Grantee Research Project Results
2018 Progress Report: UC Berkeley/Stanford Children's Environmental Health Center
EPA Grant Number: R835435Center: Center for Integrative Research on Childhood Leukemia and the Environment - 2015
Center Director: Metayer, Catherine
Title: UC Berkeley/Stanford Children's Environmental Health Center
Investigators: Hammond, S. Katharine , Shaw, Gary M. , Balmes, John R.
Institution: University of California - Berkeley
EPA Project Officer: Hahn, Intaek
Project Period: July 1, 2013 through June 30, 2018 (Extended to June 30, 2019)
Project Period Covered by this Report: July 1, 2017 through June 30,2018
Project Amount: $4,765,843
RFA: Children's Environmental Health and Disease Prevention Research Centers (with NIEHS) (2012) RFA Text | Recipients Lists
Research Category: Children's Health , Human Health
Objective:
The Children’s Health and Air Pollution Study (CHAPS) is a direct descendant of the University of California, Berkeley/Stanford Children’s Environmental Health Pre-Center with the same name. CHAPS has expanded to include research colleagues from California State University, Fresno and UCSF-Fresno. CHAPS is innovative in terms of the scientific focus, exposure assessment and methods of data analysis. We have four research projects and four cores, listed below with the leads for each:
Project 1: Exposures to Air Pollutants, Modifying Genes, and Risk of Birth Defects and Preterm Birth, John Balmes, M.D.
Objectives are to:
(1) Determine whether exposures to specific air pollutants (identified in our P20 research) are further modified by gene variants in biotransformation enzymes (e.g., NATs, GSTs, CYPH, or NOS3) for risk of selected birth defects.
(2) Determine whether ambient exposures to polycyclic aromatic hydrocarbons (PAHs), during critical periods of organogenesis, are associated with women delivering infants/fetuses with birth defects, and whether relationships are further modified by gene variants in Aim 1.
(3) Determine whether ambient exposures to PAHs, during critical periods of gestation, are associated with women delivering preterm.
(4) Determine whether the built environment is associated with preterm birth either directly or indirectly through a joint effect with ambient air pollution.
Project 2: Mechanisms of Polycyclic Aromatic Hydrocarbon-linked Immunopathogenesis in Atopy. Kari Nadeau, M.D.
Objectives: Our overall objective is to determine the molecular mechanisms by which immune dysregulation leads to human disease, specifically the atopic diseases of food allergy, allergic rhinitis, allergic conjunctivitis and allergic asthma in the children exposed to high levels of polycyclic aromatic hydrocarbons (PAHs). Our approach is to perform a cross-sectional analysis in a well defined “piece-wise” continuum of all pediatric ages in immune development: infant cohort (0-2 yrs), young children (7-9 yrs), older children (16-19 yrs), and older adolescents (19-21 yrs) from whom blood, urine and buccal samples will be collected along with detailed information on human disease. Using novel and innovative immunological studies, we will be able to determine key time points of sensitivity of the immune system to PAH exposure by defining the molecular mechanisms that play a role in immune system impairment during immune development.
Project 3: Obesity/Glucose Dysregulation and Air Pollution. John Balmes, M.D.
Objectives: The overarching goal of the Obesity/Glucose Dysregulation (OGD) project is to assess whether exposure to outdoor air pollution during childhood contributes to the development of metabolic syndrome later in life. The specific research-based goals of the peer-reviewed application are the following:
Aim 1: To determine whether oxidative stress and systemic inflammation induced by exposure to ambient air pollutants contributes to abnormal fat and glucose metabolism. We will assess whether chronic exposure to ambient air pollution (AAP), especially polycyclic aromatic hydrocarbons (PAHs), is associated with:
- increased HbA1c;
- increased BMI (ponderal index for infants);
- increased levels of 8-isoprostane (biomarker of oxidative stress), CRP (biomarker of systemic inflammation), leptin, adiponectin, and high-density lipoprotein (biomarkers of abnormal fat and glucose metabolism).
Aim 2: To determine whether air pollution-induced dysfunction of Treg and Teff contributes to the pathogenesis of impaired glucose regulation and obesity. We will assess whether chronic exposure to AAP-induced Treg and Teff dysfunction is associated with:
- increased HbA1c,
- increased BMI (ponderal index for infants).
Aim 3: To determine whether epigenetic modification of Foxp3 underlies the associations between Treg dysfunction and abnormal glucose regulation and increased BMI.
Project 4: Transit Exposures in-utero. S. Katharine Hammond, Ph.D., John Capitman, Ph.D.
Objectives: The objective of this project is to test the hypothesis that neighborhood characteristics have a direct and quantifiable relationship with an individual’s transit patterns that in turn affect personal exposures to traffic related air pollution (PAHs, PM2.5, and BC). The aims of this project are as follows:
- Aim 1: Define neighborhoods within Fresno by using both secondary and primary data to characterize assets (e.g., bus stops/routes, sidewalks, food outlets, etc.) and liabilities (e.g., neighborhood foreclosure rate, density of condemned properties, Toxic Release Inventory sites, high speed surface street traffic, etc.) of the local built environment.
- Aim 2: Estimate the indirect effects of neighborhood assets and liabilities on ambient air pollution by first assessing the impact of the built environment on transit use and then the impact of transit use on simulated personal exposures to PAHs, PM2.5, and BC.
- Aim 3: Evaluate environmental exposures by different transit methods by measuring PM2.5, ultrafine particles, BC, and particle bound PAHs in 10 neighborhoods in Fresno California.
- Aim 4: Evaluate what changes to neighborhood characteristics (i.e., interventions) would have the greatest potential to reduce transit-related exposures to PAHs, PM2.5, and BC in the population as a whole and in subgroups defined by geographic neighborhoods.
Administrative Core: S. Katharine Hammond, Ph.D.
This core provides administrative support for all of CHAPS. This includes the Fresno field office for Projects 2 and 3, the children’s health specialist and junior faculty development. In addition, this core is where we report our retreats and External Advisory Committee meetings.
Community Outreach & Translation Core: Jennifer Mann, Ph.D.
The primary objectives of the COTC are to develop and meet regularly with our Community Advisory Board and the larger stakeholder network, develop materials that explain CHAPS, and explain the results to residents, advocates and policymakers in the San Joaquin valley; work with youth to understand air quality and related health outcomes, and to build capacity of community residents to understand air quality and environmental health hazards in partnership with stakeholders in the San Joaquin Valley.
Biostatistics/Epidemiology Core: Ellen Eisen, Sc.D., Sadie Costello, Ph.D.
The Epidemiolgy/Biostatistics Core (1) provides data management and quality assurance of collected data, (2) develops structural analytic frameworks for each project with Directional Acyclic Graphs (DAGs) and (3) assists all members of the project team with their statistical analyses. They also identify methodologic challenges and develop statistical approaches to address them. This core is also where all questionnaires and study instruments are developed. A data team in this core trains interviewers and phlembotomists in the field office
Exposure Core: S. Katharine Hammond, Ph.D., Fred Lurmann
The primary goal of the Exposure Core is to assign individual exposures for relevant time-windows, from in utero to the time of last sample collection, for subjects in all four research projects. To do so, the core evaluates existing data, collects additional monitoring data and develops sophisticated models to assign weekly exposures to each study participant for criteria pollutants, as well as polycyclic aromatic hydrocarbons (PAH) and elemental carbon.
NOTE: Both projects 2 and 3 share three cohorts recruited at UCSF Fresno as part of the piece-wise cohort design. The cohorts are from three different age groups. The cohorts are:
Infants – the pregnant woman is baselined at ~20 weeks of pregnancy. Cord blood is collected at delivery. The infants are observed when they are 12- and 24-months. Pregnant women are recruited through OB/Gyn clinics throughout Fresno and Clovis. (220 pregnant women)
Young children – children ages 6 to 8 years old who attend public school in Fresno Unified School District. Schools are ranked by traffic density. Two elementary schools were randomly selected a month at a time – one each from the upper and lower quartiles of traffic density. Children are also seen 2 years after baseline (299 young children).
Adolescents/Young Adults – all recruited during our pre-Center which was the first visit of this cohort, about 2 years earlier. They will only be seen one time as part of this study. (Goal=100 adolescent/young adults).
Progress Summary:
Project 1: Exposures to Air Pollutants, Modifying Genes, and Risk of Birth Defects and Preterm Birth
(1) To determine whether exposures to specific air pollutants (identified in our P20 research) are further modified by gene variants in biotransformation enzymes (e.g., NATs, GSTs, CYPH, or NOS3) for risk of selected birth defects.
For this goal, we identified ~1400 samples buccal cells (mother and infant) and bloodspots (infants only) from available birth defect cases and controls. Those samples have had the DNA extracted and genotyping for a broad panel of biotransformation enzymes has been completed. Epidemiologic analyses on this large amount of data have begun. We have a draft manuscript that has interrogated these approximately 100 single nucleotide polymorphisms in conjunction with several air pollutant exposures for combinatorial risk on the birth defect, spina bifida. As a summary, in our previous study of air pollution exposures during the first two months of pregnancy, we found associations between high levels of CO and NO2 and risk of spina bifida (ORCO = 2.00, 95% CI: 1.06, 3.75; ORNO2 = 1.73, 95% CI: 1.01, 2.97). This newest work extends those findings and demonstrates a gene-environment interaction between each of the five criteria pollutants and several gene variants: NO (ABCC2), NO2 (ABCC2, SLC01B1), PM10 (ABCC2, CYP1A1, CYP2B6, CYP2C19, CYP2D6, NAT2, SLC01B1, SLC01B3), PM2.5 (CYP1A1 and CYP1A2). We view this investigation as exploratory even though some results showed sizable odds ratios (>4) and 95% confidence intervals excluding 1. Such caution seems prudent owing to sample sizes being relatively small, numerous comparisons being made, and a paucity of previous studies to corroborate these findings. This first paper from these rich data was published May 2018.
Our work on this goal is on schedule.
(2) To determine whether ambient exposures to polycyclic aromatic hydrocarbons (PAHs), during critical periods of organogenesis, are associated with women delivering infants/fetuses with birth defects, and whether relationships are further modified by gene variants in Aim 1.
We have geocoded all cases and controls and as indicated above have completed all of the genotyping. We are investigating whether the original targeted geographic area of study (Fresno only) where we could assign PAH exposure can be expanded to the additional surrounding areas and therefore include additional cases and controls for investigation. Our analytic work on this goal is in progress.
(3) To determine whether ambient exposures to PAHs, during critical periods of gestation, are associated with women delivering preterm.
We have published the results of this aim in Environmental Research. (Padula AM, Noth EM, Hammond SK, Lurmann FW, Yang W, Tager IB, Shaw GM. Exposure to airborne polycyclic aromatic hydrocarbons during pregnancy and risk of preterm birth. Environ Res. 2014 Nov;135:221-6. PubMed PMID: 25282280; PubMed Central PMCID: PMC4262545.) We applied the PAH exposure model to the study population within 20km of the central site in Fresno, CA. We analyzed the relationship between PAH during several periods during pregnancy (entire pregnancy, each trimester and last 6 weeks) with categories of gestational age at birth to determine the association between PAH and levels of preterm birth. We found associations between PAH during the last 6 weeks of pregnancy and birth at 20-27 weeks (OR=2.74; 95% CI: 2.24-3.34) comparing the highest quartile to the lower three quartiles. When examined for an exposure-response, the association increased across each quartile of PAH exposure. Inverse associations were also observed for exposure to PAH during the entire pregnancy and the first trimester and birth at 28-31 weeks and 20-27 weeks. We have completed this goal.
(4) To determine whether the built environment is associated with preterm birth either directly or indirectly through a joint effect with ambient air pollution.
We furthered analyses on the effects of neighborhood factors and air pollution on preterm birth using causal inference methods (i.e., targeted maximum likelihood estimation). The effects of air pollution appear to be stronger in neighborhoods with greater deprivation. Our work on a manuscript continues.
Project 2: Mechanisms of Polycyclic Aromatic Hydrocarbon-linked Immunopathogenesis in Atopy
Aim 1: Determine the extent to which Treg functional impairment in children with asthma vs. without asthma is associated with high levels of PAH cumulative exposure.
We showed that higher average PAH exposure was significantly associated with impaired regulatory T cell (Treg) function conditional on atopic status, suggesting that increased ambient PAH exposure is associated with impaired systemic immunity. In addition, the magnitude of the association increased as the length of the time-window of PAH exposure increased for both asthmatic and non-asthmatic subjects.
Aim 2: Determine the degree to which ambient PAH exposure alters Treg immunophenotypes leading to polarization of conventional CD4+ T cells towards a Th2 phenotype in children with asthma vs. without asthma.
We used mass cytometry simultaneously to analyze a large number of immune cell phenotypes and cytokines, and determined whether there were differences between non-asthmatic and healthy subjects from low- vs. high-polluted areas (LPE vs. HPE). We found distinct immunophenotypes in asthmatic subjects exposed to HPE compared to those with LPE. Significant decreases in “classical” monocytes, B cells, and the cytokines interferon-γ and TNFα, along with increases in “alternative” monocytes and activated CD4+ T cells, were associated in asthmatics with HPE, while only a reduction in CD8+ T effector cells were detected in healthy individuals with HPE. Overall, the data suggest that in healthy individuals, HPE could begin to skew the immune system towards atopy and diminished immunity. However, in those with underlying asthma, HPE could significantly worsen innate and adaptive immune responses leading to further pathogenesis and exacerbation of disease. We also identified various T cell subsets (Th1, Th2, Treg, Th17) and are currently investigating the association between T helper cell types and ambient air pollution (AAP) exposure.
Aim 3: Determine whether individual PAH exposures (short-term vs. long-term) are associated with increased DNA methylation of the FOXP3 genetic locus in Treg.
We have found that FOXP3 methylation is associated with asthma status in the promoter region, but not in the enhancer region, of FOXP3. We first found that increased PAH was associated with increased FOXP3 methylation. We then investigated other pollutants, such as O3, CO, NO2 and PM2.5, and their association with methylation, and found that the strongest association of pollution with FOXP3 methylation is for 90 days post-exposure. Finally, we examined whether the methylation levels are sustained over time by comparing percentage levels across at least a 2-year time span, and found that these methylation patterns were sustained across subjects.
Collectively, these results will demonstrate the detrimental impact of AAP on the immune system throughout development, and the role of air pollution exposure in allergic disease. Our overall objective is to determine the molecular mechanisms by which immune dysregulation leads to human disease, specifically the atopic diseases of food allergy, allergic rhinitis, allergic conjunctivitis and allergic asthma in the children exposed to high levels of ambient air pollutants. It is also our goal to use the research findings to help guide public policy to regulate air pollution levels.
Project 3: Obesity/Glucose Dysregulation and Air Pollution
This project shares three cohorts with Project 2. All three cohorts are now fully enrolled. As of this year, we have started all planned follow-up visits (visits of infants when they are 12- and 24-month, visits of young children two years after their baseline visit). All visits of the Adolescent/Young adult cohort were completed in 2014. See the administrative core for more details.
For the child cohort, to date, we have analyzed leptin (n=271), adiponectin (n=276), HbA1c (n = 275), C-reactive protein (n = 139), HDL (n=138) and 8-isoprostane (n = 290) samples at their baseline visit (6-8 years old). We have analyzed HbA1c (n = 133), C-reactive protein (n = 134), and HDL (n = 132) samples for children at their 2-year post-baseline follow-up visit (8-10 years old).
For the infant/toddler cohort, to date, we have analyzed HbA1c (n=22), C-reactive protein (n=20), and HDL (n=19) samples at their baseline visit (12-months old). We have analyzed HbA1c (n=34), C-reactive protein (n=30), and HDL (n=31) samples for children at their 1-year post-baseline follow-up visit (24-months old).
We have calculated BMI-percentile for 299 children and percent body fat for 297 children at their baseline (7-year old) visit. We have calculated BMI-percentile for 158 infants at their baseline (12-month old) visit and determined BMI category for all 100 AYA participants at baseline.
Project 4: Transit Exposures in utero
We developed a tool to assess neighborhood indicators of social and structural context that was adapted from Sampson and Raudenbush’s (1999) structured social observations (SSO) made in Chicago. Our 51-item assessment tool was designed to capture social order, social disorder, institutional order, and institutional disorder. Students and research assistants walked Fresno neighborhoods on a block-by-block basis to implement our structured social observation tool. In terms of preliminary results, we performed exploratory factor analysis (EFA) to develop factors accounting for the most variability across the items. Four factors were retained in this process: “abandoned commercial property,” “business sector,” “walkable infrastructure,” and “social disorder.” These four factors were tested for reliability using Cronbach’s alpha and we examined the effects of item-deletion from each factor to establish items that contributed most to each factor. These four factors were also aggregated to census tract (n = 58) and zip code level (n = 22) estimates in order to be examined for any association with health outcomes, secondary measures of social vulnerability such as poverty, and measures of the built environment such as the Walk Score® using Pearson’s r. The health outcomes of interest included: rates of asthma hospitalizations, premature birth, and measures of longevity. Results to date suggest we can make reliable measures of neighborhood assets and liabilities that may be linked to walking, transit use, and other behaviors associated with pollution exposure. We also found considerable variability across zip codes in these measures, which is consistent with applications of the SSO approach in other areas. These findings will assist in determining the changes that can be made to the built environment. In addition, data were collected from students who participated in the data collection process. Each student was surveyed on knowledge of health and neighborhood inequities, perception of the value of research, research skills, and on their confidence to conduct competent research. Students were surveyed prior to conducting research and then follow-up after the research was complete. Our results indicate that students who participated in the research experience tended to shift their views on accountability for health inequities from the individual to an environmental view, in comparison to students who did not participate in the research experience.
A primary aim of this study was to develop measures of social and institutional order. New analyses show the items that significantly loaded onto the constructs of social order and institutional order, respectively. We compared social and institutional order by secondary measures of the CalEnviroScreen, Regional Opportunity Index, transit behavors to work, and structural transit opportunities with Pearson’s r. Social order was negatively associated with the walk score, public transportation use, transit score and population characteristics score and positively associated with regional opportunity indicators. Institutional order was positively associated with driving alone to work and all of the regional opportunity people and place indicators. We examined counts of transportation patterns to work including public transportation and drove alone. Adjusting for many covariates social order was significant and negatively associated with public transportation to work and was positively associated with driving to work alone. Similarly, institutional order was significant and negatively associated with the use of public transportation and positively associated with driving alone to work.
Neighborhood exposure concentrations to multiple air pollutants are being characterized by real-time mobile monitoring that also collect the time-location data for proximity to traffic emission by GPS track loggers. The real time concentration of PM2.5, ultrafine particle number concentrations, BC, and particle-bound PAHs were continuously and simultaneously measured at 150 routes from 22 zip code areas. Preliminary results of neighborhood air pollution data show that PM2.5 and PAHs were significantly higher in neighborhood walking air samples compared to indoor air or Garland data. The simultaneous measurements in two neighborhoods which are distinctively different areas (High diesel High poverty vs. Low diesel Low poverty) showed that the higher pollution levels were observed when more frequent vehicular activities were around the neighborhoods.
Administrative Core
Meetings The CHAPS team continued to hold bi-weekly meetings. The three PIs also met separately on a weekly or biweekly basis and as needed. In July, 2016, the CHAPS team had a site visit with our USEPA Project Officer, Nica Louie. Two full-day meetings were held; one at Fresno State, and a second at UC Berkeley. In September, 2016, the CHAPS team met with the External Advisory Committee in Berkeley, CA.
Field Office/Data Collection (by cohort)
Adolescent/Young Adult Cohort: In 2014, we completed enrollment of 100 participants into the adolescent/young adult (AYA) cohort; all of the AYA participants were part of the P20 Immunology project and this represented the 2nd or 3rd CHAPS visit for each of these participants. Originally, we planned to recruit 100 additional participants. Data collection for this cohort has been completed.
Infant Cohort: We completed enrollment of pregnant women (18-25 weeks of pregnancy, n = 220) into the Infant cohort. As of June 30, 2018, there have been 159 follow-up visits of infants who are 12-months old (10 of these belong to 5 sets of twins, so these 159 visits represent follow-up visits for 154 mothers). Follow-up visits of toddlers who are 24-months old were started at the very end of Year 5 and we have been making good progress with these visits. As of June 30, 2018, there have been 91 followup visits of the 24-month olds (8 of these belong to 4 sets of twins, so these 91 visits represent followup for 87 mothers). Of the 91 toddlers who came in at 24 months, 12 were actually who were unable to come in for their 12-month visits, but, by maintaining contact with them, we were successfully able to bring them back in as toddlers.
Child Cohort: We recruited 299 children aged 6 to 8 who attended a school in Fresno Unified School District and their parents into the Child Cohort. The 2-year followup visits for the Child Cohort started in late June 2017 and by June 30, 2018 we had seen 151 subjects of our Child Cohort for their 2-year followup visit.
Children’s Health Specialist, John Balmes, M.D., In addition to leading the Center Project on Obesity and Glucose Dysregulation, Dr. Balmes has coordinated activities with the Pediatric Environmental Health Specialty Unit (PEHSU) at UCSF, of which he is the Principal Investigator, served as the Physician Member of the California Air Resources Board (CARB), and collaborated with the two other Children’s Environmental Health Centers (CERCH, a former center that continues to be very active through other research support mechanisms, and CIRCLE, a current center) that are housed at UC Berkeley during the reporting period. Dr. Balmes collaborated with Dr. Miller in the latter’s role as the Children’s Health Specialist for CIRCLE. With the CERCH PI, Dr. Brenda Eskenazi, and co-investigators Drs. Bradman and Kim Harley, Dr. Balmes has been collaborating on research projects to assess the respiratory health impacts of organophosphate pesticides, agricultural fumigants, and triclosan. Two publications have resulted from this collaboration. In his role as Physician Member of CARB, Dr. Balmes continues to stress the importance of policy efforts to reduce exposure of children to air pollution, such as pushing for health co-benefits with climate change mitigation strategies, and he regularly briefs both the CHAPS investigators and the Community Advisory Board on the activities of CARB. One of the most important of these current activities is the implementation of a recent California legislation, “AB-617 Nonvehicular air pollution: criteria air pollutants and toxic air contaminants,” which is considered a new frontier in air quality management.
Career development of Faculty Development Investigator and other creative junior faculty-level investigators: During this year, junior faculty from UC Berkeley, Stanford and Fresno State have done the following:
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Junior investigators have been included as full participants in biweekly center meetings, where they regularly present their research and actively participate in the discussions.
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Two junior investigators have been offered and have accepted tenure track faculty positions at other universities. They join the ranks of our other two junior investigators who had already achieved this distinction (Dr. Amanda Northcross at George Washington University and Dr. Amy Padula at UCSF).
- Dr. Sa Liu was offered and accepted a tenure-track faculty position (Assistant Professor) at Purdue University
- Dr. Neophytou was offered and accepted a tenure-track faculty position (Assistant Professor) at University of Colorado, Fort Collins.
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The junior investigators developed and submitted multiple grant proposals building on the CHAPS cohorts, exposure data, or methodologies; two of these were funded.
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Dr. Neophytou was awarded a K99 by NIEHS titled “Air pollution exposures and children’s health: mediation and interaction in a counterfactual framework,” which uses CHAPS center data.
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Dr. Noth was awarded a contract with the California Office of Environmental Health Hazard Assessment, “Pilot Air Quality Study for East Bay Diesel Exposure Project” to expand her work on polycyclic aromatic hydrocarbon monitoring in Richmond, using methodologies developed in this center.
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Dr. Noth developed and submitted an R01 grant proposal to NIEHS in June 2018 with the title “Exposure to air pollution and children's neurodevelopment in the CHAPS cohorts.” Co-Investigators included CHAPS members Mr. Lurmann, and Dr. Hammond, and Drs. Gunier and Sagiv from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) Study.
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Dr. Kwon has been a very active participant in a Community Advisory Board-initiated project on improving Environmental Public Health Literacy (with an emphasis on air pollution) among children’s advocates in the San Joaquin Valley.
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Dr. Kwon taught students from CART about portable air pollution monitors for a spring project on neighborhood characteristics and air pollution exposures.
Community Outreach & Translation Core
COTC Highlights:
Website/social media
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In October 2017, the CHAPS website (https://www.chapssjv.org/) was completely redesigned. It now features links to all publications associated with CHAPS and various pages that outline the structure and aims of the study.
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From March to May 2018, CHAPS’s Facebook page and Twitter account were updated 2-3 times a week from with information about various children’s health topics. The content for these posts, which were part of the Children's Environmental Health Toolkit featuring the #ProtectKidsHealth hashtag, was developed by the Children's Environmental Health Centers' Social Media Workgroup on the basis of the Children’s Environmental Health Impact report.
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Highlight of Transit Exposures in-utero project in Fresno State Magazine published in July 2017: http://www.fresnostate.edu/magazine/a-peek-inside-the-campus-labs/
Youth Mentoring Field Projects
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CHAPS worked with Center for Advanced Research and Technology (CART) teachers to mentor students on field research projects for the Environmental Sciences and Field Research track of CART for Spring 2018. Drs. Kwon and Zografos worked as project mentors to CART students during the Spring 2018 semester. Dr. Hammond worked with the groups at their first meeting, in February. Dr. Zografos worked with students to conduct structured social observations in various neighborhoods. These observations included assets, i.e., safe places to walk; green spaces; well-maintained yards, etc. and liabilities, i.e., graffiti; crowded streets; poorly maintained yards, etc. Dr. Kwon monitored local air quality using electronic particulate matter sensors in these same areas. Drs. Kwon and Zografos also assisted the students in preparing their final presentations, which were presented to faculty, staff, and families on May 15, 2018. Dr. Balmes attended the student presentations.
Fresno State Outreach Activities
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Two educational/outreach sessions were conducted during the July 2017 – June 2018 time period. The first educational sessions was conducted with five participants from the Fresno County Pre-Term Birth Initiative on April 17, 2018. Results from Project 4 on the structured social observation (SSO) data collection and relationships between neighborhood order and transportation use were shared. Participants engaged with graduate students from the Masters of Public Health program to discuss how these findings fit with their understanding of the factors that contribute to a healthy neighborhood for having and raising children. The outreach session was part of their course requirement in PH 225B (Foundations of Health Promotion II) course. The educational meeting was conducted with four participants from the Fresno County Black Infant Health program on June 13, 2018. Two research assistants from the Central Valley Health Policy Institute (CVHPI) helped to facilitate this process.
COTC Co-Sponsored Symposia
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November 30, 2017 COTC co-sponsored a symposium on Air Pollution’s Impacts on Allergies and Asthma – Current Advances, with the Family Allergy and Asthma Clinic held at UCSF-Fresno. Drs. Kari Nadeau and John Balmes gave presentations about CHAPS results. Emceed by Sarah Sharpe, COTC Communication and Outreach Director.
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San Joaquin Valley Asthma, Air Pollution & Health Symposium: November 30, 2016 COTC co-hosted in collaboration with Central California Asthma Collaborative held at Valley Children’s Hospital with over 60 participants including healthcare professionals and community-based organization representatives. Dr. Balmes was the keynote speaker at the event.
Biostatistics/Epidemiology Core
At the External Advisory committee held in September, 2016, we discussed recruitment challenges for the adolescent/young adult cohort and descriptive comparisons of the three cohorts. As a result of that discussion and internal CHAPS team discussions, we increased the recruitment goal for children to 320 from 220. We reduced the number of adolescents/young adults to 100. In May, 2017, we decided to limit the number of children to the 299 that had been baselined by that point.
We have completed all baseline visits for each of our three cohorts: 100 adolescent/young adults, 220 pregnant women, and 299 young children have completed a baseline evaluation. This includes the collection of blood, urine and buccal specimens, completion of a questionnaire, and relevant anthropometry. In addition, 52 cord bloods have been collected. Collection of cord blood has been a challenge, despite several attempts at re-training and reminding labor/delivery nurses and residents.
The AYA cohort had only one visit during the P01. No additional visits were planned since they were all participants of our pilot center.
During Year 4, we have worked hard on retention of the child and infant cohorts and their follow-up visits. We have seen 159 12-month old infants, as well as 91 24-month old toddlers and 151 children during their 2-year follow-up visit. All of these follow-up visits have included the collection of blood, urine (for child visits) and buccal specimens, completion of a questionnaire, and relevant anthropometry.
The 24-month questionnaire had new questions related to dietary intake and also questions pertaining to maternal use of e-cigarettes during pregnancy. The 8-10 year old questionnaire also had several new sections, including an assessment of smoking, pubertal development and psychosocial stress questions addressed to both the parent of the subject and to the subject themselves.
We developed an overarching DAG for center-level (integrated) key hypotheses. This DAG helps unite the different projects and cores and underscores the overarching biological hypothesis of molecular inflammation as central to all of our research questions. Molecular inflammation is the process by which air pollution leads to poorer birth outcomes (project 1) and obesity/dysregulation outcomes (project 3). Socioeconomic status variables, as measured in project 4 and by questionnaire, could influence air pollution exposure (exposure core) and have independent effects on methylation (project 2) and obesity/dysregulation outcomes (project 3). Air pollution can also have independent effects on methylation and obesity/dysregulation outcomes. And, lastly, methylation can lead to changes in obesity/dysregulation outcomes.
We continue to work with project investigators to construct directed acyclic graphs (DAGs) as needed to reflect the underlying assumptions and key hypotheses for each analysis. We worked closely with investigators in Projects 2 and 3 to provide support in their analysis.
Exposure Core
Substantial progress was made towards achieving the Exposure Core’s specific aims. The specific aims remain unchanged from our original plan. The two main activities in Year 5 were air monitoring and application of data and models to assign exposures to the CHAPS cohorts. The Exposure Core achieved the Year 5 accomplishments envisioned in our original project plan.
Ambient air monitoring data collections continued with continuous and speciated PAHs, black carbon, and brown carbon measurements at the central site in Fresno. These data extend one of the longest records of PAH air quality in an urban area and are being used to in paper on PAH air quality trends and probable sources in the San Joaquin Valley. The large decrease in PAH and black and brown carbon from 2001 to 2017 is a major success story for California’s air pollution control policies. The evidence suggests that reductions in biomass burning are one of the largest contributors to the improved PAH air quality in this area.
Individual daily exposures to PAH, BC, O3, NO2, NO, CO, PM2.5, and PM10 were assigned using the spatiotemporal models developed in Years 3 and 4 for all the cohorts. In the model for the greater Fresno area, the PAH metric represented lumped 4-, 5-,and 6-ring PAH compounds, and in the model for the broader San Joaquin Valley, the PAH metric represented the particle-phase PAH measured by the EcoChem PAS2000 instrument (which are closely related). The models of the greater Fresno area were used along with the geocoded residential histories and relevant covariates to estimate daily exposures for subjects in Projects 2 and 3 in the 2014-2017 time period. The models for the broader San Joaquin Valley were used to assign daily exposure assignments for PAH, O3, NO2, NO, CO, PM2.5, and PM10 from 3 months before conception to birth for the Project 1 subjects in the original cohort (1997-2007) and second cohort (1999-2011) based on their geocoded locations.
Future Activities:
Project 1: Exposures to Air Pollutants, Modifying Genes, and Risk of Birth Defects and Preterm Birth
(1) To determine whether exposures to specific air pollutants (identified in our P20 research) are further modified by gene variants in biotransformation enzymes (e.g., NATs, GSTs, CYPH, or NOS3) for risk of selected birth defects.
We will continue to analyze the interaction of air pollution and gene variants with regard to birth defects. We hope to have two manuscripts drafted in the next period.
(2) To determine whether ambient exposures to polycyclic aromatic hydrocarbons (PAHs), during critical periods of organogenesis, are associated with women delivering infants/fetuses with birth defects, and whether relationships are further modified by gene variants in Aim 1.
We plan to conduct analyses of the relationship between PAH and selected birth defects.
(3) To determine whether ambient exposures to PAHs, during critical periods of gestation, are associated with women delivering preterm.
Work on goal has been completed.
(4) To determine whether the built environment is associated with preterm birth either directly or indirectly through a joint effect with ambient air pollution.
We will continue to evaluate data we have on neighborhood deprivation and apply causal inference methods. We will also incorporate additional data on the built environment provided from Project 4.
Project 2: Mechanisms of Polycyclic Aromatic Hydrocarbon-linked Immunopathogenesis in Atopy
Subject recruitment will continue for the child cohort, 12-mo infant, 24-mo infant, and child cohort follow-up visits (two years after baseline). Data analysis and manuscript writing will also continue.
Project 3: Obesity/Glucose Dysregulation and Air Pollution
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We will continue to collect cord blood as pregnant women deliver their babies. We will continue visits of 24-month old infants and 9-year old children.
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Head circumference measurements, along with length/height and weight in the 24-month infants will be used to determine bmi-percentile of each of our infants at each follow-up visit.
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As noted above, one publication has been prepared that reports associations of traffic-related air pollution (TRAP) with OGD outcomes including adipokines, 8-isoprostane (marker of oxidative stress) and risk factors for metabolic syndrome (BMI-percentile, HbA1c, and blood pressure). The second publication involves characterization of participants as metabolically “healthy” or “unhealthy” using anthropometry data collected as part of the project and analysis of the relationship of long-term exposure to air pollution with metabolic health.
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Dr. Balmes presented preliminary results for these papers at the 2nd International Conference on Obesity and Chronic Diseases in San Francisco in July, 2017 and some of the final results of the completed TRAP-OGD outcome analysis at a UCSF conference on “The Exposome and Metabolism” in San Francisco in September 2018.
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We will continue to share all results with our Community Advisory Board. In coordination with the Community Outreach & Translation Core, we will produce fact sheets when analyses are complete.
Project 4: Transit Exposures in-utero
During the summer and early fall of 2018, we completed matching of SSO data at the census tracts with most cases in the mother/child cohort. We have begun analyses to see if our findings about social order and transportation use at the census tract level are confirmed at the individual level. We will also explore how SSO measures are related to the broad set of maternal psychological and social wellbeing indicators that will become available from follow-up surveys. We will conduct additional community conversations understanding how pregnant women and others can use findings from Project 4 and other CHAPS results to improve pregnancy experiences.
Biostatistics/Epidemiology Core
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During data collection in Year 6 (for the 9-year olds and the 24-month olds), we will perform ongoing, continuous data quality checks to identify and remedy any issues.
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In Year 6, we plan to release data across all 3 cohorts
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Although data on the 100 AYA subjects was originally released in Year 3 of the grant, we plan to release an updated data file with extended exposure data for these subjects in Year 6.
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Although data on all 299 child baseline visits was released in Year 5, we plan to release an update data file on these subjects with additional exposure data and CYTOF results for all subjects.
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Although data on the 220 pregnant women was originally released in Year 5 of the grant, we plan to release an updated data file with CYTOF data and exposure data for all 220 subjects in Year 6 (currently exposures are available only for 186 pregnant women).
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Exposure Core
The Exposure Core plans for Year 6 include operation of the PAH and carbon monitors at the Garland air monitoring site, generation of exposure assignments for more recent and earlier time periods for Projects 2 and 3 cohorts, and preparation of manuscripts. The sampling and laboratory analysis for speciated PAH will not be continued in the next reporting period.
Journal Articles: 44 Displayed | Download in RIS Format
Other center views: | All 126 publications | 45 publications in selected types | All 44 journal articles |
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Alcala E, Cisneros R, Capitman JA. Health care access, concentrated poverty, and pediatric asthma hospital care use in California's San Joaquin Valley: a multilevel approach. Journal of Asthma 2017:1-9. |
R835435 (2018) R835435 (Final) |
Exit Exit |
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Alcala E, Brown P, Capitman JA, Gonzalez M, Cisneros R. Cumulative impact of environmental pollution and population vulnerability on pediatric asthma hospitalizations:a multilevel analysis of CalEnviroScreen. International Journal of Environmental Research and Public Health. 2019;16(15):2683.. |
R835435 (Final) |
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Alderete TL, Jones RB, Chen Z, Kim JS, Habre R, Lurmann F, Gilliland FD, Goran MI. Exposure to traffic-related air pollution and the composition of the gut microbiota in overweight and obese adolescents. Environmental Research 2018;161:472-478. |
R835435 (Final) R835441 (2018) |
Exit Exit Exit |
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Cossi M, Zuta S, Padula AM, Gould JB, Stevenson DK, Shaw GM. Role of infant sex in the association between air pollution and preterm birth. Annals of Epidemiology 2015;25(11):874-876. |
R835435 (2015) R835435 (2016) R835435 (2018) R835435 (Final) |
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Gou P, Chang X, Ye Z, Yao Y, Nguyen PK, Hammond SK, Wang J, Liu S. A pilot study comparing T-regulatory cell function among healthy children in different areas of Gansu, China. Environmental Science and Pollution Research 2017;24(28):22579-22586. |
R835435 (Final) |
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Hew KM, Walker AI, Kohli A, Garcia M, Syed A, McDonald-Hyman C, Noth EM, Mann JK, Pratt B, Balmes J, Hammond SK, Eisen EA, Nadeau KC. Childhood exposure to ambient polycyclic aromatic hydrocarbons is linked to epigenetic modifications and impaired systemic immunity in T cells. Clinical & Experimental Allergy 2015;45(1):238-248. |
R835435 (2014) R835435 (2015) R835435 (2016) R835435 (Final) R834596 (2012) R834596 (Final) R834596C003 (Final) R834786 (Final) |
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Kohli A, Garcia MA, Miller RL, Maher C, Humblet O, Hammond SK, Nadeau K. Secondhand smoke in combination with ambient air pollution exposure is associated with increased CpG methylation and decreased expression of IFN-γ in T effector cells and Foxp3 in T regulatory cells in children. Clinical Epigenetics 2012;4(1):17 (16 pp.). |
R835435 (Final) R834596 (2011) R834596 (2012) R834596 (Final) R834596C003 (2011) R834596C003 (2012) R834596C003 (Final) R834786 (2012) |
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Kwon J, Weisel CP, Morandi MT, Stock TH. Source proximity and meteorological effects on residential outdoor VOCs in urban areas: results from the Houston and Los Angeles RIOPA studies. Science of the Total Environment 2016;573:954-964. |
R835435 (2018) |
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Lee EY, Lin J, Noth EM, Hammond SK, Nadeau KC, Eisen EA, Balmes JR. Traffic-related air pollution and telomere length in children and adolescents living in Fresno, CA: a pilot study. Journal of Occupational and Environmental Medicine 2017;59(5):446-452. |
R835435 (2018) R835435 (Final) |
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Lessard LN, Alcala E, Capitman JA. Pollution, poverty, and potentially preventable childhood morbidity in central California. The Journal of Pediatrics 2016;168:198-204. |
R835435 (2014) R835435 (2016) R835435 (Final) |
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Liu J, Zhang L, Winterroth LC, Garcia M, Weiman S, Wong JW, Sunwoo JB, Nadeau KC. Epigenetically mediated pathogenic effects of phenanthrene on regulatory T cells. Journal of Toxicology 2013;2013:967029. |
R835435 (Final) R834596 (2012) R834596 (Final) R834596C003 (2012) R834596C003 (Final) R834786 (2012) |
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Mann JK, Balmes JR, Bruckner TA, Mortimer KM, Margolis HG, Pratt B, Hammond SK, Lurmann FW, Tager IB. Short-term effects of air pollution on wheeze in asthmatic children in Fresno, California. Environmental Health Perspectives 2010;118(10):1497-1502. |
R835435 (Final) R834596 (2010) R834596 (2011) R834596 (2012) R834596 (Final) |
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Nadeau K, McDonald-Hyman C, Noth EM, Pratt B, Hammond SK, Balmes J, Tager I. Ambient air pollution impairs regulatory T-cell function in asthma. Journal of Allergy and Clinical Immunology 2010;126(4):845-852.e10. |
R835435 (Final) R834596 (2010) R834596 (2011) R834596C003 (2010) R834596C003 (2011) R834786 (2011) |
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Noth EM, SK Hammond, GS Biging, and IB Tager. 2011. A spatial-temporal regression model to predict daily outdoor residential PAH concentrations in an epidemiologic study in Fresno, CA. Atmospheric Environment 2011;45(14):2394-2403. |
R835435 (Final) R828678C017 (Final) |
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Noth EM, Hammond SK, Biging GS, Tager IB. Mapping and modeling airborne urban phenanthrene distribution using vegetation biomonitoring. Atmospheric Environment 2013;77:518-524. |
R835435 (Final) R834596 (Final) |
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Noth EM, Lurmann F, Northcross A, Perrino C, Vaughn D, Hammond SK. Spatial and temporal distribution of polycyclic aromatic hydrocarbons and elemental carbon in Bakersfield, California. Air Quality, Atmosphere & Health 2016;9(8):899-908. |
R835435 (2016) R835435 (2018) R835435 (Final) |
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Ortega Hinojosa AM, MacLeod K, Balmes JR, Jerrett M. Influence of school environments on childhood obesity in California. Environmental Research 2018;166:100-107. |
R835435 (2018) |
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Padula AM, Mortimer K, Hubbard A, Lurmann F, Jerrett M, Tager IB. Exposure to traffic-related air pollution during pregnancy and term low birth weight:estimation of causal associations in a semiparametric model. American Journal of Epidemiology 2012;176(9):815. |
R835435 (Final) |
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Padula AM, Tager IB, Carmichael SL, Hammond SK, Yang W, Lurmann F, Shaw GM. Ambient air pollution and traffic exposures and congenital heart defects in the San Joaquin Valley of California. Paediatric and Perinatal Epidemiology 2013;27(4):329-339. |
R835435 (Final) R834596 (2011) R834596 (2012) R834596 (Final) R834596C002 (2011) R834596C002 (2012) R834596C002 (Final) |
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Padula AM, Tager IB, Carmichael SL, Hammond SK, Lurmann F, Shaw GM. The association of ambient air pollution and traffic exposures with selected congenital anomalies in the San Joaquin Valley of California. American Journal of Epidemiology 2013;177(10):1074-1085. |
R835435 (Final) R834596 (2011) R834596 (2012) R834596 (Final) R834596C002 (2011) R834596C002 (2012) R834596C002 (Final) |
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Padula AM, Tager IB, Carmichael SL, Hammond SK, Yang W, Lurmann FW, Shaw GM. Traffic-related air pollution and selected birth defects in the San Joaquin Valley of California. Birth Defects Research, Part A: Clinical and Molecular Teratology 2013;97(11):730-735. |
R835435 (Final) R834596 (2012) R834596 (Final) R834596C002 (2012) R834596C002 (Final) |
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Padula AM, Mortimer KM, Tager IB, Hammond SK, Lurmann FW, Yang W, Stevenson DK, Shaw GM. Traffic-related air pollution and risk of preterm birth in the San Joaquin Valley of California. Annals of Epidemiology 2014;24(12):888-895e4. |
R835435 (2015) R835435 (2016) R835435 (2018) R835435 (Final) R834596 (2012) R834596 (Final) R834596C001 (2012) R834596C001 (Final) |
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Padula AM, Noth EM, Hammond SK, Lurmann FW, Yang W, Tager IB, Shaw GM. Exposure to airborne polycyclic aromatic hydrocarbons during pregnancy and risk of preterm birth. Environmental Research 2014;135:221-226. |
R835435 (2014) R835435 (2015) R835435 (2016) R835435 (2018) R835435 (Final) |
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Padula AM, Balmes JR, Eisen EA, Mann J, Noth EM, Lurmann FW, Pratt B, Tager IB, Nadeau K, Hammond SK. Ambient polycyclic aromatic hydrocarbons and pulmonary function in children. Journal of Exposure Science & Environmental Epidemiology 2015;25(3):295-302. |
R835435 (2014) R835435 (2015) R835435 (2016) R835435 (Final) R834596 (2012) R834596 (Final) |
Exit Exit |
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Padula AM, Yang W, Carmichael SL, Tager IB, Lurmann FW, Hammond SK, Shaw GM. Air pollution, neighbourhood socioeconomic factors, and neural tube defects in the San Joaquin Valley of California. Paediatric and Perinatal Epidemiology 2015;29(6):536-545. |
R835435 (2015) R835435 (2016) R835435 (2018) R835435 (Final) |
Exit Exit |
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Padula AM, Yang W, Schultz K, Tom L, Lin B, Carmichael SL, Lammer EJ, Shaw GM. Gene variants as risk factors for gastroschisis. American Journal of Medical Genetics Part A 2016;170(11):2788-2802. |
R835435 (2018) R835435 (Final) |
Exit Exit |
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Padula AM, Yang W, Carmichael SL, Lurmann F, Balmes J, Hammond K, Shaw GM. Air pollution, neighborhood acculturation factors and neural tube defects among Hispanic women in California. Birth Defects Research 2017;109(6):403-422. |
R835435 (2017) R835435 (2018) R835435 (Final) |
Exit Exit |
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Padula AM, Yang W, Schultz K, Lurmann F, Hammond SK, Shaw GM. Genetic variation in biotransformation enzymes, air pollution exposures, and risk of spina bifida. American Journal of Medical Genetics, Part A 2018 May;176(5):1055-1090. |
R835435 (2018) R835435 (Final) |
Exit Exit |
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Prunicki M, Stell L, Dinakarpandian D, de Planell-Saguer M, Lucas RW, Hammond SK, Balmes JR, Zhou X, Paglino T, Sabatti C, Miller RL, Nadeau KC. Exposure to NO2, CO, and PM2.5 is linked to regional DNA methylation differences in asthma. Clinical Epigenetics 2018;10:2. |
R835435 (2018) R835435 (Final) |
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Prunicki, M., et al., Exposure to NO2, CO, and PM2.5 Is Linked to Regional DNA Methylation Differences in Asthma (submitted). |
R835435 (2017) |
not available |
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Tager IB, Lurmann FW, Haight T, Alcorn S, Penfold B, Hammond SK. Temporal and spatial patterns of ambient endotoxin concentrations in Fresno, California. Environmental Health Perspectives 2010;118(10):1490-1496. |
R835435 (Final) |
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Zografos K, Krenz V, Yarmo K, Alcala E. College students’ utilization of protective alcohol-use behaviors. Californian Journal of Health Promotion 201;13(1): 49-58. |
R835435 (Final) |
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Gale SL, Noth EM, Mann J, Balmes J, Hammond SK, Tager IB. Polycyclic aromatic hydrocarbon exposure and wheeze in a cohort of children with asthma in Fresno, CA. Journal of Exposure Science and Environmental Epidemiology 2012;22(4):3 86. |
R835435 (Final) |
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Syed A, Hew K, Kohli A, Knowlton G, Nadeau KC. Air pollution and epigenetics. Journal of Environmental Protection 2013;4(08):114. |
R835435 (Final) |
not available |
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Sabounchi S, Bollyky J, Nadeau K. Review of environmental impact on the epigenetic regulation of atopic diseases. Current Allergy and Asthma Reports 2015;15(6):33. |
R835435 (Final) |
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Quinn C, Miller-Lionberg DD, Klunder KJ, Kwon J, Noth EM, Mehaffy J, Leith D, Magzamen S, Hammond SK, Henry CS, Volckens J. Personal exposure to PM2.5 black carbon and aerosol oxidative potential using an automated microenvironmental aerosol sampler (AMAS). Environmental Science & Technology 2018;52(19):11267-11275. |
R835435 (Final) |
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Weber KA, Yang W, Carmichael SL, Padula AM, Shaw GM. A machine learning approach to investigate potential risk factors for gastroschisis in California. Birth Defects Research 2019;111(4):212-221. |
R835435 (Final) |
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Padula AM, Yang W, Lurmann FW, Balmes J, Hammond SK, Shaw GM. Prenatal exposure to air pollution, maternal diabetes and preterm birth. Environmental Research 2019;170:160-167. |
R835435 (Final) |
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Prunicki M, Zhou X, Nadeau K. The impact of a prescribed burn versus a wildfire on the immune and cardiovascular systems of children. Journal of Allergy and Clinical Immunology 2019;143(2):AB80. |
R835435 (Final) |
Exit Exit |
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Padula AM, Yang W, Schultz K, Lee C, Lurmann F, Hammond SK, Shaw GM. Gene–environment interactions between air pollution and biotransformation enzymes and risk of birth defects. Birth Defects Research 2021; 113(9):676-686. |
R835435 (Final) |
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Prunicki, M and Nadeau, K. (2016) The Air We Breathe:How Extreme Weather Conditions Harm Us in Extreme Weather, Health, and Communities:Interdisciplinary Engagement, Springer Publishers. |
R835435 (2017) |
not available |
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Weber KA, Yang W, Lurmann F, Hammond SK, Shaw GM, Padula AM. Air pollution, maternal hypertensive disorders, and preterm birth. Environmental Epidemiology. 2019 Oct 1;3(5):e062. |
R835435 (Final) |
not available |
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Zografos, K; Alcala, E; & Capitman, J. Integrating Research Experiences into Public Health Curricula:Effects on Undergraduate Students’ Overall Educational Experience. To be submitted to:Pedagogy in Health Promotion. |
R835435 (2017) |
not available |
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Zografos K, Alcala E, Capitman J, Khang L. Integrating research experiences into public health curricula:effects on undergraduate students’ knowledge of neighborhood inequalities, perception of research, and motivation to talk about health issues. Pedagogy in Health Promotion 2019:2373379919881469. |
R835435 (Final) |
not available |
Supplemental Keywords:
Genetic polymorphisms, epidemiology, infants, pregnancy, health effects, PAH, immune system, T cells, Foxp3, epigenetics, ambient air pollution, polycyclic aromatic hydrocarbons, obesity, glucose dysregulation, immune system, structured social observation tool, built environment, air pollution, data collection, children’s healthRelevant Websites:
Children’s Health & Air Pollution Study (CHAPS) Exit
The Sean N. Parker Center for Allergy and Asthma Research Exit
Progress and Final Reports:
Original AbstractThe perspectives, information and conclusions conveyed in research project abstracts, progress reports, final reports, journal abstracts and journal publications convey the viewpoints of the principal investigator and may not represent the views and policies of ORD and EPA. Conclusions drawn by the principal investigators have not been reviewed by the Agency.
Project Research Results
- Final Report
- 2017 Progress Report
- 2016 Progress Report
- 2015 Progress Report
- 2014 Progress Report
- Original Abstract
44 journal articles for this center