2018 Progress Report: Southern California Children's Environmental Health Center

EPA Grant Number: R835441
Center: Southern California Children's Environmental Health Center
Center Director: McConnell, Rob Scot
Title: Southern California Children's Environmental Health Center
Investigators: McConnell, Rob Scot
Institution: University of Southern California
EPA Project Officer: Nolt-Helms, Cynthia
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: $4,146,875
RFA: Children's Environmental Health and Disease Prevention Research Centers (with NIEHS) (2012) RFA Text |  Recipients Lists
Research Category: Children's Health , Health

Objective:

The epidemic of childhood obesity threatens the health of a generation of children because it is a major risk factor for type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and cardiovascular diseases (CVD). Research suggests that ubiquitous ambient particulate air pollution is a potentially important cause of obesity and its metabolic consequences. Results from the Children's Health Study (CHS) found that growth trajectory of body mass index (BMI) and obesity risk were associated with prenatal and childhood exposure to the near-roadway air pollution (NRAP) mixture. In preliminary clinical studies, NRAP was associated with increased visceral adipose tissue (VAT) and expression of genes in inflammatory pathways in adipose tissue, systemic inflammation and metabolic outcomes, and abnormal pancreatic beta cell function. Together with studies in adults, this emerging science supports the hypothesis that NRAP contributes to development of obesity and metabolic disease. To investigate this broad hypothesis, the Southern California Children's Environmental Health Center (SC-CEHC) is conducting an integrated program of population-based, clinical and experimental research to address three key research questions.

Project 1: Effects of Air Pollution on the Development of Obesity in Children

Project 1 is using cutting-edge exposure assessment, imaging and metabolic phenotyping in overweight/obese CHS children to investigate the impact of prenatal and childhood exposure on obesity in the CHS cohort and the relationship to fat distribution, glucose homeostasis, lipid profile, systemic inflammation and the metabolic syndrome (MetS). The study will focus on effects of elemental carbon (EC) and transition metals (Fe and Cu) in NRAP, based on preliminary findings and their toxicological properties.

Project 2: Near-Roadway Air Pollution, Adipose Inflammation and Metabolic Consequences

Project 2 is investigating the effects of these exposures on adipose tissue inflammation, insulin resistance (IR), and gene expression in macrophages and adipocytes in adipose biopsies from a sample of overweight/obese P1 CHS participants.

Project 3: Longitudinal Effects of Air Pollution on Obesity in Mice

Project 3 is employing translational mouse models of obesity to investigate critical windows of exposure and temporal sequence of events from gestation to maturity linking NRAP exposure, adipose phenotype and inflammatory profile, and systemic metabolic dysregulation.

Results across all projects are being integrated using an innovative hierarchical statistical model to examine the mechanistic pathway of NRAP on body fat, adipose inflammation and metabolic outcomes.

Progress Summary:

Project 1: Effects of Air Pollution on the Development of Obesity in Children

1. Specific Aims

Obesity and its metabolic consequences are major public health issues. A growing body of evidence indicates that environmental exposures during the in utero, early-life and later childhood periods contribute to obesity and its metabolic consequences. In the Southern California CHS, obesity, growth trajectory of BMI and attained BMI at age 18 years were associated with traffic density and NRAP exposure during gestation and childhood, findings that were replicated for childhood exposures in a second independent cohort. Our preliminary data indicates that NRAP adversely affects body fat amount and distribution, systemic inflammation, and pancreatic beta cell function. Recent experimental studies show that early-life air pollution exposures result in fat redistribution and contribute to systemic inflammatory responses and alterations of metabolic function, including IR and MetS. Studies in animal models have shown that early-life particulate matter (PM) inhalation increases VAT, a fat depot that is associated with systemic inflammation and increased risk for later-life metabolic and cardiovascular diseases. The effects of air pollution on fat redistribution are reflected in increased hepatic fat fraction (HFF), which could contribute to the emergence of NAFLD in children. Taken together, these studies indicate that early-life traffic exposures have the potential to increase childhood obesity and contribute to fat redistribution, systemic inflammation and metabolic changes associated with increased risk for type 2 diabetes, NAFLD and CVD.

Although studies support the hypotheses that exposures to air pollution during developmental periods play a role in the trajectory toward childhood obesity, adipose tissue redistribution, inflammation and metabolic dysfunction, little is known about the responsible mechanisms or the causal components of air pollution that could be targets for prevention. We aim to fill critical gaps in the scientific knowledge base by investigating the effects of elevated NRAP exposures during the in utero and childhood periods on clinically important obesity phenotypes, obesity-related inflammation and adipokines, insulin sensitivity, pancreatic beta cell function, and components of MetS at age 18 years. We have identified NRAP as the exposures of interest, as traffic-related PM produces systemic oxidative stress and inflammation that may be responsible for adverse health effects.

Using newly assembled data, we will employ state-of-the-art spatiotemporal models to provide time-resolved (prenatal and childhood) EC and PM less than 2.5 µg/m (EC2.5 and PM2.5) transition metals exposures to examine their effects during critical developmental periods on obesity among a subset of 4,560 Southern California-born CHS participants. This subset of subjects from the CHS has linked birth certificate data and extensive data on lifetime air pollution and tobacco smoke exposures, community contextual information, time-activity patterns, BMI trajectory, physical activity and health status. To investigate mechanism and mediation effects, we propose to examine adipose tissue distribution using advanced magnetic resonance imaging (MRI) techniques, measures of inflammation, adipokines, insulin sensitivity and beta-cell function by frequently sampled intravenous glucose tolerance test and the prevalence of MetS and in a subsample of 200 overweight or obese CHS participants.

Aim 1 will investigate the longitudinal effects of prenatal, early and later childhood exposures to traffic-related air pollutants on BMI trajectory and obesity in the CHS cohort. We hypothesize that elevated exposure to traffic-related air pollutants during the in utero and childhood periods are obesogenic and result in a steeper, gender-specific trajectory of BMI increase with age and that cumulative exposures increase the prevalence of obesity at ages 5, 10 and 16 years.

Aim 2 will examine the effects of lifetime traffic-related air pollutant exposures on the VAT, HFF, subcutaneous adipose tissue (SAT), deep SAT (dSAT) and superficial SAT (sSAT) in 200 overweight or obese 18-year-old CHS participants sampled informatively based on EC2.5 exposure. We hypothesize that elevated exposure to EC2.5 will increase (1) the amount of VAT and dSAT relative to SAT and (2) HFF and the prevalence of NAFLD.

Aim 3 will investigate the effects of traffic-related air pollutant exposures on insulin sensitivity, pancreatic beta cell function, MetS and its components (blood pressure, glucose, lipid profile), adipokines, and markers of inflammation (CRP, IL-6, TNF-α, MCP-1, leptin, resistin, adiponectin) in the 200 overweight or obese CHS 18-year-olds studied in Aim 2. We will assess VAT as a mediator for the chronic effects of exposure on adipokines, inflammatory markers, insulin sensitivity, pancreatic beta cell function and MetS using a novel quantile regression mediation approach. We hypothesize that, after accounting for recent air pollution exposures, (1) chronic traffic-related air pollutant exposures will increase metabolic dysfunction and the risk for MetS, and (2) these adverse effects of chronic traffic exposures are mediated through VAT.

2. Studies and Results

We have investigated the longitudinal effects of prenatal, early and later childhood exposure to traffic-related air pollutants on BMI trajectory and obesity in the CHS cohort. The exposure assessment was completed from primary data, including review of residential address histories, geocoding with state-of-the-art methods and updated models for exposure. A manuscript is now published in Environmental Health showing early-life traffic pollution is associated with later childhood BMI growth.

For aims 2 and 3, we have completed 160 participant study visits. Assays and exposure assessment have been completed. We have assembled analytic datasets and are examining the data. We aim to begin submitting manuscripts by the end of the year.

3. Significance

The epidemiologic evidence is supported by experimental studies using animal models, which show that particulate air pollutant increases visceral adiposity, adipose inflammation, systemic inflammation, metabolic dysfunction and atherosclerotic lesions. These data suggest that near-roadway exposures to motor vehicle emissions are not only obesogenic, but increase the metabolic and inflammatory consequences of obesity. These obesogenic mobile source emissions are substantial in the Los Angeles (LA) region, and many of the 3 million children in LA are highly exposed because they reside, play and go to school in close proximity to major roads. These children may be at increased lifetime risk for chronic diseases from chronically elevated exposures occurring during critical developmental periods, including the in utero, early childhood (ages 0-5 years) and later childhood (ages 5-18 years) periods.

Project 2: Near-Roadway Air Pollution, Adipose Inflammation and Metabolic Consequences

1. Specific Aims

Animal toxicological studies suggest that adipose tissue inflammation plays a critical role in mediating the effects of air pollution on IR, systemic inflammation and the metabolic risk that is associated with obesity. These relationships have not previously been studied in humans. In Project 2 we will investigate specific toxicologically relevant pro-inflammatory components of the near-roadway PM mixture. The specific aims are as follow:

Aim 1 will investigate the effects of lifetime cumulative exposure to ambient NRAP EC and NOx on macrophage polarization in dSAT from macrophage subtype 2 (M2) to pro-inflammatory macrophage subtype 1 (M1). We hypothesize that exposure to markers of the NRAP mixture (EC and NOx) will be associated with increased proportion of M1/M2 macrophages and with the presence of clusters of necrotic macrophates (crown-like structures [CLS]) in biopsy samples obtained from a novel dSAT biopsy.

Aim 2 will investigate the effects of lifetime exposure to NRAP on adipose tissue function and cell-specific gene expression. We hypothesize that high lifetime exposure to EC and NOx will be associated with (Aim 2a) increased expression of NFĸB inflammatory and insulin signaling pathway genes in macrophages and adipocyte subfractions of SAT and (Aim 2b) greater release of adipocytokines and biochemical markers of IR from SAT biopsies incubated ex vivo.

Aim 3 will integrate information from P1 and P2 using a novel latent variable model to examine quantitatively the mechanisms underlying the entire pathway of NRAP effects on metabolic outcomes. The model will quantify the effects of exposure at different ages on a latent quantity, such as underlying adipose tissue inflammation. This variable cannot be measured directly, but can be informed by measures of surrogates like SAT inflammation (from n = 60 in P2) and abdominal visceral adipose tissue volume (from n = 200 in P1). Information on systemic metabolic outcomes from P1 and lifetime BMI trajectory and other CHS covariates from the entire cohort effectively increases sample size. Understanding these mechanisms would strengthen our causal inference on NRAP health effects and identify new targets for intervention. We have modified the exposure aims based on the CSR comments to focus on NOx and EC as markers for NRAP exposure. Intracommunity variation in metals have proven difficult to model.

2. Studies and Results

We have completed data collection. We have sorted cells in adipose tissue and blood for M1 and M2 macrophages and T-regulatory (Treg) and T-effector (Teff) cells, and we have completed analyses showing reduced M2 and Treg cell number concentration in association with increasing ozone, a pattern that is stronger if there are higher concentrations of M1 or Teff cells, respectively. We see an opposite pattern of increased Tregs associated with an interaction of NO2 with Teff cells and with M1 cells. However, the NO2 associations are explained by the ozone pattern of effects. Ozone has an immune modulatory pattern that reduces Treg cell number. A manuscript is nearing completion. Adipocytokines in serum and BMI do not show a consistent pattern of associations with either adipose tissue cell counts or air pollution. Thus, T- and M-cell effects of air pollution do not explain the systemic associations observed in other studies. The analyses of adipocytokines in adipose tissue and the integrated analysis are pending.

3. Significance

The role of ozone as an immune modulator of anti-inflammatory Treg and M2 cell number in adipose tissue was unexpected and merits further investigation.

Project 3: Longitudinal Effects of Air Pollution on Obesity in Mice

1. Specific Aims

The overall goals of Project 3 are to carry out comprehensive experiments in mice to determine the effect of NRAP on obesity and related metabolic traits. We will use a longitudinal study design and will focus on nanoscale PM (nPM) as the pollutant of interest, since these particles reflect the NRAP that is associated with obesity in the CHS, as described in Project 1. Using the well-established C57BL/6 mouse model, we will induce obesity through combination of litter reduction at birth to promote overnutrition during early life with high-fat feeding at the time of weaning. Mice will be exposed to a novel near-roadway source of nPM (exposed group) or filtered air (control group) during prenatal, postnatal, or both pre- and postnatal development and will be characterized for obesity-related metabolic, molecular, biochemical and neurobiological phenotypes at 5 weeks of age (puberty period), 9 weeks of age (late adolescence) and 13 weeks of age (young adulthood). These proposed experiments are well integrated with the overall focus of the Center and may provide causal information that could guide informed analyses in Projects 1 and 2, as analogous obesity-related parameters are collected in humans.

Aim 1. We will determine the longitudinal effects of nPM exposure on the development of obesity and relevant physiological metabolic phenotypes. Mice in the control and exposed groups will undergo MRIs to determine body composition (lean tissue mass and whole-body fat) and fat distribution. We will also perform intraperitoneal glucose tolerance tests to assess glucose/insulin metabolism, measure a panel of adipocytokines in plasma and determine hepatic lipid content.

Aim 2. We will characterize adipose tissue from mice for molecular, histological and biochemical phenotypes. Immunohistochemistry will be used to determine the presence of CLS in adipose tissue, which is indicative of macrophage infiltration and inflammation. Adipocytes will be separated from the stromal vascular fraction, which will be used to perform flow cytometry to determine M1 and M2. The effects of nPM exposure on inflammatory and metabolic gene expression will be investigated in both isolated adipocytes and macrophages. Explant incubation studies will be carried out to determine in vitro production of adipocytokines. We hypothesize that nPM exposure will have progressively adverse effects on adipose tissue homeostasis, with increased inflammation at the cellular, secretory and gene expression levels.

Aim 3. We will investigate whether the effects of nPM exposure on obesity are mediated through neurobiological pathways involved in metabolic regulation. Immunohistochemical techniques and morphometric analyses will be used to characterize the hypothalamus from nPM-exposed and control mice with respect to the organization of neural projections involved in feeding regulation. Expression of metabolically relevant neuropeptide genes will also be investigated in a nucleus-specific manner by real-time PCR, and food intake will be assessed to determine whether nPM exposure results in altered feeding behavior. 

2. Studies and Results

We continued to determine the effects of NRAP on obesity in mice and focused our studies during Year 3 on prenatal exposure. At the time of pregnancy, female C57Bl/6J mice were exposed to either filtered air or 300 µg/m3 nPM for 5 hours per day, 3 days per week, and exposure was discontinued after birth of the pups. At the time of weaning (4 weeks of age), male and female mice were put on a regular chow diet (n = 30 males and n = 15 females) and maintained for 14 weeks. Similar to our lifelong exposure study (manuscript currently under revision at Scientific Reports), we carried out several non-invasive measurements, including body weight and glucose metabolism. We found in utero exposure to nPM led to differences in the body weight gains after weaning and out to 14 weeks of age, with more pronounced effects in females than males. The increase in body weight in females was mostly attributable to increased fat mass, particularly at 12 and 16 weeks of age. By comparison, nPM effects on body composition in males were no longer observed at 16 weeks of age. This was accompanied by both male and female nPM-exposed mice exhibiting impaired glucose clearance after being administered intraperitoneal glucose tolerance tests, with significantly higher area under the glucose tolerance curve than control-exposed mice. We are now in the process of characterizing various tissues with respect to gene expression and cell biology traits to determine whether changes in these phenotypes could explain the mechanism for the observed whole-body physiological differences. Interestingly, male mice exposed to nPM showed a 77 percent reduction in neurogenesis in the dentate gyrus of the hippocampus as measured by EdU-positive cells colocalized with NeuN. However, astrogenesis, measured by EdU-positive cells colocalized with GFAP, and the total number of EdU-positive cells was not altered by nPM exposure.

3. Significance

In summary, our data indicate that mice fed a chow fat with exposure to nPM in utero exhibit increased accumulation of adipose tissue, possibly through increased food intake, and decreased glucose clearance that is likely the result of increased IR at the level of adipose tissue. However, we do not believe these metabolic abnormalities are due to differences in the inflammatory profile of adipose. Furthermore, the similarity of these metabolic effects to those from our whole-life exposure study suggest that in utero exposure to nPM is sufficient to disturb metabolic homeostasis. The results of these studies will also be of direct relevance to those collected in humans as part of Projects 1 and 2, and more broadly could have important implications for the observed associations between traffic-related air pollution exposure and obesity-related outcomes in children.

Administrative Core

1. Specific Aims

The primary goal of the Administrative Core is to provide an efficient infrastructure coordinating and facilitating activities across the Center and to promote scientific integration and community engagement. Drs. Rob McConnell and Michael Goran provide leadership to achieve these goals, bringing expertise in environmental health and childhood obesity/metabolic function, respectively. The goal of the Core is to ensure multidisciplinary interactions among basic, clinical and public health scientists and community outreach faculty and staff to enhance a world-class research and outreach program in children’s health. Major goals are as follow:

Aim 1. Coordinate a program of research that integrates state-of-the-art exposure assessment with innovative health effects research to achieve rapid advances in understanding the impact of air pollution on childhood obesity and metabolic dysregulation.The Core mechanisms will facilitate maturing collaboration between two University of Southern California (USC) teams conducting research on (1) exposure assessment and health effects of air pollution in children and (2) childhood obesity and diabetes. An important resource is the rich institutional scientific environment, including complementary centers and an administrative infrastructure that will be leveraged to co-sponsor seminars and workshops and build scientific synergy within and outside the Center.

Aim 2. Facilitate the translation/application of research findings to prevention, policy and clinical decision-making arenas and provide valuable information to communities, clinicians and policymakers.The Core will provide administrative support to community engagement activities and to the Pediatric Health Specialist to help identify scientific and outreach opportunities for enhancing translation of Center research findings.

Aim 3. Provide fiscal management and reporting and coordinate interactions with the National Institute of Environmental Health Sciences (NIEHS) and the U.S. Environmental Protection Agency (EPA).The Core will manage all aspects of the budget, including subcontracts, and will assist the research projects and the Community Outreach and Translation Core (COTC) with purchasing and reimbursements. The Core will prepare all reports and coordinate with NIEHS and EPA.

Aim 4. Foster the career development program of junior investigators into independent contributors to pediatric environmental health research.The Core will coordinate a robust career development program to promote the progress of the faculty development investigator to research independence. They will provide opportunities for mock peer review of grant applications, review of presentation skills, and networking with other investigators within the USC research community and beyond. Career development activities have been part of the existing Southern California Environmental Health Sciences Center (SCEHSC), a program that ranked highly in that center’s external review. In addition, participation in COTC activities will be an opportunity to develop skills in non-technical presentations that will be a valuable career asset.

Aim 5. Make important contributions to national networks that foster communication, innovation and research excellence in the area of children’s environmental health.The Core, COTC and SC-CEHC leadership will participate in conference calls and the annual meetings of SC-CEHC directors. Opportunities for inter-center collaboration will be sought. In addition, SC-CEHC investigators will participate in national conference calls including those of the NIEHS Programs in Environmental Public Health Network, and of other groups, to present the SC-CEHC’s most recent research findings on air pollution, obesity and metabolic consequences.

2. Studies and Results

Administratively, an Executive Committee consisting of the SC-CEHC Director, Deputy Director, Project and COTC Directors, the Public Health Specialist, and the Center Administrator integrates the perspective of exposure assessment, air pollution health effects, childhood obesity and diabetes. The Executive Committee continues to meet monthly to foster scientific interaction and coordinate internal/external activities. Activities and challenges in each project and core are reviewed, and at the conclusion of the meeting a more in-depth review of one project analysis or of an emerging area of research is presented, usually by a postdoctoral or graduate student in an informal setting designed to foster collaboration. These informal seminars are complementary to seminars co-organized with the Diabetes and Obesity Research Institute, the NIEHS-supported SCEHSC, and the Air Pollution and Brain Initiative focused on the role of the brain as a target organ for obesogenic and metabolic effects of air pollution.

The Core External Advisory Committee continues to consist of Dr. Staci Bilbo from Duke University, Dr. Andrew Rundle from Columbia University, Dr. Michael Brauer from the University of British Columbia, Dr. David Diaz-Sanchez from the EPA Office of Research and Development, and Mr. Angelo Logan from Occidental College. The committee will not meet formally during the no-cost extension period, but individual committee members continue to provide advice at the request of the Executive Committee as issues in their area of expertise arise.

The Core has provided administrative support to a wide variety of activities led by the COTC, including the Public Health Specialist, that have facilitated the translation of research findings to communities, clinicians and policymakers. An inter-center partnership (USC; University of Illinois; Emory University; Columbia University; and University of California [UC], San Francisco) has developed materials for efforts to use social media more effectively for communicating health risk and the results of Center research. A training session by this social media working group (SWG) for other Centers was held at the conclusion of the yearly Children’s Centers meeting in RTP in October. A major effort was the organization of a conference on Parks, Obesity and Air Pollution, which brought together community groups, planners and urban design experts from academia and commerce, policy makers, and Center scientists. A rich collaboration has resulted that is focused on integrating considerations of air pollution into planning efforts to redevelop Southern California and into plans for new parks funded by a recent bond initiative. Other activities, including development of internships for high school students, undergraduates and graduate students, as well as presentations in various communities, are ongoing. Center members also continue to be interviewed in traditional media. Additional details are provided in the COTC report.

A key task of the Core leadership and staff is responsibility for fiscal management/reporting and for coordinating interactions and reports with NIEHS/EPA. The Administrative Core continues to administer all financial aspects of the Center, purchasing, reimbursement, and progress and other reports to NIEHS and EPA.

The Center supported Rima Habre, the Center Faculty Development Investigator (5% in the Administrative Core and 20% in Project 1), to develop exposure models for the Center, especially for Project 1. In the no-cost extension, the Center is providing support to Leda Chatzi, an early-stage investigator recently recruited to USC from the University of Heraklion in Crete. She is helping develop new directions for the Center on endocrine-disrupting chemicals and metabolic disease for a possible renewal application.

Center members have been active contributors to the annual and monthly meetings of investigators from all CEH Centers. Several junior investigators or postdoctoral students presented at the International Society for Environmental Epidemiology on topics ranging from environmental determinants of NAFLD to new strategies for community engagement in air pollution health science. Several inter-center collaborations, in addition to the SWG, continue, including with the UC Davis Center around autism and neurocognitive effects of air pollution. A collaboration with the Columbia University and Johns Hopkins University Centers recently resulted in a publication evaluating new biological markers of near-roadway pollution exposure using archived blood samples.

3. Significance

The Core coordinates a shared Career Development Program (CDP) with the SCEHSC that promotes the progress of postdoctoral fellows, the FDI and other junior faculty in both Centers to research independence. The CDP Director is the Center Director, Dr. McConnell. The CDP continues to provide broad opportunities for mock peer review of grant applications, response to reviews and resubmissions, review of presentation skills, and sessions with the COTC on opportunities for participation in outreach and in dealing with the press in the context of recent papers on Center research. The Core organizes a small group (junior investigator only) networking opportunity with senior investigators visiting or presenting to NIEHS-supported (and other EH) seminars. Complementary activities supported partially by the Administrative Core are described in the COTC report. Several Center junior investigators have received F31, F32 and K awards.

Community Outreach and Translation Core

1. Specific Aims

The COTC’s goal is to protect children’s health through educating new constituencies to understand the complex land use, public health and public policy dilemma between the need for increased outdoor physical activity to reduce obesity and the potential risks of active recreation near traffic pollution. The COTC is an integral part of the SC-CEHC, with the COTC director a member of the Center’s Executive Committee, which meets monthly.

Aim 1. Develop new constituencies and new media outlets for dissemination of research findings on NRAP and its adverse health effects on children, including (a) advocates of physical activity to reduce obesity and (b) advocates for new parks and outdoor exercise facilities and equitable access to green space in the city, including elected officials, urban planners, architects/landscape architects, land conservation and environmental justice groups.

Aim 2. Build civic engagement in environmental health around the issues of air pollution and physical activity by using youth-based participatory engagement techniques, working with youth from two communities with significant NRAP and high obesity rates.

Aim 3. Enhance the capacity of current community partners, new constituencies and youth to educate policymakers about the need to consider research findings on the adverse health effects of near-roadway air pollution, including obesity, when (a) siting new facilities to encourage physical activity, (b) expanding or building new highways or major roads close to where children play or exercise, and (c) considering new regulations to reduce air pollution to protect children’s health.

Aim 4. Evaluate COTC efforts and share successful strategies and models with others at the local and national level; meet with community advisors and a formal community advisory committee.

2. Studies and Results

The COTC aims to serve as a bridge between the scientists in the SC-CEHC and the public so that the public better understands concerns about near roadway air pollution, especially the potential impacts of air pollution, obesity and metabolic outcomes. We aim to engage a broad array of stakeholders, from health professionals to architects, urban planners and youth.

Over the past year, the COTC continued to partner with community organizations throughout the greater LA area. These targeted areas face high ambient air pollution, cumulative environmental burdens and health disparities, and a lack of open space and parks. Working with the organizations and utilizing participatory engagement techniques, the COTC developed and implemented a participatory air pollution monitoring program with youth from environmental justice communities around urban LA, conducted popular education-based air pollution monitoring workshops and activities around LA to environmental justice and community health-based organizations, and local high school and college students. We have reached over 1,200 residents in the past year through events, workshops and trainings.

Air Pollution and Community Workshops

Several organizations have partnered with the COTC to investigate air pollution in their neighborhoods through community air monitoring, including the Clean Air Coalition of North Whittier and Avocado Heights, East Yard Communities for Environmental Justice (EYCEJ), Long Beach Alliance for Children with Asthma, Communities for a Better Environment, South Central Youth Leadership Coalition, Asian Pacific Islander Forward Movement, and Legacy LA.

During the past year, the COTC redeveloped their air pollution monitoring curriculum and developed a manual for how to operate AirBeams, low cost real-time PM2.5 sensors. The curriculum included environmental health and justice, goods movement, sources of PM, health effects of NRAP and the positive benefits of urban green space. The curriculum is rooted in a popular education framework that engages participants through their own lived experiences.

Participants in air monitoring workshops received a hands-on air monitoring activity, including training on how to operate and understand AirBeams and the P-trak ultrafine particle counter. Participants developed a hypothesis and then chose parks or schools near hot spots of traffic in their neighborhoods, as well as comparison locations. They were trained on the use of real-time ultra-fine particle monitors and conducted monitoring at several locations in the area near the workshop.

Monitoring activities were also conducted in the context of educational leadership institute activities. We engaged with hundreds of students at Occidental College, University of Southern California and California State University, Los Angeles targeting students from low-income communities of color. Additionally, COTC staff conducted several workshops with students in grades 3-8 at Andrews School in North Whittier along a goods movement corridor. Through a connection with the Clean Air Coalition of North Whittier and Avocado Heights, these workshops fed into a GATE (honors) student project about Air Pollution, during which COTC supported students with air monitors and air pollution education resources and gave project topic ideas to students who then performed independent air quality related projects with guidance from their GATE teacher. The project culminated with a student poster session attended by 25 students and 75 parents and teachers.

COTC staff presented air pollution workshops and conducted monitoring activities at several environmental justice youth conferences in East LA hosted by Legacy LA and in Southeast LA hosted by Communities for a Better Environment.

Community partner EYCEJ continues to call upon the COTC to educate their members about air pollution monitoring as they ask questions about their exposures along the I-710 goods movement corridor and in the port community of West Long Beach. To that end, the COTC supported two toxic tours hosted by EYCEJ via bike route. The COTC outfitted bike tour participants with AirBeams to record PM2.5 exposures throughout the half-day and day-long tours. Debrief meetings after the conclusion of the tours are done either on the same day or soon after to discuss monitoring data, participant observations, and community questions and concerns. Together, this information is used in presentations to educate other residents about air pollution, as well as inform plans for projects to reduce air pollution and examine the needs for more green space. The AirBeam manual that the COTC developed was disseminated during air pollution monitoring activities and projects and shared with users across the country.

The COTC co-facilitated a bus tour with the local community-based organizations to show members of EPA, CalEPA, South Coast Air Quality Management District and public health offices environmental health concerns related to siting housing and parks near freeways and other industrial activities. Over 50 people participated, and 10 community members gave testimony to the public officials during the tour.

A Day in the Life Program

Launched in summer 2017, “A Day in the Life” was developed as part of a collaboration with USC and community-based organizations with high school youth memberships. With a goal to increase environmental health literacy, collect community-owned data and promote awareness about exposures to pollution at the neighborhood level in environmental justice, youth participated in a series of workshops. In these workshops, participants learned about air pollution, PM2.5, sources of pollution and the impacts on health. Participants were trained to use AirBeams, low-cost portable air monitoring devices, to record the air pollution along their daily routes of travel from their homes to school and around their communities. In collaboration with Sandy Navarro of LA Grit Media, students also participated in a Storytelling for Social Change workshop, where they learned the skills needed to capture and craft a story, such as story boarding, framing shots, and becoming familiar with photo and video editing tools.

Participating youth were already involved and connected with USCEHC community partners, including Communities for a Better Environment; South Central Youth Leadership Coalition; and Promoting Youth Advocacy, a school-based club in Alhambra that long-time partner Asian and Pacific Islander Forward Movement works with. All communities were located near freeways and ports, and 17 youth participated. More information about the program can be found on the program website: https://envhealthcenters.usc.edu/resources/community-air-monitoring/a-day-in-the-life and in a blog post: https://envhealthcenters.usc.edu/2018/08/dayinthelife2018.html.

Program youth-based projects are showcased on the Day in the Life StoryMap here: http://arcg.is/CXfen.

The initial program year culminated with a youth event, LA Youth for Environmental Justice Forum (https://envhealthcenters.usc.edu/2018/08/layouth4ejevent.html%20%E2%80%8E) that showcased participant projects and featured most program participants on a panel describing their experiences and lessons learned as a result of their participation. Over 100 youth and families participated in this day-long youth-led event, which fostered cross-neighborhood collaboration.

Social Media Workgroup: A Collaboration Between Children’s Centers

COTC staff Wendy Gutschow assumed a leadership role within the cross-center collaboration around children’s environmental health messaging and CEHC research dissemination on social media. The SMW began as a result of the charge to COTCs at the October 2017 CEHC meeting in San Francisco to disseminate the contents of the Children’s Environmental Health Impact Report. The workgroup began by creating social media content from the Impact Report to be used by all CEHCs. In spring 2018, the collaborative group applied for and received Administrative Supplement funding from NIEHS. The funding of the work has enabled the group to expand their capacity to include social media assessment, training and capacity building for CEHCs and other environmental health centers and PEHSUs.

Parks, Green Spaces and Urban Design

Obesity is a public health problem of epidemic proportions in California and elsewhere in the country, resulting in illness, disease and huge costs. In Los Angeles County, developing obesity is strongly associated with economic hardship; that is, obesity most heavily impacts working poor and communities of color. These same communities face the highest cumulative burden of environmental pollution and the least park space per resident. Recognizing the complexity of these problems, we developed a collaboration with the USC urbanism and landscape architect program and local landscape firms to expand experts engaged in this issue. We have hosted three meetings among a diverse set of actors interested in exploring the “collision of best intentions” between parks and pollution.

As a result of this ongoing collaboration, the COTC hosted USC landscape architecture and urbanism Master's students at the SC-CEHC to frame the context of environmental health impacts on the built environment, including siting of parks and urban green space, and giving the students a broader perspective on NRAP and its effects on public health. Later in the year, the COTC staff members and Rob McConnell served as panelists for USC landscape architecture and urbanism Master's students' final project presentations.

The Outreach Core has continued to keep informed about projects regarding parks improvement and development in LA through the Los Angeles County Parks Needs Assessment. The Core has developed a new partnership with local Boyle Heights/East LA nonprofit Promesa Boyle Heights, an organization that provides leadership development to community members around issues of park equity and access. The Core has implemented workshops and arranged trainings with community volunteers to learn more about air pollution impacts in their community.

At the request of the LA City Council, COTC Director and Center Scientists spoke to the City Council and the Planning and Land-Use Committee to answer questions regarding traffic-related air pollution, discuss health effects associated with building housing adjacent to busy roadways, and evaluate design and policies to protect public health. We met on four occasions with the public officials at their invitation to discuss this and ongoing research findings.

3. Significance

The COTC holds trainings, workshops and conferences to disseminate research and hear from the community. The COTC is often asked to make presentations, including speaking at parent meetings at schools, community asthma coalition meetings and meetings about EH disparities. The COTC has also developed expertise in the multimedia area, training community members to develop videos telling stories about their communities’ concerns or their achievements, and also in developing print and online interactive infographics on EH topics. The COTC has implemented community participatory pollution monitoring programs for community volunteers and students.

The COTC has refined its methodology for communicating science through infographics. In collaboration with community partners, we have developed and published multiple bilingual infographics focused on air pollution, parks and health, green cleaning products, neighborhood oil drilling, goods movement, the Salton Sea, lead, and arsenic. The materials have been featured at several community events and professional conferences and highlighted through social media.

The COTC documents its work and shares information through online media, including the Environmental Health blog with current news, events, research projects and outreach activities: https://envhealthcenters.usc.edu.

 

Future Activities:

Project 1: Effects of Air Pollution on the Development of Obesity in Children

We will continue to investigate the effects of prenatal, early and later childhood exposure traffic-related air pollutant on metabolic outcomes (Aims 2 and 3). We are analyzing the data and will be preparing manuscripts to report findings.

Project 2: Near-Roadway Air Pollution, Adipose Inflammation and Metabolic Consequences

The coming year will be focused on conducting all remaining assays on the final data set and completing analyses and manuscripts.

Project 3: Longitudinal Effects of Air Pollution on Obesity in Mice

Based on our findings from the whole-life and prenatal exposure studies, we have chosen to focus more on the prenatal period as a developmental window that is particularly vulnerable to the effects of nPM. Therefore, our plans during the last year of Project 3 are to further characterize the prenatal period with respect to other pollutants, such as polycyclic aromatic hydrocarbons, that have also been associated with obesity-related traits and other adverse health outcomes. Based on the exposure studies thus far and feedback from the external advisory committee, we will focus mostly on using a chow diet, since nPM reproducibly affected metabolic homeostasis under these conditions, and we wish to exclude any confounding effects of combining exposures with an obesifying diet. However, we will still consider a high fat-fed group of mice as well, possibly by using a diet that has lower fat content. In combination with the results from the already completed whole-life and prenatal exposure studies using nPM, we expect to obtain additional insight into the critical windows of susceptibility during development that are important for exposure to NRAP.

Administrative Core

The Administrative Core is functioning well. The coming year will be focused on supporting the Projects and the COTC to complete all analyses and manuscripts and to provide investigators with administrative support in planning for new directions based on results to date. Activities of the COTC, described in the COTC progress report, will continue to be supported. The Core will provide fiscal management and reporting. Administrative Core and other Center investigators will continue to contribute to inter-Center meetings and inter-center collaboration.

Community Outreach and Translation Core

The COTC will continue to respond to invitations to speak at community meetings and conferences, respond to technical assistance requests, and update community and political stakeholders on the latest research coming out of the center and on related children’s environmental health topics. We anticipate actively engaging with communities developing air pollution trainings and community air monitoring in Southern California through the AB 617 legislation. We continue to leverage relationships with urban planners to engage in dialogue about the role of air pollution in land-use decisionmaking. We are actively working with community organizations to support adding new PM monitors to parks in Long Beach and Alahambra cities. We expect to develop a manuscript on the Day in the Life program and best practices for youth-based participatory air monitoring.


Journal Articles: 59 Displayed | Download in RIS Format

Other center views: All 62 publications 59 publications in selected types All 59 journal articles
Type Citation Sub Project Document Sources
Journal Article Alderete TL, Autran C, Brekke BE, Knight R, Bode L, Goran MI, Fields DA. Associations between human milk oligosaccharides and infant body composition in the first 6 mo of life. American Journal of Clinical Nutrition 2015;102(6):1381-1388. R835441 (2016)
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  • Journal Article Alderete TL, Habre R, Toledo-Corral CM, Berhane K, Chen Z, Lurmann FW, Weigensberg MJ, Goran MI, Gilliland FD. Longitudinal associations between ambient air pollution with insulin sensitivity, β-cell function, and adiposity in Los Angeles Latino children. Diabetes 2017;66(7):1789-1796. R835441 (2018)
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  • Journal Article 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. R835441 (2018)
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  • Journal Article Alderete TL, Song AY, Bastain T, Habre R, Toledo-Corral CM, Salam MT, Lurmann F, Gilliland FD, Breton CV. Prenatal traffic-related air pollution exposures, cord blood adipokines and infant weight. Pediatric Obesity 2018:13(6):348-356. R835441 (2018)
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  • Journal Article Allayee H, Hazen SL. Contribution of gut bacteria to lipid levels: another metabolic role for microbes? Circulation Research 2015;117(9):750-754. R835441 (2016)
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  • Journal Article Berger PK, Fields DA, Demerath EW, Fujiwara H, Goran MI. High-fructose corn-syrup-sweetened beverage intake increases 5-hour breast milk fructose concentrations in lactating women. Nutrients 2018;10(6):669 (9 pp.). R835441 (2018)
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  • Journal Article Bouret S, Levin BE, Ozanne SE. Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity. Physiological Reviews 2015;95(1):47-82. R835441 (2016)
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  • Journal Article Breton CV, Mack WJ, Yao J, Berhane K, Amadeus M, Lurmann F, Gilliland F, McConnell R, Hodis HN, Kunzli N, Avol E. Prenatal air pollution exposure and early cardiovascular phenotypes in young adults. PLoS One 2016;11(3):e0150825 (12 pp.). R835441 (2016)
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  • Journal Article Chen Z, Salam MT, Toledo-Corral C, Watanabe RM, Xiang AH, Buchanan TA, Habre R, Bastain TM, Lurmann F, Wilson JP, Trigo E, Gilliland FD. Ambient air pollutants have adverse effects on insulin and glucose homeostasis in Mexican Americans. Diabetes Care 2016;39(4):547-554. R835441 (2016)
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  • Journal Article Chen Z, Salam MT, Alderete TL, Habre R, Bastain TM, Berhane K, Gilliland FD. Effects of childhood asthma on the development of obesity among school-aged children. American Journal of Respiratory and Critical Care Medicine 2017;195(9):1181-1188. R835441 (2018)
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  • Journal Article Cheng H, Davis DA, Hasheminassab S, Sioutas C, Morgan TE, Finch CE. Urban traffic-derived nanoparticulate matter reduces neurite outgrowth via TNFα in vitro. Journal of Neuroinflammation 2016;13:19 (11 pp.). R835441 (2016)
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  • Journal Article Cho J, Goldenson NI, Pester MS, Khoddam R, Bello MS, Dunton GF, Belcher BR, Leventhal AM. Longitudinal associations between anhedonia and body mass index trajectory groups among adolescents. Journal of Adolescent Health 2018;63(1):81-87. R835441 (2018)
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  • Journal Article Cui X, Gong J, Han H, He L, Teng Y, Tetley T, Sinharay R, Chung KF, Islam T, Gilliland F, Grady S, Garshick E, Li Z, Zhang JJ. Relationship between free and total malondialdehyde, a well-established marker of oxidative stress, in various types of human biospecimens. Journal of Thoracic Disease 2018;10(5):3088-3097. R835441 (2018)
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  • Journal Article Dueker D, Taher M, Wilson J, McConnell R. Evaluating children's location using a personal GPS logging instrument: limitations and lessons learned. Journal of Exposure Science and Environmental Epidemiology 2014;24(3):244-252. R835441 (2015)
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  • Journal Article Dunton GF, O'Connor SG, Belcher BR, Maher JP, Schembre SM. Objectively-measured physical activity and sedentary time are differentially related to dietary fat and carbohydrate intake in children. Frontiers in Public Health 2018;6:198 (6 pp.). R835441 (2018)
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  • Journal Article Fruin S, Urman R, Lurmann F, McConnell R, Gauderman J, Rappaport E, Franklin M, Gilliland FD, Shafer M, Gorski P, Avol E. Spatial variation in particulate matter components over a large urban area. Atmospheric Environment 2014;83:211-219. R835441 (2015)
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  • Journal Article Ghazalpour A, Cespedes I, Bennett BJ, Allayee H. Expanding role of gut microbiota in lipid metabolism. Current Opinion in Lipidology 2016;27(2):141-147. R835441 (2016)
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  • Journal Article Ghosh R, Lurmann F, Perez L, Penfold B, Brandt S, Wilson J, Milet M, Kunzli N, McConnell R. Near-roadway air pollution and coronary heart disease: burden of disease and potential impact of a greenhouse gas reduction strategy in Southern California. Environmental Health Perspectives 2016;124(2):193-200. R835441 (2016)
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  • Journal Article Ghosh R, Gauderman WJ, Minor H, Youn HA, Lurmann F, Cromar KR, Chatzi L, Belcher B, Fielding CR, McConnell R. Air pollution, weight loss and metabolic benefits of bariatric surgery: a potential model for study of metabolic effects of environmental exposures. Pediatric Obesity 2018;13(5):312-320. R835441 (2017)
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  • Journal Article Goran MI, Martin AA, Alderete TL, Fujiwara H, Fields DA. Fructose in breast milk is positively associated with infant body composition at 6 months of age. Nutrients 2017;9(2)146 (11 pp.). R835441 (2018)
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  • Journal Article Habre R, Zhou H, Eckel SP, Enebish T, Fruin S, Bastain T, Rappaport E, Gilliland F. Short-term effects of airport-associated ultrafine particle exposure on lung function and inflammation in adults with asthma. Environment International 2018;118:48-59. R835441 (2018)
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  • Journal Article Hasson RE, Hsu YJ, Davis JN, Goran MI, Spruijt-Metz D. The influence of parental education on dietary intake in Latino youth. Journal of Immigrant and Minority Health 2018;20(1):250-254. R835441 (2018)
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  • Journal Article Hsieh S, Klassen AC, Curriero FC, Caulfield LE, Cheskin LJ, Davis JN, Goran MI, Weigensberg MJ, Spruijt-Metz D. Built environment associations with adiposity parameters among overweight and obese Hispanic youth. Preventive Medicine Reports 2015;2:406-412. R835441 (2016)
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  • Journal Article Hsieh S, Leaderer BP, Feldstein AE, Santoro N, McKay LA, Caprio S, McConnell R. Traffic-related air pollution associations with cytokeratin-18, a marker of hepatocellular apoptosis, in an overweight and obese paediatric population. Pediatric Obesity 2018;13(6):342-347. R835441 (2017)
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  • Journal Article Hsu TM, Konanur VR, Taing L, Usui R, Kayser BD, Goran MI, Kanoski SE. Effects of sucrose and high fructose corn syrup consumption on spatial memory function and hippocampal neuroinflammation in adolescent rats. Hippocampus 2015;25(2):227-239. R835441 (2016)
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  • Journal Article Jerrett M, Shankardass K, Berhane K, Gauderman WJ, Künzli N, Avol E, Gilliland F, Lurmann F, Molitor JN, Molitor JT, Thomas DC, Peters J, McConnell R. Traffic-related air pollution and asthma onset in children: a prospective cohort study with individual exposure measurement. Environmental Health Perspectives 2008;116(10):1433-1438. R835441 (2017)
    R831861 (Final)
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  • Journal Article Jerrett M, McConnell R, Wolch J, Chang R, Lam C, Dunton G, Gilliland F, Lurmann F, Islam T, Berhane K. Traffic-related air pollution and obesity formation in children: a longitudinal, multilevel analysis. Environmental Health 2014;13:49 (9 pp.). R835441 (2015)
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  • Journal Article Kayser BD, Goran MI, Bouret SG. Perinatal overnutrition exacerbates adipose tissue inflammation caused by high-fat feeding in C57BL/6J mice. PLoS One 2015;10(3):e0121954 (15 pp.). R835441 (2016)
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  • Journal Article Kayser BD, Toledo-Corral CM, Alderete TL, Weigensberg MJ, Goran MI. Temporal relationships between adipocytokines and diabetes risk in Hispanic adolescents with obesity. Obesity 2015;23(7):1479-1485. R835441 (2016)
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  • Journal Article Kim JS, Alderete TL, Chen Z, Lurmann F, Rappaport E, Habre R, Berhane K, Gilliland FD. Longitudinal associations of in utero and early life near-roadway air pollution with trajectories of childhood body mass index. Environmental Health 2018;17(1):64 (10 pp.). R835441 (2018)
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  • Journal Article Kim JY, Goran MI, Toledo-Corral CM, Weigensberg MJ, Shaibi GQ. Comparing glycemic indicators of prediabetes: a prospective study of obese Latino Youth. Pediatric Diabetes 2015;16(8):640-643. R835441 (2016)
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  • Journal Article Li L, Lurmann F, Habre R, Urman R, Rappaport E, Ritz B, Chen JC, Gilliland FD, Wu J. Constrained mixed-effect models with ensemble learning for prediction of nitrogen oxides concentrations at high spatiotemporal resolution. Environmental Science & Technology 2017;51(17):9920-9929. R835441 (2018)
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  • Journal Article Lopez NV, Schembre S, Belcher BR, O'Connor S, Maher JP, Arbel R, Margolin G, Dunton GF. Parenting styles, food-related parenting practices, and children's healthy eating: a mediation analysis to examine relationships between parenting and child diet. Appetite 2018;128:205-213. R835441 (2018)
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  • Journal Article Luo S, O'Connor SG, Belcher BR, Page KA. Effects of physical activity and sedentary behavior on brain response to high-calorie food cues in young adults. Obesity 2018;26(3):540-546. R835441 (2018)
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  • Journal Article Lurmann F, Avol E, Gilliland F. Emissions reduction policies and recent trends in Southern California's ambient air quality. Journal of the Air & Waste Management Association 2015;65(3):324-335. R835441 (2016)
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  • Journal Article McConnell R, Shen E, Gilliland FD, Jerrett M, Wolch J, Chang C-C, Lurmann F, Berhane K. A longitudinal cohort study of body mass index and childhood exposure to secondhand tobacco smoke and air pollution: the Southern California Children's Health Study. Environmental Health Perspectives 2015;123(4):360-366. R835441 (2015)
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  • Journal Article McConnell R, Gilliland FD, Goran M, Allayee H, Hricko A, Mittelman S. Does near-roadway air pollution contribute to childhood obesity? Pediatric Obesity 2016;11(1):1-3. R835441 (2015)
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  • Journal Article Noble EE, Hsu TM, Jones RB, Fodor AA, Goran MI, Kanoski SE. Early-life sugar consumption affects the rat microbiome independently of obesity. The Journal of Nutrition 2017;147(1):20-28. R835441 (2018)
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  • Journal Article O'Connor SG, Ke W, Dzubur E, Schembre S, Dunton GF. Concordance and predictors of concordance of children's dietary intake as reported via ecological momentary assessment and 24 h recall. Public Health Nutrition 2018;21(6):1019-1027. R835441 (2018)
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  • Journal Article O'Reilly GA, Belcher BR, Davis JN, Martinez LT, Huh J, Antunez-Castillo L, Weigensberg M, Goran MI, Spruijt-Metz D. Effects of high-sugar and high-fiber meals on physical activity behaviors in Latino and African American adolescents. Obesity 2015;23(9):1886-1894. R835441 (2016)
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  • Journal Article Pomatto LCD, Cline M, Woodward N, Pakbin P, Sioutas C, Morgan TE, Finch CE, Forman HJ, Davies KJA. Aging attenuates redox adaptive homeostasis and proteostasis in female mice exposed to traffic-derived nanoparticles ('vehicular smog'). Free Radical Biology and Medicine 2018;121:86-97. R835441 (2018)
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  • Journal Article Ritz B, Qiu J, Lee PC, Lurmann F, Penfold B, Erin Weiss R, McConnell R, Arora C, Hobel C, Wilhelm M. Prenatal air pollution exposure and ultrasound measures of fetal growth in Los Angeles, California. Environmental Research 2014;130:7-13. R835441 (2015)
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  • Journal Article Shankardass K, McConnell R, Jerrett M, Lam C, Wolch J, Milam J, Gilliland F, Berhane K. Parental stress increases body mass index trajectory in pre-adolescents. Pediatric Obesity 2014;9(6):435-442. R835441 (2015)
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  • Journal Article Smallwood T, Allayee H, Bennett BJ. Choline metabolites: gene by diet interactions. Current Opinion in Lipidology 2016;27(1):33-39. R835441 (2017)
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  • Journal Article Su JG, Jerrett M, McConnell R, Berhane K, Dunton G, Shankardass K, Reynolds K, Chang R, Wolch J. Factors influencing whether children walk to school. Health & Place 2013;22:153-161. R835441 (2015)
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  • Journal Article Tellez-Rojo MM, Bellinger DC, Arroyo-Quiroz C, Lamadrid-Figueroa H, Mercado-Garcia A, Schnaas-Arrieta L, Wright RO, Hernandez-Avila M, Hu H. Longitudinal associations between blood lead concentrations lower than 10 μg/dL and neurobehavioral development in environmentally exposed children in Mexico City. Pediatrics 2006;118(2):e323-e330. R835441 (2017)
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  • Journal Article Toledo-Corral CM, Alderete TL, Richey J, Sequeira P, Goran MI, Weigensberg MJ. Fasting, post-OGTT challenge, and nocturnal free fatty acids in prediabetic versus normal glucose tolerant overweight and obese Latino adolescents. Acta Diabetologica 2015;52(2):277-284. R835441 (2016)
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  • Journal Article Toledo-Corral CM, Alderete TL, Habre R, Berhane K, Lurmann FW, Weigensberg MJ, Goran MI, Gilliland FD. Effects of air pollution exposure on glucose metabolism in Los Angeles minority children. Pediatric Obesity 2018;13(1):54-62. R835441 (2018)
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  • Journal Article Urman R, Gauderman J, Fruin S, Lurmann F, Liu F, Hosseini R, Franklin M, Avol E, Penfold B, Gilliland F, Brunekreef B, McConnell R. Determinants of the spatial distributions of elemental carbon and particulate matter in eight Southern Californian communities. Atmospheric Environment 2014;86:84-92. R835441 (2015)
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  • Journal Article Urman R, McConnell R, Islam T, Avol EL, Lurmann FW, Vora H, Linn WS, Rappaport EB, Gilliland FD, Gauderman WJ. Associations of children's lung function with ambient air pollution: joint effects of regional and near-roadway pollutants. Thorax 2014;69(6):540-547. R835441 (2015)
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  • Journal Article Vos MB, Goran MI. Sugar, sugar ... not so sweet for the liver.Gastroenterology 2017;153(3):642-645. R835441 (2018)
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  • Journal Article Wang P, Tuvblad C, Younan D, Franklin M, Lurmann F, Wu J, Baker LA, Chen JC. Socioeconomic disparities and sexual dimorphism in neurotoxic effects of ambient fine particles on youth IQ: a longitudinal analysis. PLoS One 2017;12(12):e0188731 (15 pp.). R835441 (2018)
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  • Journal Article Wheelock K, Zhang JJ, McConnell R, Tang D, Volk HE, Wang Y, Herbstman JB, Wang S, Phillips DH, Camann D, Gong J, Perera F. A novel method for source-specific hemoglobin adducts of nitro-polycyclic aromatic hydrocarbons. Environmental Science: Processes & Impacts 2018;20(5):780-789. R835441 (2018)
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  • Journal Article Wu W, Muller R, Berhane K, Fruin S, Liu F, Jaspers I, Diaz-Sanchez D, Peden DB, McConnell R. Inflammatory response of monocytes to ambient particles varies by highway proximity. American Journal of Respiratory Cell and Molecular Biology 2014;51(6):802-809. R835441 (2015)
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  • Journal Article Younan D, Tuvblad C, Li L, Wu J, Lurmann F, Franklin M, Berhane K, McConnell R, Wu AH, Baker LA, Chen JC. Environmental determinants of aggression in adolescents: role of urban neighborhood greenspace. Journal of the American Academy of Child and Adolescent Psychiatry 2016;55(7):591-601. R835441 (2018)
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  • Journal Article Younan D, Tuvblad C, Franklin M, Lurmann F, Li L, Wu J, Berhane K, Baker LA, Chen JC. Longitudinal analysis of particulate air pollutants and adolescent delinquent behavior in Southern California. Journal of Abnormal Child Psychology 2018;46(6):1283-1293. R835441 (2018)
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  • Journal Article Zigman JM, Bouret SG, Andrews ZB. Obesity impairs the action of the neuroendocrine ghrelin system. Trends in Endocrinology and Metabolism 2016;27(1):54-63. R835441 (2016)
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  • Journal Article Zink J, Belcher BR, Dzubur E, Ke W, O'Connor S, Huh J, Lopez N, Maher JP, Dunton GF. Association between self-reported and objective activity levels by demographic factors: ecological momentary assessment study in children. JMIR mHealth and uHealth 2018;6(6):e150 (12 pp.). R835441 (2018)
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  • Journal Article Volk HE, Lurmann F, Penfold B, Hertz-Picciotto I, McConnell R. Traffic related air pollution, particulate matter, and autism. JAMA Psychiatry 2013;70(1):71-77. R835441 (2017)
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  • Progress and Final Reports:

    Original Abstract
  • 2014 Progress Report
  • 2015 Progress Report
  • 2016 Progress Report
  • 2017 Progress Report