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2002 Progress Report: CECEHDPR - University of Southern California
EPA Grant Number: R826708Center: CECEHDPR - University of Southern California
Center Director: Gong, Henry
Title: CECEHDPR - University of Southern California
Investigators: Gong, Henry
Current Investigators: Gong, Henry , Avol, Edward L. , Diaz-Sanchez, David , Gauderman, William , Gilliland, Frank , Hinds, William C. , Jones, Craig , McConnell, Rob , Peters, John M.
Institution: University of California - Los Angeles
EPA Project Officer: Fields, Nigel
Project Period: August 1, 1998 through July 31, 2003
Project Period Covered by this Report: August 1, 2001 through July 31, 2002
Project Amount: $2,895,926
RFA: Centers for Children's Environmental Health and Disease Prevention Research (1998)
Research Category: Children's Health , Health Effects
Description:
Objective:The focus of the University of Southern California (USC) Children's Environmental Health Center is to develop a better understanding of how host susceptibility and environmental exposures contribute to children's respiratory disease. This research will provide health and environmental officials with a variety of useful intervention tools. USC intends to investigate the relationship between environmental tobacco smoke (ETS) and asthma in children. This project will determine the biological mechanisms by which ETS alters normal allergic responses in children.
The Community Outreach and Education Program (COEP) of the Children's Environmental Health Center (CEHC) attempts to connect an interdisciplinary team of scientists from USC and UCLA with other researchers studying issues of children's environmental health, as well as with community-based organizations and others interested in children's environmental health issues. The COEP program at the Keck School of Medicine at USC began when NIEHS funded the Southern California Environmental Health Sciences Center in 1996. The CEHC has allowed an expansion of partnerships with community-based and public health organizations, as well as with health care providers and schools, particularly around issues of asthma.
The primary objectives of CEHC's COEP activities are:
- ·To create awareness of new problems and research opportunities in children's
environmental health that are relevant to the community;
·To collaborate with community-based organizations and community-focused institutions on projects involving children's environmental health issues;
·To provide support to Center members by linking their research efforts with interested community organizations;
·To identify and respond to programmatic needs and requests concerning environmental health issues that affect children that are raised within the community;
·To promote education about children and environmental health issues in K-12 school programs.
In addition to the objectives detailed above, the Center has received funding for the following three projects, which will be discussed below:
Project 1: Children's Susceptibility to Air Pollution (Children's Environmental Health Center)
This study builds on an ongoing prospective cohort study of children in 12 California communities to assess the hypotheses that 1) dietary intake of fruits, vegetables and antioxidants; and 2) polymorphisms in genes involved in lung defenses (GSTMI, GSTFI, GSTPI, MPO, TNFA) affect children's susceptibility for slow lung function growth and increased occurrence of respiratory illnesses from chronic exposure to ozone (O3) nitrogen dioxide (NO2), and respirable particles (PM10 and PM2.5).
Project 2: Children's Exposure to Environmental Tobacco Smoke: Changes in Allergic Response
The objective of this study is to design a carefully-controlled experiment for deposit accumulation and HC emission measurement. (2) To assess the effects of combustion chamber deposits on the hydrocarbon emissions from a modern production spark-ignition engine. (3) To measure the effect of CCD on HC emissions from single-component fuels. (4) To develop and validate a model for the mechanism(s) by which combustion chamber deposits lead to additional HC emissions. (5) To study the effects of combustion chamber deposits on NOx emissions.
Project 3: Asthma in Children: A Community-based Intervention Project
Asthma is the most common chronic disease in childhood. Asthma is now associated with increasing frequency, hospitalization, and mortality, especially in nonwhite, poor, inner-city children. Research is needed to develop and evaluate comprehensive community-based programs designed to reduce asthma triggers in the home environment, such as house dust mites and cockroaches. In this study, inner-city, primarily minority, children with asthma are being identified through a school-based mobile asthma clinic, the Breathmobile, which delivers high quality asthma care to these children. Working with school nurses and community organizations and 3 Breathmobile units, we propose a community-based intervention aimed at reducing asthma triggers in the home. The major goal of this study is to determine whether a comprehensive environmental health education program, enhanced by least-toxic integrated pest management for cockroach control, will result in reduction of dust mites or cockroaches in children's homes and clinical improvement in asthma.
Progress Summary:Project 1: Children's Susceptibility to Air Pollution (Children’s Environmental Health Center)
Studies and Results
The cohort of children and adolescents who have participated in the Children's Health Study (CHS) form the base population for the longitudinal study of childhood determinants of susceptibility. Investigators are collecting updated medical histories, dietary information, buccal cells for genotyping and verifying medical history of asthma. Tracing subjects has proved to be a major challenge requiring substantial effort. Based on the findings that in utero exposure to maternal smoking is associated with decreased lung function especially in children with asthma and is also associated with increased risk of early onset asthma, Investigators have continued validating medical histories of asthma by contacting parents for telephone interviews and have completed a counter-matched prevalence case-control study nested in the cohort. As of 5/24/2002, they have interviewed 194 parents or guardians for the incident asthma cases and a set of controls. They are continuing to collect buccal cells by mail. They have found that extraction of the DNA from cells using a commercial kit (Purgene) provides stable DNA specimens for cleaner genotyping results. They have genotyped 3200 specimens at GSTM1, T1, and P1 and TNFa using Taqman assays and have conducted several analyses. They have been delayed in genotyping MPO because of difficulties in designing the probe for the wild type allele. They found that polymorphisms of GSTM1 and GSTP1 are associated with early onset asthma (before age five years) and severity of wheezing. They have observed an additive interaction between GSTP1 and GSTM1 for wheezing. They found that polymorphisms of GSTM1 and GSTP1 are associated with early onset asthma (before age five years) and severity of wheezing in those exposed to in utero smoking. A manuscript has been accepted for publication. They have observed a 3-way interaction between in utero exposure, GSTP1 and GSTM1 in the occurrence of wheezing.
Investigators have conducted preliminary analyses of the risk for newly diagnosed asthma among CHS participants with available genotyping data. They found a significant protective effect for the GSTP1 Val allele. A manuscript is in preparation. They have observed a two-fold increased risk of asthma among participants who begin to smoke cigarettes as well as who became obese. Manuscripts are in preparation.
They have observed a statistically significant effect of GSTM1 and PI on lung function growth, especially measures of small airway flows. They have examined the effects of GSTM1, PI and Tl on respiratory illness-related school absenteeism. In preliminary analyses of our 1996 school absenteeism cohort, they found that GSTP1, but not GSTM1 or TI, was associated with rates of respiratory related absences. A manuscript reporting these findings is in press.
They are currently examining the effect of the TNF -308 polymorphism on lung function growth, asthma and wheezing occurrence, and absences. They are continuing to examine the effects o diet on lung function and asthma outcomes. A manuscript is in preparation to report the findings relating Vitamin C and A to lung function level in children. They are planning to examine gene - air pollution and diet air pollution interactions in detail in the next year.
Project 2: Children's Exposure to Environmental Tobacco Smoke: Changes in Allergic Response
Studies and Results
Specific Aim #1: Investigators will determine the mechanisms by which ETS
alters the in vivo IgE antibody response in the human upper airway.
As with other inhaled pollutants, ETS is thought to exert major effects
through the production of reactive oxygen species (ROS). Antioxidants have
been shown
to reduce the allergic inflammatory effects of chemicals present in ETS
in vitro. Glutathione-S-Transferases (GSTS) are a family of enzymatic antioxidants
involved in metabolism of ROS and detoxification of chemicals present in
ETS. Functional polymorphisms in the GST genes are very common in the population
(up to 50%) and are candidates for modulating individual susceptibility
to
the adjuvant effects of ETS on allergic inflammation. Investigators tested
the effects of GSTM1 and GSTTI null genotypes, (which results in an absence
of these enzymes) and GSTP1 codon 105 variants (which determines GSTP1
activity) on the ETS adjuvant effect. They have used their previously established
human
ETS exposure model performed in collaboration with Dr. Gong at the Los
Amigos Research and Education Institute. In this model subjects are exposed
to the
side-stream smoke of five Kentucky Reference cigarettes in a two-hour period.
Nineteen ragweed allergen sensitive subjects were challenged intranasally
with
allergen following 2 hours exposure to either clean air or ETS. As they
have previously reported exposure to ETS prior to allergen challenge significantly
enhanced ragweed-specific IgE levels in nasal ravages obtained 4 days after
exposure. In collaboration with Dr. Gilliland (Project 2) and the Molecular
Biology Core they determined GST genotypes using DNA from buccal cell specimens.
Individuals with either a GSTM1 present or the GSTP1 vallO5 variant genotypes showed markedly reduced ETS enhancement of the nasal response to allergen. In subjects with the GSTM1 null genotype, allergen specific-IgE levels were 26 fold higher following ETS/allergen exposure than clean air/allergen exposure. In contrast subjects with GSTM1 present genotype showed only a 4 fold in Acreage. A similar significantly larger increase in IgE was observed in subjects with GSTP1 val105 variant genotypes compared with subjects with wildtype GSTP1 genotype. The same pattern was observed in histamine levels obtained 10 mins after allergen challenge. ETS potentiated the response to a significantly greater degree in subjects with the GSTM1 null and GSTP1 wild type genotypes. None of the GSTs modified the allergic response following allergen challenge alone. G8TT1 genotype was not associated with allergic response following ETS.
Aim #2): Investigators will determine how exposure to ETS alters IQE-independent inflammatory responses in the human upper airway.
Investigators have previously established that ETS will synergise with allergen to produce a local Th2 cytokine milieu. This cytokine response is characteristic of an enhanced allergic response and is critical to allergic inflammation. Following challenge of allergic subjects with allergen alone they observed little or no change in nasal cytokine levels. In contrast if allergen-challenge was performed following ETS exposure, there was a rise in IL-4, IL-5 and IL-13 levels in nasal washes obtained 24 hours later. In contrast, IFN-Y levels were riot significantly changed by ETS plus allergen exposure. They tested the hypothesis that the increased responsiveness to ETS in IgE production in individuals with certain GST genotypes was due to regulation of cytokines by these natural antioxidants. Although an increase in IL-4 and a decrease in INF-Y were associated with GSTM1 null and GSTP1 wild type genotype, the changes did not achieve statistical significance. This may be because of the limited number of subjects used.
They have also previously shown that eosinophil influx in the nasal mucosa is significantly greater if allergen challenge followed ETS exposure. Thus while less than 1% of total cells were identified as eosinophils in baseline ravages, and 19% eosinophils were measured 24 hours after allergen challenge, this number rose to 32% following ETS plus allergen exposure. Investigators hypothesized that this is due to changes in chemokine levels. They have obtain nasal ravages from subjects before and 1, 6 and 14 hours after exposure to either ETS/allergen or clean air/allergen. These samples are currently being measured for levels of RANTES, GM-CSF, IL-8, MIP-1alpha and MCP-1. These are CC and CXC chemokines implicated in eosinophil and lymphocyte attraction and activation.
Aim #3) Investigators will test the hypothesis that the in vivo allergic antibody response due to chronic exposure to ETS is controlled by genetic back-ground and age.
Investigators have previously succeeded in establishing an animal model of chronic exposure to ETS using two strains (a poor and a good IgE responder) and shown that ETS could increase antigen-specific IgE responses to an aerosolized protein in both. This model is characterized by increased eosinophils in BAL fluid and increased IL-4 levels. We tested the hypothesis that this key TH2 promoting cytokine is responsible for both the humural and cellular responses observed in our model. Therefore, we compared untreated mice to mice treated with i.p. injections of a IL-4 receptor antagonist. This antagonist blocks the binding of both IL4 and IL-13. As before untreated BALB/c mice exposed to 10 days exposure of ETS+ aerosolized OVA made significantly more OVA-IGE than those exposed to OVA alone. However, in mice treated with 10µg IL-4R antagonist given immediately prior to each ETS exposure, there was no enhancement of OVA-IGE by ETS, thus OVA-IGE in OVA or OVA+ETS exposed animals were the same. Furthermore, eosinophil enhancement by ETS was significantly inhibited in the antagonist-treated animals.
Project 3: Asthma in Children: A Community-based Intervention Project
Phase 1
Investigators completed a study of repeated measurements of cockroach allergen in a study of 49 homes of allergic children with cockroaches, which were treated and professionally cleaned and had repeated subsequent professional treatment during up to one year of follow-up. In the kitchens of homes heavily infested with cockroaches, the intervention produced a marked reduction in allergen (Bla g 2), large enough that effects on health might be expected, based on other studies which have evaluated health outcomes. However, concentrations which have been associated with health effects in other studies continued to be observed in many homes. In less heavily infested homes, there was minimal effect of the intervention. Important experience about sampling strategy and design were gained, which have been applied to the educational intervention. A manuscript is under review
In a sample of homes, repeated measurements have been made of allergen levels at co-located sites within the home, at different time intervals, and using different methods of collection (wipe and vacuum methods). They have demonstrated adequate recovery of allergen from vacuumed samples of bedding, even when covered with allergen impermeable covers, and of accessible dust within the kitchen (on counters and floors, but not behind or under appliances), even in homes where subjects are encouraged to clean to reduce allergen levels. Within home correlations exceeding .40 (similar to reports from other studies) are as good or better using a wipe collection technique, which is suitable for subjects to collect themselves, as from vacuum collected dust by a technician. The wipe test would be suitable for large-scale epidemiologic studies, in which it would be too expensive to make home visits. A manuscript is under preparation. Based on these analyses, an appropriate strategy has been finalized to assay 2 archived dust samples from each visit. These analysis have been a joint effort with the CEHC at the University of Iowa (Peter Thome), rather than at USC, as originally proposed. Dr. Thome has unique expertise in the analysis of endotoxin, which is being assayed as part of a complementary research effort.
Investigators have 160 subjects. Fourteen have been lost to follow-up and eight have completed the study. We have examined the knowledge of caretakers of their children's allergies from their physicians (by skin test), a key intermediate variable in the intervention to control exposure to allergens. Caretakers accurately report those allergens to which their children are allergic (although there are many false positive reports). A manuscript is under preparation. Analysis of the relationship of intervention to health outcomes from the first two home visits is nearing completion, and a manuscript is under preparation. Data for the third visit is available and being prepared for analysis.
Phase II (expansion to broader community) and Health Education
The core of the educational effort is a flip chart and accompanying training manual for families in a comic book style format. Other tools developed include a coloring book for children and reinforcement messages on magnets for refrigerators. During the past year Investigators have refined reinforcement educational messages for the final two visits to participants' homes, tailored to the problems in individual homes. A brief video demonstrating the impact of house dust mite allergen on the lung has been adapted from materials available in the public domain (with permission). They have posted to the Center web site our educational manual and review of indoor allergen health education materials In Spanish and English. We described last year a (now county wide) community based asthma coalition, in which Center investigators are active participants, which includes some of our community partners to the CEHC, and which also uses community health workers for teaching families. The CEHC organized jointly with the coalition a series of workshops for community health educators on how to better control indoor allergens (house dust mite, mold, and cockroach). The development of a research component to this growing effort has been slow, because the coalition has focused during this year on developing a proposal for a large grant, which was recently awarded by the California Endowment, and which relies heavily on our curriculum for training community outreach workers and for teaching subjects. Center investigators and staff are largely responsible for the design of the environmental intervention, including the proposed research evaluation, which the coalition has asked be expanded to include community concerns around the effect of air pollution on asthmatic children.
Future Activities:The CEHC COEP Director will spend significant effort in distributing a documentary video on air pollution's impact to various organizations concerned with children's environmental health around the state of California, especially in those counties experiencing the most serious air pollution problems. These will include focused campaigns to reach school PTAS, AYSO soccer groups, school nurses, nursing organizations, pediatricians, local and regional air pollution control districts, middle and high school science and health classes, and many others. The CEHC director will form partnerships with nonprofit organizations to assist in distribution efforts, will speak at gatherings where the video is shown, and will write articles for newsletters to promote the documentary video.
The Environmental Justice collaboration with EHC will be ongoing during the next year and it is anticipated that the collaboration between the CEHC and the Long Beach Asthma Alliance will be expanded. Planned activities for individual projects are outlined below :
Project 1: Children's Susceptibility to Air Pollution (Children's Environmental Health Center)
Investigators plan to analyze the nested case-control study of early life events and asthma and the medical records validation study. We will begin genotyping subjects for MPO and continue TNFA and the GSTS. They will continue to collect buccal cells, health update and diet questionnaires for cohort members. The ongoing longitudinal study will collect exposure data. They plan additional analyses of the dietary data in the next year and continued examination of the effects of tobacco smoke and ambient air pollution on children's respiratory health.
Project 2: Children's Exposure to Environmental Tobacco Smoke: Changes in Allergic Response
Investigators have shown that ETS has the potential to exacerbate on-going
allergic diseases and presumably increase severity of allergic disease. During
this next year of support they intend to further study the importance of
genotype on susceptibility to the adjuvant effects of ETS. They believe
that the association
between IL-4/ INF-
levels and GST genotypes although not statistical significant
is real. They believe that the study at the moment is under-powered. They
therefore, propose to increase the number of subjects studied to test this
assertion.
During this same time they will make use of the availability of mice whose
gene for a key natural antioxidant is absent (NQO14' mice).
Project 3: Asthma in Children: A Community-based Intervention Project
Urgent tasks are to complete the manuscripts described above and to complete and incorporate the allergen assay results into the health analyses. Investigators will extend the analysis to subsequent visits as families complete the study and data become available. They will complete the design and collect preliminary data from the research evaluation of the broader intervention by the community asthma coalition.
Journal Articles: 50 Displayed | Download in RIS Format
| Other center views: | All 80 publications | 52 publications in selected types | All 50 journal articles |
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Berhane K, McConnell R, Gilliland F, Islam T, Gauderman WJ, Avol E, London SJ, Rappaport E, Margolis HG, Peters JM. Sex specific effects of asthma on pulmonary function in children. American Journal of Respiratory and Critical Care Medicine 2000;162(5):1723-1730. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2001) R826708C003 (2001) R831861 (2004) R831861 (2005) |
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Chang MC, Sioutas C, Kim S, Gong Jr H, Linn WS. Reduction of nitrate losses from filter and impactor samplers by means of concentration enrichment. Atmospheric Environment 2000;34(1):85-98. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) |
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Corren J, Diaz-Sanchez D, Saxon A, Deniz Y, Reimann J, Sinclair D, Davancaze T, Adelman D. Effects of omalizumab, a humanized monoclonal anti-IgE antibody, on nasal reactivity to allergen and local IgE synthesis. Annals of Allergy, Asthma and Immunology 2004;93(3):243-248. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Diaz-Sanchez D, Proietti L, Polosa R. Diesel fumes and the rising prevalence of atopy: an urban legend? Current Allergy and Asthma Reports 2003;3(2):146-152. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Diaz-Sanchez D, Riedl M. Diesel effects on human health: a question of stress? American Journal of Physiology—Lung Cellular and Molecular Physiology 2005;289(5):L722-L723. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Enright PL, Linn WS, Avol EL, Margolis HG, Gong H Jr, Peters JM. Quality of spirometry test performance in children and adolescents: experience in a large field study. Chest 2000;118(3):665-671. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2005) |
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Finkelman FD, Yang M, Orekhova T, Clyne E, Bernstein J, Whitekus M, Diaz-Sanchez D, Morris SC. Diesel exhaust particles suppress in vivo IFN-γ production by inhibiting cytokine effects on NK and NKT cells. Journal of Immunology 2004;172(6):3808-3813. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Gauderman WJ, McConnell R, Gilliland F, London S, Thomas D, Avol E, Vora H, Berhane K, Rappaport EB, Lurmann F, Margolis HG, Peters J. Association between air pollution and lung function growth in southern California children. American Journal of Respiratory and Critical Care Medicine 2000;162(4 Pt 1):1383-1390. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2000) R826708C001 (2001) R826708C003 (2001) R831861 (2004) R831861 (2005) |
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Gilliland FD, McConnell R, Peters J, Gong H Jr. A theoretical basis for investigating ambient air pollution and children’s respiratory health. Environmental Health Perspectives 1999;107(Suppl 3):403-407. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2000) R826708C003 (2000) R831861 (2004) R831861 (2005) |
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Gilliland FD, Linn W, Rappaport E, Avol E, Gong H, Peters J. Effect of spirometer temperature on FEV1 in a longitudinal epidemiological study. Occupational and Environmental Medicine 1999;56(10):718-720. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2005) |
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Gilliland FD, Berhane K, McConnell R, Gauderman WJ, Vora H, Rappaport EB, Avol E, Peters JM. Maternal smoking during pregnancy, environmental tobacco smoke exposure and childhood lung function. Thorax 2000;55(4):271-276. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2000) R826708C003 (2000) R831861 (2004) R831861 (2005) |
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Gilliland FD, Li YF, Peters JM. Effects of maternal smoking during pregnancy and environmental tobacco smoke on asthma and wheezing in children. American Journal of Respiratory and Critical Care Medicine 2001;163(2):429-436. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C003 (2001) R831861 (2005) |
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Gilliland FD, Berhane K, Rappaport EB, Thomas DC, Avol E, Gauderman WJ, London SJ, Margolis HG, McConnell R, Islam KT, Peters JM. The effects of ambient air pollution on school absenteeism due to respiratory illnesses. Epidemiology 2001;12(1):43-54. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C003 (2001) R831861 (2004) R831861 (2005) |
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Gilliland FD, Berhane KT, Li YF, Kim DH, Margolis HG. Dietary magnesium, potassium, sodium, and children’s lung function. American Journal of Epidemiology 2002;155(2):125-131. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C003 (2000) R831861 (2005) |
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Gilliland FD, Berhane KT, Li Y-F, Gauderman WJ, McConnell R, Peters J. Children’s lung function and antioxidant vitamin, fruit, juice, and vegetable intake. American Journal of Epidemiology 2003;158(6):576-584. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) |
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Gilliland FD, Berhane K, Islam T, McConnell R, Gauderman WJ, Gilliland SS, Avol E, Peters JM. Obesity and the risk of newly diagnosed asthma in school-age children. American Journal of Epidemiology 2003;158(5):406-415. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Gilliland FD, Li Y-F, Saxon A, Diaz-Sanchez D. Glutathione-S-Transferase M1 and P1 genotypes protect against xenobiotic enhancement of allergic responses. Lancet 2004;363:119-125. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C002 (Final) R831861 (2004) R831861 (2005) |
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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. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826710 (Final) R827027 (2002) R831845 (2005) R831861 (2004) R831861 (2005) R832141 (2006) |
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Gong H, Sioutas C, Linn WS, Clark KW, Terrell SL, Terrell LL, Anderson KR, Kim S, Chang M-C. Controlled human exposures to concentrated ambient fine particles in metropolitan Los Angeles: methodology and preliminary health-effect findings. Inhalation Toxicology 2000;12(1):107-119. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R827352 (2004) R827352 (Final) R827352C012 (Final) R827352C014 (Final) |
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Gong H. Urban air pollution and health inequities: a workshop report. Environmental Health Perspectives 2001;109(Suppl 3):357-374. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2005) |
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Gong Jr H, Linn WS, Terrell SL, Anderson KR, Clark KW. Anti-inflammatory and lung function effects of montelukast in asthmatic volunteers exposed to sulfur dioxide. Chest 2001;119:402-408. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2005) |
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Harrington-Brock K, Cabrera M, Collard DD, Doerr CL, McConnell R, Moore MM, Sandoval H, Fuscoe JC. Effects of arsenic exposure on the frequency of HPRT-mutant lymphocytes in a population of copper roasters in Antofagasta, Chile: a pilot study. Mutation Research – Fundamental and Molecular Mechanisms of Mutagenesis 1999;431(2):247-257. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2000) |
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Kim S, Sioutas C, Chang M-C, Gong Jr H. Factors affecting the stability of the performance of ambient fine-particle concentrators. Inhalation Toxicology 2000;12(11, Suppl 4):281-298. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R825513C024 (Final) R827352 (2004) R827352 (Final) R827352C012 (Final) R827352C014 (Final) R828598C700 (Final) R829095C004 (2005) |
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Kunzli N, McConnell R, Bates D, Bastain TM, Hricko A, Lurmann F, Avol E, Gilliland FD, Peters JM. Breathless in Los Angeles: The exhausting search for clean air. American Journal of Public Health 2003;93(9):1494-1499. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Li YF, Gilliland FD, Berhane K, McConnell R, Gauderman WJ, Rappaport EB, Peters JM. Effects of in utero and environmental tobacco smoke exposure on lung function in boys and girls with and without asthma. American Journal of Respiratory and Critical Care Medicine 2000;162(6):2097-2104. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2001) R826708C003 (2001) R831861 (2005) |
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Li YF, Tsao YH, Gauderman WJ, Conti DV, Avol E, Dubeau L, Gilliland FD. Intercellular adhesion molecule-1 and childhood asthma. Human Genetics 2005;117(5):476-484. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Li Y-F, Langholz B, Salam MT, Gilliland FD. Maternal and grandmaternal smoking patterns are associated with early childhood asthma. Chest 2005;127:1232-1241. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Li Y-F, Gauderman WJ, Avol E, Dubeau L, Gilliland FD. Associations of tumor necrosis factor G-308A with childhood asthma and wheezing. American Journal of Respiratory and Critical Care Medicine 2006;173(9):970-976. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Linn WS, Gong Jr H, Clark KW, Anderson KR. Day-to-day particulate exposures and health changes in Los Angeles area residents with severe lung disease. Journal of the Air & Waste Management Association 1999;49(9 PM):108-115. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) |
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Linn WS, Szlachcic Y, Gong Jr H, Kinney PL, Berhane KT. Air pollution and daily hospital admissions in metropolitan Los Angeles. Environmental Health Perspectives 2000;108(5):427-434. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2000) R827352 (2004) R827352 (Final) R827352C012 (Final) |
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Linn WS, Adkins RH, Gong Jr H, Waters RL. Pulmonary function in chronic spinal cord injury: a cross-sectional survey of 222 Southern California adult outpatients. Archives of Physical Medicine and Rehabilitation 2000;81(6):757-763. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) |
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McConnell R, Berhane K, Gilliland F, London SJ, Vora H, Avol E, Gauderman WJ, Margolis HG, Lurmann F, Thomas DC, Peters JM. Air pollution and bronchitic symptoms in Southern California children with asthma. Environmental Health Perspectives 1999;107(9):757-760. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (2000) R831861 (2004) R831861 (2005) |
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McConnell R, Berhane K, Gilliland F, London SJ, Islam T, Gauderman WJ, Avol E, Margolis HG, Peters JM. Asthma in exercising children exposed to ozone: A cohort study. Lancet 2002;359(9304):386-391. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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McConnell R, Berhane K, Gilliland FD, Molitor J, Thomas D, Lurmann F, Avol E, Gauderman WJ, Peters JM. Prospective study of air pollution and bronchitic symptoms in children with asthma. American Journal of Respiratory and Critical Care Medicine 2003;168(7):790-797. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C003 (Final) R827352 (2004) R827352 (Final) R827352C007 (Final) R827352C009 (Final) R831861 (2004) R831861 (2005) |
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McConnell R, Milam J, Richardson J, Galvan J, Jones C, Thorne PS, Berhane K. Educational intervention to control cockroach allergen exposure in the homes of hispanic children in Los Angeles: results of the La Casa study. Clinical & Experimental Allergy 2005;35(4):426-433. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C003 (Final) R831861 (2004) R831861 (2005) R831861C001 (2005) |
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Peters JM, Avol E, Navidi W, London SJ, Gauderman WJ, Lurmann F, Linn WS, Margolis H, Rappaport E, Gong H, Thomas DC. A study of twelve Southern California communities with differing levels and types of air pollution. I. Prevalence of respiratory morbidity. American Journal of Respiratory and Critical Care Medicine 1999;159(3):760-767. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Peters JM, Avol E, Gauderman WJ, Linn WS, Navidi W, London SJ, Margolis H, Rappaport E, Vora H, Gong H Jr, Thomas DC. A study of twelve Southern California communities with differing levels and types of air pollution. II. Effects on pulmonary function. American Journal of Respiratory and Critical Care Medicine 1999;159(3):768-775. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Richardson JL, Milam JE, Galvan J, Jones C, McConnell R. Knowledge of skin test results among parents of asthmatic children. Journal of Asthma 2005;41(2):199-204. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Riedl MA, Landaw EM, Saxon A, Diaz-Sanchez D. Initial high-dose nasal allergen exposure prevents allergic sensitization to a neoantigen. Journal of Immunology 2005;174(11):7440-7445. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Riedl M, Diaz-Sanchez D. Biology of diesel exhaust effects on respiratory function. Journal of Allergy and Clinical Immunology 2005;115(2):221-228. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Rumold R, Jyrala M, Diaz-Sanchez D. Secondhand smoke induces allergic sensitization in mice. The Journal of Immunology 2001;167(8):4765-4770. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C002 (2001) R831861 (2005) |
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Salam MT, Gilliland F, Li Y-F, Langholz B. Early life environmental risk factors for asthma: Findings from the Children’s Health Study. Environmental Health Perspectives 2004;112(6):760-765. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) R831861C001 (2005) |
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Salam MT, Langholz B, Li Y-F, Gilliland FD. Maternal fish consumption during pregnancy and risk of childhood asthma. Journal of Asthma 2005;42(6):513-518. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Saxon A, Diaz-Sanchez D. Air pollution and allergy: you are what you breathe. Nature Immunology 2005;6(3):223-226. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Sioutas C, Kim S, Chang M, Terrell LL, Gong Jr H. Field evaluation of a modified DataRAM MIE scattering monitor for real-time PM2.5 mass concentration measurements. Atmospheric Environment 2000;34(28):4829-4838. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R827352 (Final) R827352C012 (Final) R827352C014 (Final) |
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Thorne PS, Metwali N, Avol E, McConnell RS. Surface sampling for endotoxin assessment using electrostatic wiping cloths. Annals of Occupational Hygiene 2005;49(5):401-406. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Wan J, Diaz-Sanchez D. Phase II enzymes induction blocks the enhanced IgE production in B cells by diesel exhaust particles. Journal of Immunology 2006;177(5):3477-3483. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2005) |
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Wenten M, Berhane K, Rappaport EB, Avol E, Tsai WW, Gauderman WJ, McConnell R, Dubeau L, Gilliland FD. TNF-308 modifies the effect of second-hand smoke on respiratory illness-related school absences. American Journal of Respiratory and Critical Care Medicine 2005;172:1563-1568. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Whitekus MJ, Li N, Zhang M, Wang M, Horwitz MA, Nelson SK, Horwitz LD, Brechun N, Diaz-Sanchez D, Nel AE. Thiol antioxidants inhibit the adjuvant effects of aerosolized diesel exhaust particles in a murine model for ovalbumin sensitization. The Journal of Immunology 2002;168(5):2560-2567. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R826708C001 (Final) R826708C002 (Final) R827352 (Final) R827352C002 (Final) R831861 (2004) R831861 (2005) |
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Xie B, Gilliland FD, Li YF, Rockett HR. Effects of ethnicity, family income, and education on dietary intake among adolescents. Preventive Medicine 2003;36(1):30-40. |
R826708 (2000) R826708 (2001) R826708 (2002) R826708 (Final) R831861 (2004) R831861 (2005) |
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Allergens, Asthma, Biochemistry, Children's Health, Disease & Cumulative Effects, Ecological Risk Assessment, Human Health Risk Assessment, airway disease, airway inflammation, community-based intervention, environmental health, epidemiology, human exposure, endotoxin, California, Los Angeles. , Geographic Area, Scientific Discipline, Health, RFA, Risk Assessments, Health Risk Assessment, Epidemiology, Children's Health, Allergens/Asthma, State, California (CA), asthma indices, allergen, respiratory problems, respiratory disease, children's environmental health, asthmatic children, second hand smoke, cigarette smoke, childhood respiratory disease, human health risk, susceptibility, acute lung injury, air pollution, airborne pollutants, airway disease, children, tobacco smoke, exposure, children's vulnerablity, asthma triggers, allergic response, asthma, human exposure
Relevant Websites:
The link to University of Southern California is:
http://es.epa.gov/ncer/centers/cecehdpr/98/socal/
Progress and Final Reports:
2000 Progress Report
2001 Progress Report
Original Abstract
Final Report
Subprojects under this Center:
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R826708C001 Asthma in Children: A Community-based Intervention Project
R826708C002 Children's Exposure to Environmental Tobacco Smoke: Changes in Allergic Response
R826708C003 Respiratory Disease and Prevention Center