Grantee Research Project Results
2012 Progress Report: Berkeley/Stanford Children’s Environmental Health Center
EPA Grant Number: R834596Center: UC Berkeley/Stanford Children’s Environment Health Center
Center Director: Tager, Ira
Title: Berkeley/Stanford Children’s Environmental Health Center
Investigators: Hammond, S. Katharine , Tager, Ira , Gale, Sara L , Shaw, Gary M. , Balmes, John R. , Padula, Amy , Eisen, Ellen , Mann, Jennifer , Nadeau, Kari
Institution: University of California - Berkeley , Stanford University
EPA Project Officer: Callan, Richard
Project Period: May 7, 2010 through May 6, 2013 (Extended to May 6, 2014)
Project Period Covered by this Report: May 7, 2012 through May 6,2013
Project Amount: $1,091,783
RFA: Children's Environmental Health and Disease Prevention Research Centers: Formative Centers (with NIEHS) (2009) RFA Text | Recipients Lists
Research Category: Children's Health , Human Health
Objective:
Project 1: Effect of multi-level environmental exposure on birth outcomes
Hypothesis: The associations between adverse pregnancy outcomes (low birth weight [LBW], pre-term and small for gestation age) and exposure to ambient air pollutants and endotoxin are increased in women who reside in impoverished neighborhoods and are socially disadvantaged at the individual level.
Specific Aim: To determine if the associations between adverse pregnancy outcomes (low birth weight, pre-term and small for gestation age) and exposure to ambient air pollutants and endotoxin are increased in women who reside in impoverished neighborhoods and are socially disadvantaged at the individual level.
Project 2: Exposure to Air Pollutants and Risk of Birth Defects
Hypothesis: Exposure to specific air pollutants and mixtures of air pollutants during critical periods of fetal organogenesis are associated with structural birth defects (so-called “congenital” anomalies or birth defects).
Specific Aim: Birth defects are the leading cause of infant mortality in the United States. Our Center’s research efforts will enhance scientific understanding of the potential environmental etiologies of birth defects, which will undoubtedly have important implications for risk assessment and prevention of these common, costly, and often deadly outcomes of pregnancy. Specifically in this project, we are conducting a rigorous population-based epidemiologic study to address the following research aim: to determine whether exposures to specific air pollutants and mixtures of air pollutants, during critical periods of fetal organogenesis, are associated with women delivering infants/fetuses with structural birth defects.
Project 3: Ambient Pollutant/Bioaerosol Effects on Treg Function
Hypothesis: The reported associations between ambient air pollution and endotoxin and asthma onset and exacerbation are mediated through pollutant/endotoxin alterations of regulatory T-cells (Treg), and these effects on Treg are related to exposure in the year prior to specimen collection and exposure during the late 1st and early 2nd trimesters when T-cell differentiation and function begin to develop.
Specific Aim: The overall goal of this research is to further understand the link between indicators of exposure and outcomes on human health by studying immune system changes in subjects exposed to elevated levels of ambient air pollution. We hypothesize that immunological indicators linked to environmental exposure and health outcomes will elucidate the role and mechanism of air pollution in asthma, a link that is theoretically understood, circumstantially clear, but not yet proven. We have developed a comprehensive novel indicator of hazard exposure that can be performed on one drop of blood. We will correlate cellular, serological, and epigenetic biomarker changes in peripheral blood, which can be broadly applied to an individual health outcome. The objectives of the research are (1) to examine the link between specific immune indicators and ambient air pollution exposure (level of exposure, chronicity of exposure, and type of exposure: ozone, NO/NO2, CO, PM2.5, PM10, sulfate, elemental carbon, polyaromatic hydrocarbons, daily naphthalene, endotoxin, fungal spores, and/or pollens) through a database collected in a large population in Fresno, CA; and (2) to characterize the relationship between immune indicators and health outcomes of asthma.
Community Outreach and Translation Core (COTC)
To engage community-based stakeholders in the ongoing conduct of studies of the effects of air pollution in children in the San Joaquin Valley by Center investigators and to facilitate translation of results of these studies into useful information for such stakeholders.
Exposure Core (ExC)
The purpose of the Exposure Core was to supply exposure data for the three projects, which involves acquisition and processing of routinely measured ambient air pollutants, and collection of new PAH and endotoxin data in the San Joaquin Valley (SJV).
Progress Summary:
Overview
During the past year, the entire study group has continued to meet biweekly to share progress in individual projects, discuss challenges, and integrate these results. Recruitment for Project 3 was completed in May 2012, and the field office was closed. Excellent progress has been made on all three projects, with intellectual support from the Biostatistics and Exposure Cores and logistical support from the Administrative Core; the Community Outreach and Translation Core has continued to participate in both the science and interactions with the community.
We have observed relationships between air pollution, especially polycyclic aromatic hydrocarbons, and the adverse health effects under study, birth outcomes, birth defects, impaired immune function, asthma, and pulmonary function. Furthermore, we have developed new metrics of neighborhood and found enhanced air pollution adverse health effects in those neighborhoods with low socioeconomic status. We also are finding that exposure to traffic-related air pollution at specific periods during pregnancy increases the odds of prematurity; exposure to selected traffic-related air pollution at different periods during pregnancy increases the odds of neural tube defects, while exposure to different traffic-related air pollution at different periods during pregnancy increases the odds of other birth defects. We have observed significant immunotoxic effects of polycyclic aromatic hydrocarbons using in vivo and ex vivo studies. These results provide mechanistic evidence to support the pulmonary function and asthma outcomes we are observing among our participants in both the CHAPS-SJV cohort and the Fresno Asthmatic Children’s Environment Study cohort.
Project 1: Effect of Multi-level Environmental Exposure on Birth Outcomes
In this project we are using data from the Study of Air Pollution, Genetics and the Environment, which include birth certificates in the four most populous counties of the San Joaquin Valley of California from 2000-2006. Ambient air pollution measurements and traffic metrics were assigned to the geocoded maternal residences. The exposures included: ozone (O3), nitrogen dioxide (NO2), nitrogen oxide (NO), carbon monoxide (CO), particulate matter < 10 μg/m3 (PM10), and PM < 2.5 μg/m3 (PM2.5) and traffic density. In addition, we have used land use regression to assign PAH (rings 4, 5, 6) estimates for the entire pregnancy (and the last 6 weeks) of each of the maternal residences within 20 km of Fresno's central site monitor for births between 2000-2006. These exposure metrics currently are being analyzed to identify the relationship between PAH exposure during pregnancy and preterm birth.
We have found associations between air pollution and adverse birth outcomes. We used targeted maximum likelihood estimation to examine the relationship between traffic and term low birth weight. We found that if everyone lived near high volume freeways (estimated by 4th quartile of traffic density), the estimated probability of term low birth weight would be 2.27% (95% confidence interval: 2.16, 2.38) compared to 2.02% (95% confidence interval: 1.90, 2.12) had everyone lived near smaller local roads (1st quartile of traffic density). This paper was recently published in the American Journal of Epidemiology.
Most recently, we have drafted a manuscript on traffic-related air pollution and four levels of prematurity based on gestational age at birth (20-27 weeks, 28-31 weeks, 32-33 weeks and 34-36 weeks) versus term (37-42 weeks). There were increased odds of prematurity at 20-27 weeks gestation for those exposed to the highest quartile of each pollutant during the 2nd trimester of pregnancy with adjusted odds ratios ranging from 1.6 to 2.5. The associations were substantially stronger in those with low neighborhood socioeconomic status with adjusted odds ratios ranging from 1.8 to 3.7. Exposure to particulate matter, particularly during mid to late pregnancy was associated with all gestational definitions of prematurity with the strongest associations for the earliest premature births. These results confirm previous studies that have found associations between traffic-related air pollution and prematurity. This study adds that the association is driven by very early preterm births and low SES.
To further explore our findings of neighborhood SES as a modifier in the relationship between air pollution and prematurity, we intend to build a more robust indicator of neighborhood deprivation. We have constructed the ½ mile neighborhood surrounding each of the maternal residences for births between 2000-2006 in Fresno county (N = 90,196). These neighborhoods include the GIS data that were previously collected (road network and traffic, alcohol and cigarette sales, wildfires, Superfund sites, grocery stores and farmers markets, schools and daycares, hospitals, water quality, and crime). To understand the complex neighborhood environment, we used item response theory to help characterize the variables that make up a deprived neighborhood. The item parameters are all of the covariates, which we converted to be positive and negative (0 = negative neighborhood influence, 1 = positive neighborhood influence). We used the FACES cohort (N = 315) to pilot the program of the IRT analysis. The next step is to examine neighborhood deprivation as an effect modifier in the relationship between traffic-related air pollution and adverse birth outcomes in the CHAPS study population.
Significance: Elevated air pollution levels and higher traffic density have been implicated as having adverse effects on the health of children and adults. Outcomes include reduced birth weight and gestational duration, decreased pulmonary function and coronary heart disease. Many of the outcomes are more common within communities with lower socioeconomic status (SES) and more ethnic diversity; these are the same communities that tend to have higher air pollution and traffic density, at least in the United States. It may be a case of environmental justice with important health consequences and may invoke policy change to address such potential injustice.
Project 2: Exposure to Air Pollutants and Risk of Birth Defects
In this project we are using data from the largest case-control study conducted to date in the United States on birth defects – the National Birth Defects Prevention Study. We limit our inquiries to the California study site in the San Joaquin Valley – an area with demonstrated poor air quality. We examined a total of 2,455 cases of 36 defects and their relationship with air pollution and traffic metrics. The first analysis targeted specific birth defect phenotypes that appear to be more environmentally sensitive in their etiologies (neural tube defects, cleft lip with or without cleft palate, cleft palate only, gastroschisis) and included 802 cases and 849 controls. Our second analysis focused on 822 congenital heart defects, which were categorized into 19 specific defects. Our most recent analysis evaluated the remaining defects for which there were sufficient power to detect associations (12 defects and 830 cases).
Ambient air pollution measurements and traffic metrics were assigned to each of the geocoded residences reported by the study subjects during the first and second month of pregnancy. The exposures included: ozone (O3), nitrogen dioxide (NO2), nitrogen oxide (NO), carbon monoxide (CO), particulate matter < 10 μg/m3 (PM10), PM < 2.5 μg/m3 (PM2.5), and traffic density. The station-specific daily air quality data from the U.S. EPA Air Quality System were spatially interpolated using inverse distance-squared weighting. Traffic density indicators were calculated to represent the amount of traffic counts within a 300 m radius of the early pregnancy residence.
Our analyses find evidence that higher exposure to traffic-related ambient air pollutants CO, NO and NO2, and lower exposure to O3 during the first 2 months of pregnancy appears to be associated with increased odds of neural tube defects in the San Joaquin Valley of California after adjusting for maternal race-ethnicity, education and multi-vitamin use. In contrast, higher ozone was associated with an increased odds of gastroschisis and higher CO was associated with decreased odds of cleft lip with/without cleft palate. Exposure to increased levels of traffic density (and in some cases PM10) during the first 2 months of pregnancy was associated with ventricular septal defects, hypospadias, hydrocephaly and esophageal atresia.
Significance: The etiologies of most structural birth defects are unknown. There have been a few observations that point toward ambient air pollutants as risk factors for human birth defects. However, this important public health hypothesis has been under studied owing to the lack of good exposure and outcome data. Thus, Project 2 uniquely fills an important gap in our understanding of the role of environmental exposure on the risk of human birth defects.
Project 3: Ambient Pollutant/Bioaerosol Effects on Treg Function
The work on the project aims has proceeded smoothly and at the pace anticipated. All has progressed according to timelines and all subjects have been recruited and are enrolled in the study. We are in the process of performing all cellular and molecular analyses on the blood samples obtained from the subjects. Some preliminary results and publications have occurred and these are detailed below. The aims of the project are unchanged.
As described in the preliminary results section below, significant immunotoxic effects were observed using in vivo and ex vivo studies. Our preliminary data demonstrate that:
- DNA methylation of the Foxp3 gene results in decreased FoxP3 protein levels in Treg and that the levels of FoxP3 decrease are associated with increases in levels of exposure to polycyclic aromatic hydrocarbons.
- Downregulation of chemokine receptor/cognate ligand pairs (CCR8/CCL1) is worsened by exposure to polycyclic aromatic hydrocarbons.
- Decreases in Treg-associated (TGF-ß and IL-10) and increases in Th2-associated plasma markers (IL-4 and IL-13) correlate with increased levels of exposure to ambient air pollution.
- Higher degrees of Treg impairment correlate with severity of asthma.
- Lower levels of Treg immune indicators can be detected in non-asthmatic children exposed to elevated levels of ambient air pollution and that if the Treg immune indicators increase over the four time points of the study (baseline, 6 mo, 12 mo and 18 mo), then these children might be at risk for developing asthma. Definitive analysis for the positive predictive value of a Treg immune indicator is outside the scope of this study but we plan to collect evidence in this proposed research to further test predictive value in the future.
We expect our results to:
- Provide sufficient evidence to help understand the link between the environmental hazard, exposure (individual estimate exposures), and health outcomes (asthma) through the database collected in a large population in the Fresno, CA.
- Characterize the relationship between ambient air pollution exposure and biomarkers that can be used to indicate the health outcomes of asthma.
Significance/Overall Impact: The proposal is aimed to innovatively examine whether chronic ambient air pollution exposures, the health outcomes of individual children, and changes in the immune system are correlated. The results are essential for understanding immune mechanisms that could be related to exposure and health outcomes. Overall, the results would help in decreasing and preventing the burden of asthma and allergy and reducing exposure to air pollution.
Biostatistics Core:
The Biostatistics Core worked closely with each of the projects to implement the causal inference (semiparametric) framework that was the centerpiece of the P20. New statistical methods have been developed to provide fully adjusted (confounders) exposure-response functions for pollutants that make use of an advanced algorithm (Super Learner), which provides optimal models (variance, bias tradeoff) simultaneously from a large library of user-specified algorithms. The method obviates the need from assumptions about the data generating distributions and is justified by an important theoretical result (Oracle Inequality). The figure below illustrates how the Super Learner is able to show a distinct population threshold between lag 1 individual level NO2 concentrations and a.m. wheeze, compared to the best model included in a five model library. These methods allow us to produce marginal, public health relevant exposure-response function without having to pre-specify any one, single a priori model. This will provide great flexibility in our health analyses as well as improved utility for health impact assessment speciated data collected in fall/winter 2010/2011.
Significance: Project 2 has provided preliminary evidence for an association between neural tube defects and increased levels of traffic-generated air pollutants in one of the largest samples of NTDs studied. Project 3 has provided additional evidence for the impairment in Treg function and morbidity in asthmatic children. These data continue to support the hypothesis that these effects may be occurring early in life. Our Biostatistics Core has developed powerful new methods to provide population-level exposure response function curves that overcome many of the limitations of existing methods. These will allow us to provide finer scale analyses of health effects over the full range of exposures without the need to group exposures into arbitrary groups.
Community Outreach and Translation Core (COTC)
During this reporting period, the Community Advisory Board (CAB) met three times. A meeting on 5/17/2012 was the final of three where we discussed potential grant activities and collaborations as a group for the grant proposal to become a full Children’s Environmental Health Center. The emphasis was on projects that would enhance and not compete with current efforts in the San Joaquin Valley on improved Children’s Environmental Health. The group decided to propose a project with a local organization’s Fresno Youth Council for Sustainable Communities that also would support the new Fresno Environmental Reporting Network (FERN). A collaborative project with CHAPS and Fresno State also emerged because of work with the CAB.
The group met again on November 19, 2012. Dr. Noth gave a presentation on a land use regression model that she developed to estimate daily concentrations to PAH in children living in Fresno. Dr. Mann presented how these exposures were associated with wheeze in asthmatic children in Fresno (Gale, et al., 2012). On 2/20/13, interested CAB members met with a reporter for Discover Magazine who was interested in doing a story on CHAPS and air quality and asthma in the SJV. During this reporting year, CAB members were instrumental in helping us plan how to contact pregnant mothers for recruitment of infants through clinics in the Fresno area, both in discussions during meetings and subsequent conversations. Two CAB members, who have collaborated with us on previous projects in Fresno, met with investigators on multiple occasions to discuss recruitment and will be in charge of the proposed field office.
Ms. Saklar, Director of Outreach and Communications, represented CHAPS at four monthly FERN meetings during this time period including the network launch and environmental justice tour. Issues raised ranged from black smoke being emitted at a local winery to black dust being reported coming from a metal company; agricultural burnings to pesticide drift; illegal alleyway dumping to high levels of arsenic in the drinking water in Lenare; and inadequate rental property conditions to loose dogs. Ms. Saklar also has been an active participant with organizations represented by CAB members, including the Central Valley Air Quality Coalition and Fresno Metro Ministry.
Finally, as results from CHAPS begin to be published, the COTC has taken an opportunity to improve the website and set up Facebook and Twitter accounts. We are preparing for presentations in Fresno that will be reported on in the next report.
The CAB continues to be a good venue for concerns about air quality monitoring conducted by the San Joaquin Air Pollution Control District to be communicated to Dr. Balmes, who is the physician member of the California Air Resources Board (CARB).
Exposure Core (ExC)
Task 1 – Routine Air Quality Data. As part of FACES and SAGE, STI had acquired and quality assured air quality data for NO, NO2, ozone, CO, PM2.5, PM10, and PM2.5 chemical constituents for 2000-2006 that are routinely collected at air monitoring stations in Fresno and Kern Counties. The database was extended geographically to include all eight counties in the SJV and extended temporally to include 1997-1999 and 2007-2011 ambient air quality data. These data have been used to generate individual level exposure assignments for Projects 1, 2 and 3. In Year 3, the exposure database was extended into 2012 and assignments were made for additional subjects with later test dates.
Task 2 – Bakersfield Central Site PAH Monitoring and Endotoxin Sampling. Work under this task in Year 3 involved comparing Bakersfield continuous PAH concentrations to those measured in fall/winter 2011/2012 in Stockton, Madera, Fresno, and Visalia to obtain an understanding of how PAH varies spatially up and down the valley. In addition, both laboratory and field intercomparison of the six ECOCHEM PAS2000 instruments used in this task were conducted. The laboratory evaluations were conducted in the DHS indoor air chamber with zero air and various combustion sources. The field intercomparison was conducted in winter 2013 in Fresno. These were carried out not only to characterize precision of the measurements but also to guide development of calibration procedures that can be used in future studies. Another work element involved generating individual level PAH exposure assignments to support health analyses. The Noth, et al. (2011) model was applied to estimate PAH exposures for subjects in Projects 1, 2 and 3.
Task 3 – Bakersfield Spatial PAH Monitoring and Endotoxin Sampling. Additional analyses of the PAH data collected in Bakersfield were conducted in Year 3. These data are being used to evaluate the similarities in parameters (traffic, population density, agricultural burning) that explain spatial PAH variations in Bakersfield and Fresno. These data also are being used as pilot study data for larger scale saturation experiments than are being planned in the future (e.g., the proposed P01).
Future Activities:
Project 1: The next step is to examine neighborhood deprivation as an effect modifier in the relationship between traffic-related air pollution and adverse birth outcomes in the CHAPS study population.
Project 2: Our plans and goal have essentially not changed. Many more analyses are planned in the coming year.
Project 3: We plan to:
- Complete all collection of samples and clinical outcome measures every 6 months.
- Complete our analysis of repeat immune measures (i.e., Treg function, Foxp3 expression, DNA methylation of Foxp3 locus) and repeat clinical outcomes (pulmonary function tests and health questionnaires) on each subject.
- Obtain short term and long term individual estimate exposures to ambient air PAHs, PM2.5, black carbon and ozone, and then test whether there is an association of the extent of exposure in each subject to immune outcome measures in the same subject.
- If data represent interesting findings, we will submit a manuscript on the EPA-funded cohorts.
COTC: Our plans are to complete the analysis of PAH spatial and temporal variation on both the urban scale (in Bakersfield) and the regional scale, extending from Bakersfield in the south to Stockton in the north, and complete the PAH analyzer intercomparison work and study documentation.
Journal Articles: 15 Displayed | Download in RIS Format
Other center views: | All 50 publications | 15 publications in selected types | All 15 journal articles |
---|
Type | Citation | ||
---|---|---|---|
|
Balmes JR. How does diesel exhaust impact asthma? Thorax 2011;66(1):4-6. |
R834596 (2010) R834596 (2011) R834596 (2012) R834596 (Final) R834596C003 (2012) |
Exit Exit Exit |
|
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 & Environmental Epidemiology 2012;22(4):386-392. |
R834596 (2010) R834596 (2011) R834596 (2012) R834596 (Final) R834596C003 (2012) |
Exit |
|
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. |
R834596 (2012) R834596 (Final) R834596C003 (Final) R834786 (Final) R835435 (2014) R835435 (2015) R835435 (2016) R835435 (Final) |
Exit Exit Exit |
|
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.). |
R834596 (2011) R834596 (2012) R834596 (Final) R834596C003 (2011) R834596C003 (2012) R834596C003 (Final) R834786 (2012) R835435 (Final) |
Exit |
|
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. |
R834596 (2012) R834596 (Final) R834596C003 (2012) R834596C003 (Final) R834786 (2012) R835435 (Final) |
Exit |
|
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. |
R834596 (2010) R834596 (2011) R834596 (2012) R834596 (Final) R835435 (Final) |
|
|
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. |
R834596 (2010) R834596 (2011) R834596C003 (2010) R834596C003 (2011) R834786 (2011) R835435 (Final) |
Exit Exit |
|
Noth EM, Hammond SK, Biging GS, Tager IB. Mapping and modeling airborne urban phenanthrene distribution using vegetation biomonitoring. Atmospheric Environment 2013;77:518-524. |
R834596 (Final) R835435 (Final) |
Exit Exit Exit |
|
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):815-824. |
R834596 (2010) R834596 (2011) R834596 (2012) R834596 (Final) R834596C001 (2011) R834596C001 (2012) R834596C001 (Final) |
Exit Exit Exit |
|
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. |
R834596 (2011) R834596 (2012) R834596 (Final) R834596C002 (2011) R834596C002 (2012) R834596C002 (Final) R835435 (Final) |
|
|
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. |
R834596 (2011) R834596 (2012) R834596 (Final) R834596C002 (2011) R834596C002 (2012) R834596C002 (Final) R835435 (Final) |
Exit |
|
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. |
R834596 (2012) R834596 (Final) R834596C002 (2012) R834596C002 (Final) R835435 (Final) |
|
|
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. |
R834596 (2012) R834596 (Final) R834596C001 (2012) R834596C001 (Final) R835435 (2015) R835435 (2016) R835435 (2018) R835435 (Final) |
Exit Exit Exit |
|
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. |
R834596 (2012) R834596 (Final) R835435 (2014) R835435 (2015) R835435 (2016) R835435 (Final) |
Exit Exit |
|
Yang W, Carmichael SL, Roberts EM, Kegley SE, Padula AM, English PB, Shaw GM. Residential agricultural pesticide exposures and risk of neural tube defects and orofacial clefts among offspring in the San Joaquin Valley of California. American Journal of Epidemiology 2014;179(6):740-748. |
R834596 (Final) R834596C002 (Final) |
Exit Exit Exit |
Supplemental Keywords:
air pollution, low birthweight, preterm births, neighborhood effects, cumulative impact, congenital abnormalities, pregnancy, immune function, Foxp3, immune system, epigenetic effectsProgress and Final Reports:
Original Abstract Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
R834596C001 Effect of Multi-Level Environmental Exposure on Birth Outcomes
R834596C002 Exposure to Air Pollutants and Risk of Birth Defects
R834596C003 Ambient Pollutant/Bioaerosol Effects on Treg Function
The 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.