a microscopic analysis of the lung as well as an assessment of the nerves within the airways. The second specific aim is to develop a mouse model of asthma-like pulmonary inflammation in response to cockroach allergens. For this specific aim, a model in mice which is similar to humans will be set up to attempt to decipher the specific mediators that cause the lung injury. This model will be established by locating households with high levels of cockroach allergens and using this material to immunize the mice. The mice will be challenged by exposure to aerosols containing the dust with the cockroach allergens and the pulmonary injury carefully quantitated including an analysis of innervation of the airways. The third specific aim is to investigate the signals responsible for inducing the cells to make the chemokines. This will be done in cells sensitized and then challenged with cockroach allergens. This will focus on reactive oxygen and reactive nitrogen intermediates since they have been demonstrated to increase the synthesis of chemokines. The last specific aim is to rigorously test the central hypothesis that chemokines are important in causing asthma. This will be tested by blocking the biological activity of the chemokines with specific therapies to inhibit the chemokines and then determining if there is a reduction in the pulmonary inflammation induced by repeated exposures to the cockroach allergens. Successful completion of this project will both delineate the underlying mechanisms of disease and identify potential novel targets for intervention.
Progress Summary:Core 1: Community-Based Intervention to Reduce Environmental Triggers for Asthma Among Children, and Core 2: Indoor and Outdoor Air Contaminant Exposures. The Intervention and Exposure Cores of MCECH continue to have the same specific aims as stated in the proposal, but because the two are so integrated and have the same participants and current goals, their research teams and activities have been combined into one "meta"-project called: Community Action Against Asthma, or CAAA. A Steering Committee, which meets monthly and is comprised of the university and Detroit community partners involved in both projects, oversees and is directly involved in decision making and other activities regarding the implementation of the research protocol. A separate Research Work Group, comprised of the university-based faculty and staff for CAAA, oversees the technical aspects of research issues and works closely and in coordination with the CAAA Steering Committee.
There have been no changes in the specific aims. The asthma intervention core will test the ability of individually tailored interventions to reduce exposure to environmental contaminants and to improve asthma related health status. At the same time, the intervention will provide direct benefit to the children and families enrolled in the study. The central hypothesis being addressed in the asthma exposure core is that exposure to ambient air contaminants will aggravate the health status of asthmatic children largely through the potentiation of the adverse effects of common indoor air contaminants. Proving or refuting this hypothesis will lead to substantial advances in scientific knowledge and have a direct impact on public health recommendations.
The most critical element in the success of the project to date has been the establishment at the outset of a dynamic Steering Committee (SC) comprised of representatives from all of the partner organizations: Butzel Family Center, Community Health and Social Services, Inc. (CHASS Center), Detroit Health Department, Detroiters Working for Environmental Justice, Friends of Parkside, Henry Ford Health System, Kettering/Butzel Health Initiative, Latino Family Services, United Community Housing Coalition, Warren/Conner Development Coalition, and the University of Michigan Schools of Public Health and Medicine. The Detroit Public Schools also are collaborating with the project. The SC meets on at least a monthly basis. The SC has, through a process of consensus, been responsible for all major decisions regarding study design as well as numerous more specific decisions concerning, for example, recruitment strategies, wording of instruments, and hiring of personnel.
A screening questionnaire was distributed in the Fall of 1999 to identify children with asthma then ages 6 to 10. Over 7,500 questionnaires were successfully mailed and about 2,000 were distributed in elementary schools. A total of 3,342 screening questionnaires were completed and returned in 1999. Among the returned questionnaires, 1,655 (49.7 %) were consistent with probable or known asthma of any severity. Among these, 387 (11.5 % of the total returned) had probable or known moderate to severe asthma based on National Asthma Education and Prevention Program diagnostic guidelines and another 116 had mild persistent asthma severe enough for eligibility for the study. Calculated minimum population-based estimates of
prevalence for any asthma (18.9 %) and moderate to severe asthma
(4.4 %) substantially exceed national averages. Among those with known or
probable moderate to severe asthma, over 30 percent had not been diagnosed by a
physician, over one-half were not taking daily asthma medication, and
approximately one-quarter had not taken any physician-prescribed asthma
medication in the past 12 months.
Of the 503 initially considered eligible for the study, approximately 30 were
excluded because of living or having moved to an address outside of the target
area. Of the remaining approximately 470 eligible children, 302 have been
successfully enrolled into at least one aspect of the study (skin testing,
baseline questionnaire, and/or first seasonal intensive data collection). Most
of those not yet enrolled have proved difficult to contact by phone or mail.
Fewer than 20 families have refused participation.
Other important steps accomplished in 1999-2000 include:
- Development and pilot testing of written instruments in both English and Spanish including the screening questionnaire, adult (caregiver) questionnaire, child questionnaire, a household environmental checklist, and a neighborhood environmental checklist.
- Elaboration of study protocols for skin test "fairs", training on use of the Airwatch airway monitor and symptom diary, administration of adult and children baseline questionnaires, completion of household and neighborhood environmental checklists, collection of household dust for allergen analysis, and measurement of personal and indoor household PM levels.
- Hiring and training of staff from the community to serve as interviewers, air monitor and diary trainers, environmental checklist administrators, household dust collectors, and community environmental specialists ("CESs", or Outreach Workers).
- Allergen skin testing of 272 children at 17 skin test "fairs".
- Completion with 279 of the 302 participating families of the adult baseline questionnaires, household walk-through, and household dust collection for allergen analysis.
- Participation by 205 families in the first 2-week intensive seasonal assessment through daily use of airway monitors and diaries, and, in a subset of about 80 households, measurement of vapor phase nicotine.
- Installation of two tapered element oscillating microbalance instruments (TEOMs), for continuous measurement of ambient PM, on the rooftops of two Detroit elementary schools.
- Development and production of customized indoor air sampling pump units, which were used to collect PM levels in each of the two elementary schools and in participant households during the first 2-week intensive seasonal assessment.
- Creation and distribution of a newsletter for households participating in the study.
- Distribution of vacuum cleaners and mattress and pillow covers to all wave one study participants as part of the intervention, and development of personalized plans for each of the households in wave one.
- Participation by project faculty and staff in a 2-day training on Integrated Pest Management conducted by the Michigan Department of Agriculture, with plans underway to begin working with Abell Pest Management Services as part of the intervention.
- Establishment of a Dissemination Committee, comprised of university and community representatives, to make information about the work of the project known to Detroit and the academic community. The Committee has developed a protocol consisting of guidelines for dissemination activities (including authorship on articles and on presentations, participation at national conferences, and promotion of project activities and findings within the Detroit community).
Results of Allergen Skin Testing. Based on preliminary analyses, the proportion of children with positive response to skin prick testing for each allergen is shown below:
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The substantial proportion of children positive for allergens of outdoor origin (ragweed, grass, and Alternaria) was somewhat unexpected, and may have important implications for the customization of intervention strategies beyond those that were already envisioned for children allergic to roach and dust mite.
Core 3: Chemokines in the Pathogenesis of Asthma. We have initiated our investigations into the immuno pathologic alterations that occur in asthma. Our studies began shortly after the initial grant award was given. We started with the first specific aim of the grant. The data indicated that the recombinant chemokines would recruit neutrophils to the lung in a dose dependent manner. Inbred strains of mice have been divided into high responder mice that are termed TH1 and low responder mice that are termed TH2. We additionally tested in the capacity for the chemokines to recruit neutrophils in TH1 (C57/Bl6) and TH2 (Balb/c) mice. These results demonstrated that either the high responder mice, or the low responder mice would respond equally well to the chemokines. Both strains of mice will actively and briskly recruit neutrophils into the pulmonary airspace following a local challenge.
The next step was to begin to develop a new murine model of asthma. Our original proposal intended to collect house dust from homes where children are experiencing symptoms of asthma. We collected dust from 10 such homes and prepared an aqueous extract of the material. This extract was then tested for the presence of several allergens including cockroach (Bla g I and II), dust mite (Der p1 and f1), cat (Fel d1) and dog (Can f1). Table 1 shows the results that we obtained from these analyses. As can be observed, the sample from number five contained high levels of the cockroach allergens.
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Table 1. Concentrations of allergens in dust collected from
10 households in Detroit where children have asthma.
With these results, we revisited house number five and obtained a significant quantity of house dust. An aqueous extract was prepared from this material to be used for future studies. We next initiated our studies to develop the model of mouse asthma. The following protocol was used for this study. First, mice were immunized with the household dust extract combined with adjuvants. After 14 days, the lungs of the immunized mice were exposed to the host dust extract using the same protocol that had been devised for the exposure to the recombinant chemokines developed in year one. The mice were anesthetized, the tongue gently pulled forward, and the host dust extract placed in the back of the hypopharynx. Seven days after the second exposure the mice were once again re-exposed to the host dust extract. Forty-eight hours after the third exposure the mice were sacrificed and bronchoalveolar lavage performed to determine the inflammatory cell infiltrate. The results showed that the model could actively recruit eosinophils, the hallmark inflammatory cell of asthmatic attack, into the lung. We next conducted a dose response study where the house dust extract was diluted 1:1, 1:10, and 1:50 prior to immunization of the mice. These data demonstrated that, in a dose response manner, eosinophils are recruited into the lung (Figure 1). This figure also shows that the number of neutrophils did not vary significantly, but the number of lymphocytes (another marker of specific immune activation) did decrease.
These data indicate that the proposed model of murine asthma has been
initially developed and characterized. We are in the process of purchasing a
small animal pulmonary function apparatus in order to rigorously determine that
airway hyperreactivity has been established in this model.
The intervention activities as described above for the wave one families will continue during the 2000-2001 year. In March 2001, families who have been randomized into wave two will begin to receive their intervention. In addition, the neighborhood-level community awareness and mobilization campaign will begin in the upcoming year. This phase of the intervention will include educational events on environmental triggers for asthma, working with neighborhood block clubs and associations, advocacy for families attempting to adopt new health behaviors, assisting with housing issues, and organizing and conducting activities to reduce physical environmental hazards in their neighborhoods. Air monitoring activities, as described above, will be ongoing throughout the upcoming year.
We will continue our investigations as planned. We should have completed our complete characterization of the most model within the next 6 months. We will then begin to assay for the pathogenic factors.
Journal Articles: 26 Displayed | Download in RIS Format
| Other center views: | All 46 publications | 26 publications in selected types | All 26 journal articles |
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Clark NM, Brown RW, Parker EA, Robins TG, Remick DG, Philbert MA, et al. Childhood asthma. Environmental Health Perspectives. 1999;107:421-429. |
R826710 (Final) R826710C001 (1999) R826710C002 (1999) R826710C003 (1999) |
not available |
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Dvonch T, Marsik FJ, Keeler GJ, Robins TG, Yip F, Morishita M. Field comparison of PM2.5 TEOM and PM2.5 manual filter-based measurement methods in urban atmospheres. Journal of Aerosol Science. 2000;31:S190-S191 |
R826710 (Final) |
not available |
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Edgren KK, Parker EA, Israel BA, Lewis TC, Salinas M, Robins TG, Hill YR. Conducting a health education intervention and an epidemiological research project involving community members and community partner organizations: The Community Action Against Asthma Project.Health Promotion Practice2005;6(3):263-269. |
R826710 (Final) |
not available |
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Eggleston PA, Diette G, Lipsett M, Lewis T, Tager I, McConnell R, Chrischilles E, Lanphear B, Miller R, Krishnan J. Lessons learned from the study of childhood asthma from the Centers for Children’s Environmental Health and Disease Prevention research. Environmental Health Perspectives 2005;113(10):1430-1436. |
R826710 (Final) R827027 (2002) R829389 (2003) R829389 (2004) R829389 (2005) R831710 (2004) R831710 (2005) R831861 (2005) R832139 (2004) R832139 (2005) R832139C002 (2005) R832139C003 (2005) R832141 (2006) |
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Farquhar SA, Parker EA, Israel BA. In their words: A qualitative analysis of the effects of the physical environment on Detroit residents.Local Environment2005;10(3): 259-274. |
R826710 (Final) |
not available |
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Farquhar SA, Parker EA, Schulz AJ, Israel BA. In their words: How Detroit residents perceive the effects of their physical environment. Local Environment. 2005;10(3):259-274. |
R826710 (Final) |
not available |
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Farquhar SA, Parker EA, Israel BA, Schulz AS. The effects of the physical environment on health and well-being in residents of eastside and southwest Detroit, Michigan. Journal of Environmental Psychology. |
R826710 (2002) |
not available |
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Gilliland F, Avol E, Kinney P, Jerrett M, Dvonch T, Lurmann F, Buckley T, Breysse P, Keeler G, de Villiers T, McConnell R. Air pollution exposure assessment for epidemiologic studies of pregnant women and children: lessons learned from the Centers for Children’s Environmental Health and Disease Prevention Research. Environmental Health Perspectives 2005;113(10):1447-1454. |
R826710 (Final) R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R827027 (2002) R831845 (2005) R831861 (2004) R831861 (2005) R832141 (2006) |
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Israel BA, Parker EA, Rowe Z, Salvatore A, Minkler M, Lopez J, Butz A, Mosley A, Coates L, Lambert G, Potito PA, Brenner B, Rivera M, Romero H, Thompson B, Coronado G, Halstead S. Community-based participatory research: lessons learned from the Centers for Children's Environmental Health and Disease Prevention Research. Environmental Health Perspectives 2005;113(10):1463-1471. |
R826710 (Final) R829391 (2004) R829391 (2005) R829391 (2006) R829391C005 (2006) R831709 (2005) R831709C003 (2005) R831709C003 (2006) R831710 (2004) R831710 (2005) R831711 (2005) R831711 (2006) R831711 (2007) R831711C001 (2006) R831711C002 (2006) R831711C003 (2006) |
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Israel BA, Schulz AJ, Parker EA, Becker AB, Allen AJ, Guzman JR. Critical issues in developing and following community-based participatory research principles. In: M Minkler and N Wallerstein, editors. Community-Based Participatory Research for Health. San Francisco, CA: Jossey-Bass; 2003:56-73. |
R826710 (Final) |
not available |
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Keeler GJ, Dvonch JT, Yip F, Parker EA, Israel BA, Marsik FJ, et al. Assessment of personal and community-level exposures to particulate matter among children with asthma in Detroit, Michigan, as part of Community Action Against Asthma (CAAA). Environmental Health Perspectives. 2002;110:173-181. |
R826710 (2002) R826710 (Final) |
not available |
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Kim J, Merry AC, Nemzek JA, Bolgos GL, Siddiqui J, Remick DG. Eotaxin Represents the Principal Eosinophil Chemoattractant in a Novel Murine Asthma Model Induced by House Dust Containing Cockroach Allergens. Journal of Immunology 2001;167:2808-2815. |
R826710 (2002) R826710 (Final) |
not available |
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Kim J, McKinley L, Natarajan S, Bolgos GL, Siddiqui J, Copeland S, Remick DG. Anti-tumor necrosis factor-alpha antibody treatment reduces pulmonary inflammation and methacholine hyper-responsiveness in a murine asthma model induced by house dust.Clinical and Experimental Allergy2006;36(1):122-132. |
R826710 (Final) |
not available |
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Kim J, McKinley L, Siddiqui J, Bolgos G, Remick DG. Prevention and reversal of pulmonary inflammation and airway hyperresponsiveness by dexamethasone treatment in a murine model of asthma induced by house dust. American Journal of Physiology - Lung Cellular & Molecular Physiology. 2004;287(3):L503-L509. |
R826710 (Final) |
not available |
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Lewis TC, Robins TG, Dvonch JT, Keeler GJ, Yip FY, Mentz GB, et al. Air pollution associated changes in lung function among asthmatic children in Detroit. Environmental Health Perspectives2005;113(8):1068-1075. |
R826710 (Final) |
not available |
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Lopéz ED, Parker EA, Edgren KK, Brakefield-Caldwell W. Lessons learned while using a CBPR approach to plan and conduct forums to disseminate research findings back to partnering communities. Metropolitan Universities Journal 2005;16(1):57-76. |
R826710 (Final) |
not available |
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McKinley L, Kim J, Bolgos GL, Siddiqui J, Remick DG. CXC chemokines modulate IgE secretion and pulmonary inflammation in a model of allergic asthma. Cytokine2005;32(3-4):178-85. |
R826710 (Final) |
not available |
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McKinley L, Kim J, Bolgos GL, Siddiqui J, Remick DG.Allergens induce enhanced bronchoconstriction and leukotriene production in C5 deficient mice.Respiratory Research2006;7:129. |
R826710 (Final) |
not available |
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McKinley L, Kim J, Bolgos GL, Siddiqui J, Remick DG. Reproducibility of a novel model of murine asthma-like pulmonary inflammation. Clinical & Experimental Immunology. 2004;136:224-231. |
R826710 (Final) |
not available |
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Parker EA, Israel BA, Robins TG, Mentz G, Lin X, Brakefield-Caldwell W, Ramirez E, Edgren KK, Salinas M, Lewis TC. Evaluation of Community Action Against Asthma: A community health worker intervention to improve children's asthma-related health by reducing household environmental triggers for asthma. Health Education and Behavior2008;35(3):376-395. |
R826710 (Final) |
not available |
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Parker EA, Israel BA, Brakefield-Caldwell W, Keeler GJ, Lewis TC, Ramirez E, et al. Community Action Against Asthma: Examining the partnership process of a community-based participatory research project. Journal of General Internal Medicine. 2003;18(7):558-567. |
R826710 (Final) |
not available |
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Parker EA, Robins TG, Israel BA, Brakefield-Caldwell W, Edgren KK, Wilkins D. Developing and implementing guidelines for dissemination: The experience of the Community Action Against Asthma project. In: BA Israel, E Eng, AJ Schulz and E Parker, editors. Methods in Community-Based Participatory Research for Health. San Francisco, CA: Jossey-Bass; 2005:285-306. |
R826710 (Final) |
not available |
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Parker EA, Baldwin GT, Israel BA. Health promotion models and theories for environmental health. Health Education & Behavior. 2004;31(4):491-509. |
R826710 (Final) |
not available |
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Trout D, Weissman DN, Lewis D, Brundage RA, Franzblau A, Remick D. Evaluation of hypersensitivity pneumonitis among workers exposed to metal removal fluids. Applied Occupational and Environmental Hygiene2003;18: 953-60. |
R826710 (Final) |
not available |
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Yip F, Keeler GJ, Dvonch JT, Robins T, Parker E, Israel BA, et al. Personal exposures to particulate matter among children with asthma in Detroit, Michigan. Atmospheric Environment. 2004;38:5227-5236. |
R826710 (Final) |
not available |
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Lewis TC, Robins TG, Joseph CLM, Parker EA, Israel BA, Rowe Z, et al. Identification of gaps in the diagnosis and treatment of childhood asthma using a community-based participatory research approach. Journal of Urban Health. 2004;81(3):472-488. |
R826710 (Final) |
not available |
asthma, ambient air, indoor air, exposure, health effects, children, stressor, pathogens, community-based, social science, pathology, monitoring, Detroit. Children, health, asthma, exposure, home, indoor air, inner city, cockroach, chemokines, allergen. , HUMAN HEALTH, Air, Geographic Area, Scientific Discipline, Health, RFA, Molecular Biology/Genetics, Health Effects, Indoor Air Pollution, indoor air, Risk Assessments, Health Risk Assessment, Children's Health, Environmental Chemistry, Allergens/Asthma, State, exposure assessment, asthma indices, airborne urban contaminants, allergen, environmental tobacco smoke, inhalation, respiratory problems, respiratory disease, children's environmental health, asthmatic children, air quality, second hand smoke, cigarette smoke, assessment of exposure, childhood respiratory disease, human health risk, susceptibility, cockroaches, acute lung injury, air pollution, airborne pollutants, airway disease, children, exposure, children's vulnerablity, indoor air chemistry, asthma triggers, allergic response, asthma, human exposure, Human Health Risk Assessment, airway inflammation
Relevant Websites:
Progress and Final Reports:
Original Abstract
2002 Progress Report
Final Report
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R826710C001 Indoor and Outdoor Air Contaminant Exposures and Asthma Aggravation Among Children (Asthma Exposure)
R826710C002 Chemokines in the Pathogenesis of Asthma (Asthma Chemokines)
R826710C003 A Community-Based Intervention to Reduce Environmental Triggers for Asthma Among Children (Asthma Intervention)