2007 Progress Report: Urban Air Pollution and Persistent Early Life Asthma

EPA Grant Number: R831861C001
Subproject: this is subproject number 001 , established and managed by the Center Director under grant R831861
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).

Center: USC Center for Children’s Environmental Health
Center Director: Gilliland, Frank D.
Title: Urban Air Pollution and Persistent Early Life Asthma
Investigators: Gilliland, Frank D.
Institution: University of Southern California
EPA Project Officer: Callan, Richard
Project Period: November 1, 2003 through October 31, 2008 (Extended to October 31, 2010)
Project Period Covered by this Report: November 1, 2006 through October 31, 2007
RFA: Centers for Children's Environmental Health and Disease Prevention Research (2003) RFA Text |  Recipients Lists
Research Category: Children's Health , Health Effects , Health

Objective:

The Community Based Participatory Research project will evaluate the relationship between early life asthma and traffic–related air pollution. We are examining this question in a case–control study of asthma persisting to school entry, but with onset earlier in life, in children resident in the same home since before age 2. We also hypothesize that susceptibility to ambient air pollution will vary based on genotype for GSTM1, GSTP1, NQO1, HO-1, and TNF-alpha, genes involved in the biologic response to oxidant air pollutants. Lifetime exposure will be assessed by calibrating home measurements to the extensive historical exposure assessment from a monitor in each community operating continuously during the lifetime of participants. Community participation in study promotion to participants and in data collection and interpretation is enhancing both the quality of Center research and of the environmental action plans for families of children with asthma in ongoing projects of the community partners. A steering committee representing university and community research partners, and policy makers, works closely with the Community Outreach and Translation Core to provide the scientific basis necessary for developing policy for the more widespread protection of children from the effects of air pollution. Specific aims include:

  1. Identify the population for the proposed case-control study
  2. Collect information from parents of participants to assess asthma, activity patterns, and risk factors for asthma, using a structured telephone interview, also to be administered by Community Study Liaisons;
  3. Assess the relationship between residential exposure to ambient traffic related air pollutants and asthma among cases and controls, using information from the Exposure Assessment and Modeling Core;
  4. Develop tools for assessment of traffic within 100 meters of homes with COTC Neighborhood Assessment Teams composed of community volunteers selected by community research partners;
  5. Genotype cases and controls for polymorphisms in GSTM1, GSTP1, HO-1, NQO1 and TNF, and assess how these polymorphisms modify the relationship between air pollutants and asthma;
  6. Assess the burden of asthma-related disease attributable to air pollution in all children living in two communities represented by the community partners, using results from this study and from existing literature;
  7. Develop a series of community forums with the COTC to discuss the public health burden of air pollution for asthma;
  8. Integrate new information on air pollution into the environmental action plans developed with families of children with asthma by all community health workers working in service programs of community partners;
  9. Foster discussion among partners through an active steering committee and through presentation of results at meetings of partner organizations;
  10. Participate with the COTC in seminars, community forums and in the critique of policy initiatives by providing the best scientific evidence available on air pollution and childhood asthma.

Progress Summary:

Questionnaire interviews have been completed in the asthma case-control study (with 75% participation). Extensive data clean-up has been required in the exposure data at the c-c locations, and this resulted in more time than anticipated for the modeling procedures (conducted by the exposure assessment and modeling core). However, prediction models explain 50% to almost 90% of the variation in NOx in all communities, and a ms is in preparation. Analysis of the c-c data is puzzling, as the exposure predicted from these models in the entire cohort is associated with asthma, but the conditional logistic analysis of measured exposure at homes of c-c is not. Analysis is ongoing to resolve this inconsistency. Genotyping has been completed and analyses of gene main effects are underway (to be followed by gene-air pollution analyses). A methods paper on the burden of disease in a CBPR partner community demonstrates that (conservatively) 8% of all childhood asthma in Long Beach can be attributed to local traffic exposure (see abstract citation below, ms in review). A more comprehensive childhood burden of air pollution paper is being developed covering both of our partner communities and multiple respiratory outcomes. We have worked closely with CBPR partners so that all participating are well versed in the new science developing from these efforts. All press releases on important papers are coordinated so that community partners are well prepared to comment on relevance to local air pollution and traffic issues. This has been quite successful, and the collaboration with scientists and community partners has resulted in the results having greater relevance for policy, as reflected in the COTC progress report, and in complementary grant funding focused on policy. Community partners have been trained to use a tool kit for evaluating near road exposure, as described in the COTC report. Efforts to obtain better data on traffic counts at schools continues to be a priority but has been challenging to realize.

In several complementary analyses, we have found associations with modeled traffic exposure and incident asthma in this cohort (see abstract citation below, ms in preparation). In a novel analysis, we have found that stress modifies the effect of traffic-modeled exposure and of in utero tobacco smoke exposure (ms in preparation), and preliminary results indicate that commuting time is associated with asthma. We have published results on the effect of wildfire exposures on asthma symptoms in several of our study communities, and we have found these effects to be modified by GSTM1 genotype, information that will be important for the further analysis of traffic related pollution effects. An important paper has been published demonstrating that the traffic exposure metrics developed in the Center are associated with lung function growth in an older cohort.

A relatively consistent pattern of association of traffic exposure with asthma developing in early life and incident asthma developing during school years across multiple cohorts is emerging.

Future Activities:

We plan to finalize case-control and burden of disease analyses, using results from the main analyses of asthma and air pollution. We will finalize genetic analyses. We will be working on a major community forum planned for year 5 by the COTC to highlight results from the Center.


Journal Articles on this Report : 6 Displayed | Download in RIS Format

Other subproject views: All 145 publications 93 publications in selected types All 92 journal articles
Other center views: All 195 publications 127 publications in selected types All 126 journal articles
Type Citation Sub Project Document Sources
Journal Article Gauderman WJ, Vora H, McConnell R, Berhane K, Gilliland F, Thomas D, Lurmann F, Avol E, Kunzli N, Jerrett M, Peters J. Effect of exposure to traffic on lung development from 10 to 18 years of age: a cohort study. Lancet 2007;369(9561):571-577. R831861 (2005)
R831861 (Final)
R831861C001 (2007)
R831861C001 (Final)
R831861C002 (Final)
R831861C003 (2007)
R831861C003 (Final)
R827352 (Final)
R827352C007 (Final)
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  • Journal Article Islam T, Gauderman WJ, Berhane K, McConnell R, Avol E, Peters JM, Gilliland FD. Relationship between air pollution, lung function and asthma in adolescents. Thorax 2007;62(11):957-963. R831861 (Final)
    R831861C001 (2007)
    R831861C001 (Final)
    R831861C002 (Final)
    R831861C003 (2007)
    R831861C003 (Final)
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  • Journal Article Islam T, McConnell R, Gauderman WJ, Avol E, Peters JM, Gilliland FD. Ozone, oxidant defense genes, and risk of asthma during adolescence. American Journal of Respiratory and Critical Care Medicine 2008;177(4):388-395. R831861 (Final)
    R831861C001 (2007)
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  • Journal Article Kunzli N, Perez L, Lurmann F, Hricko A, Penfold B, McConnell R. An attributable risk model for exposures assumed to cause both chronic disease and its exacerbations. Epidemiology 2008;19(2):179-185. R831861 (Final)
    R831861C001 (2007)
    R831861C001 (Final)
    R831861C002 (Final)
    R831861C003 (Final)
    R827352 (Final)
    R831845 (2005)
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  • Journal Article Molitor J, Jerrett M, Chang CC, Molitor NT, Gauderman J, Berhane K, McConnell R, Lurmann F, Wu J, Winer A, Thomas D. Assessing uncertainty in spatial exposure models for air pollution health effects assessment. Environmental Health Perspectives 2007;115(8):1147-1153. R831861 (Final)
    R831861C001 (2007)
    R831861C001 (Final)
    R831861C002 (Final)
    R831861C003 (Final)
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  • Journal Article Salam MT, Gauderman WJ, McConnell R, Lin PC, Gilliland FD. Transforming growth factor-β1 C-509T polymorphism, oxidant stress, and early-onset childhood asthma. American Journal of Respiratory and Critical Care Medicine 2007;176(12):1192-1199. R831861 (Final)
    R831861C001 (2007)
    R831861C001 (Final)
    R831861C002 (Final)
    R831861C003 (2007)
    R831861C003 (Final)
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  • Abstract: ATS Journals - Abstract
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  • Supplemental Keywords:

    RFA, Health, Scientific Discipline, Air, ENVIRONMENTAL MANAGEMENT, HUMAN HEALTH, Environmental Chemistry, Health Risk Assessment, mobile sources, Biochemistry, Environmental Monitoring, Health Effects, Children's Health, Risk Assessment, asthma, traffic, engine exhaust, community-based intervention, airway disease, respiratory problems, automotive emissions, automotive exhaust, Human Health Risk Assessment, susceptibility, childhood respiratory disease, ambient particle pollution, children's environmental health, outreach and education

    Progress and Final Reports:

    Original Abstract
  • 2004 Progress Report
  • 2005 Progress Report
  • 2006 Progress Report
  • 2008
  • 2009
  • Final Report

  • Main Center Abstract and Reports:

    R831861    USC Center for Children’s Environmental Health

    Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
    R831861C001 Urban Air Pollution and Persistent Early Life Asthma
    R831861C002 Pollution-Enhanced Allergic Inflammation and Phase II Enzymes
    R831861C003 Air Pollution, Exhaled Breath Markers, and Asthma in Susceptible Children