Grantee Research Project Results
2017 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, 2016 through June 30,2017
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 anlaysis. We have four research projects and four cores:
Project 1: Exposures to Air Pollutants, Modifying Genes, and Risk of Birth Defects and Preterm Birth.
Project 2: Mechanisms of Polycyclic Aromatic Hydrocarbon-linked Immunopathogenesis in Atopy.
Project 3: Obesity/Glucose Dysregulation and Air Pollution
Project 4: Transit Exposures in-utero.
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 submitted May 2017.
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 work on this goal is on schedule.
3) To determine whether ambient exposures to PAHs, during critical periods of gestation, are associated with women delivering preterm.
This aim was completed before Year 4. We have published the results of this aim in Environmental Research. 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 have begun 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.
As of the end of Year 4, baseline data collection for all three cohorts has been completed. The initial child cohort target of 220 samples was reached and was extended to include 299 subjects, .
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 analysed leptin (n=230), adiponectin (n=234), hba1c (n=275), C-reactive protein (n=139), HDL (n=138) and 8-isoprostane (n=253) samples at baseline. We have completed analysis of leptin, adiponectin, 8-isoprostane and HbA1c for 96 participants in the adolescent/young adult cohort. We have calculated BMI-percentile for 221 children, and determined BMI category for AYA and all Child.
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.
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.
Future Activities:
Project 1: Exposures to Air Pollutants, Modifying Genes, and Risk of Birth Defects and Preterm Birth.
We will continue to analyze the interaction of air pollution and gene variants with regard to birth defects. We hope to have one paper accepted and at least 2 others drafted in the next period. We plan to conduct analyses of the relationship between PAH and selected birth defects. 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
- We will continue to collect cord blood as pregnant women deliver their babies. We will continue visits of 12- and 24-month old infants and 9-year old children during the next reporting period.
- Head circumference measurements, along with length/height and weight in the 12- and 24-month infants will be used to determine bmi-percentile of each of our infants at each follow-up visit.
- Two publications are being prepared. The first is a descriptive account of air pollution and OGD outcomes including adipokines, 8-isoprostane (marker of oxidative stress) and risk factors for metabolic syndrome (increased HbA1c and blood pressure). The second publication is characterization of participants as “metabolically healthy and unhealthy” using anthropometry data collected as part of the project.
- We will continue to share all preliminary 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.
The The PM2.5, ultrafine particles, BC, and particle-bound PAHs concentrations will be geocoded for the routes in the neighborhood areas and will be compared with stationary PAHs concentrations and other species PM2.5 that measured continuously in the Fresno Stationary Air Monitoring Sites. The data will be used to estimate the personal exposure of pregnant participants for the transit exposures. We plan on testing the structured social observation for its predictive power of health outcomes among the child, adolescent, and parent cohorts that are being tracked in this project. A cluster analysis will be used to identify clusters of associations between poor health outcomes in the neighborhoods with the greatest social and environmental challenges. In the subsequent reporting period, we will be evaluating the changes to neighborhood characteristics (i.e. interventions) that have the greatest potential to reduced transit-related exposures during pregnancy to PAHs, PM2.5, and BC in the population as a whole and in subgroups defined by geographic neighborhoods.
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) |
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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) |
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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) |
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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) |
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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) |
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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) |
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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) |
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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. |
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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) |
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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) |
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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:
Ambient air pollution, genetic polymorphisms, epidemiology, infants, pregnancy, health effects, PAH, Immune system, T cells, Foxp3, epigenetics, ambient air pollution, polycyclic aromatic hydrocarbons, Obesity, Glucose dysregulation, Structured social observation tool; built environment;Relevant Websites:
Children's Health and Air Pollution Study Exit 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
- 2018 Progress Report
- 2016 Progress Report
- 2015 Progress Report
- 2014 Progress Report
- Original Abstract
44 journal articles for this center