UG3OD035550
Cooperative Agreement
Overview
Grant Description
Prenatal Environment and Child Health (PEACH) in ECHO - Prenatal Environment and Child Health (PEACH) in ECHO
Abstract
Few modifiable factors have been identified that improve neurodevelopmental (ND) outcomes. One such factor, supplemental folic acid (SFA), taken before and during the first weeks post-conception, reduced risk for neural tube defects (NTDs) by up to 70% in randomized trials, initiating mandatory food grain fortification and guidelines for SFA intake for people who could or had become pregnant, with subsequent increases in blood folate concentrations and reduced NTD prevalence.
While generally regarded as a public health success, the impacts have not been evenly distributed across sub-populations within the US, with Hispanic populations at higher risk for NTDs, more likely to have suboptimal folate status, and less likely to take SFA. Further, the biologic mechanisms behind this protection remain unclear.
Prenatal SFA and adequate folate status has since been associated with improved behavioral and language outcomes, higher executive functioning, and reduced risk for attention deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and associated traits. High folate/SFA has also been shown to attenuate increased risks associated with several contaminant exposures that are more prevalent in groups that are under-represented in research and/or more likely to have sub-optimal folate status and less likely to meet SFA intake recommendations. One example includes plasticizers in personal care products that are more prevalent in Hispanic populations and are linked to increased ND risk which is attenuated with prenatal SFA.
Many gaps in understanding and implementation of SFA measures need to be addressed to increase the public health impact of SFA interventions to their fullest potential:
1) How does the timing of SFA initiation and its association with blood folate differ across subpopulations?
2) What other child health outcomes are associated with prenatal SFA and blood folate?
3) How do these associations differ by the timing and dose of SFA intake?
4) How do doses and timing of SFA and folate concentrations linked with improved child outcomes differ across people with different genetic, environmental, and nutritional backgrounds?
5) Does periconceptional SFA/folate status modify associations between environmental contaminants, including novel chemicals, and ND outcomes including behavioral problems and high autistic traits?
6) What biologic pathways are modified in utero by periconceptional SFA and suboptimal folate status?
7) How do those biologic pathways relate to known ND pathways?
8) How does the conceiving partner's preconception folate status relate to placenta epigenetics and the child's outcomes?
Our strong team with relevant expertise in reproductive, environmental and nutritional epidemiology, interactions, epigenetics and ND assessment, plus ample experience engaging community partners, will recruit 740 expecting families in Northern California representing diverse racial, ethnic, socioeconomic, genetic, and environmental backgrounds to enrich the ECHO cohort with participants traditionally underrepresented in research to address these gaps and produce findings that will substantially inform public health policies for more effective improvement of child developmental outcomes.
Abstract
Few modifiable factors have been identified that improve neurodevelopmental (ND) outcomes. One such factor, supplemental folic acid (SFA), taken before and during the first weeks post-conception, reduced risk for neural tube defects (NTDs) by up to 70% in randomized trials, initiating mandatory food grain fortification and guidelines for SFA intake for people who could or had become pregnant, with subsequent increases in blood folate concentrations and reduced NTD prevalence.
While generally regarded as a public health success, the impacts have not been evenly distributed across sub-populations within the US, with Hispanic populations at higher risk for NTDs, more likely to have suboptimal folate status, and less likely to take SFA. Further, the biologic mechanisms behind this protection remain unclear.
Prenatal SFA and adequate folate status has since been associated with improved behavioral and language outcomes, higher executive functioning, and reduced risk for attention deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and associated traits. High folate/SFA has also been shown to attenuate increased risks associated with several contaminant exposures that are more prevalent in groups that are under-represented in research and/or more likely to have sub-optimal folate status and less likely to meet SFA intake recommendations. One example includes plasticizers in personal care products that are more prevalent in Hispanic populations and are linked to increased ND risk which is attenuated with prenatal SFA.
Many gaps in understanding and implementation of SFA measures need to be addressed to increase the public health impact of SFA interventions to their fullest potential:
1) How does the timing of SFA initiation and its association with blood folate differ across subpopulations?
2) What other child health outcomes are associated with prenatal SFA and blood folate?
3) How do these associations differ by the timing and dose of SFA intake?
4) How do doses and timing of SFA and folate concentrations linked with improved child outcomes differ across people with different genetic, environmental, and nutritional backgrounds?
5) Does periconceptional SFA/folate status modify associations between environmental contaminants, including novel chemicals, and ND outcomes including behavioral problems and high autistic traits?
6) What biologic pathways are modified in utero by periconceptional SFA and suboptimal folate status?
7) How do those biologic pathways relate to known ND pathways?
8) How does the conceiving partner's preconception folate status relate to placenta epigenetics and the child's outcomes?
Our strong team with relevant expertise in reproductive, environmental and nutritional epidemiology, interactions, epigenetics and ND assessment, plus ample experience engaging community partners, will recruit 740 expecting families in Northern California representing diverse racial, ethnic, socioeconomic, genetic, and environmental backgrounds to enrich the ECHO cohort with participants traditionally underrepresented in research to address these gaps and produce findings that will substantially inform public health policies for more effective improvement of child developmental outcomes.
Awardee
Funding Goals
NOT APPLICABLE
Grant Program (CFDA)
Awarding Agency
Place of Performance
Davis,
California
95616
United States
Geographic Scope
Single Zip Code
Related Opportunity
Analysis Notes
Amendment Since initial award the total obligations have increased 149% from $1,273,600 to $3,172,491.
Davis University Of California was awarded
Prenatal SFA Impact on Child Health Disparities
Cooperative Agreement UG3OD035550
worth $3,172,491
from the National Institute of Allergy and Infectious Diseases in September 2023 with work to be completed primarily in Davis California United States.
The grant
has a duration of 1 year 8 months and
was awarded through assistance program 93.310 Trans-NIH Research Support.
The Cooperative Agreement was awarded through grant opportunity Open Competition: Environmental influences on Child Health Outcomes (ECHO) Pregnancy Cohort Study Sites. Clinical Trial Not Allowed (UG3/UH3).
Status
(Complete)
Last Modified 6/20/24
Period of Performance
9/1/23
Start Date
5/31/25
End Date
Funding Split
$3.2M
Federal Obligation
$0.0
Non-Federal Obligation
$3.2M
Total Obligated
Activity Timeline
Transaction History
Modifications to UG3OD035550
Additional Detail
Award ID FAIN
UG3OD035550
SAI Number
UG3OD035550-237029789
Award ID URI
SAI UNAVAILABLE
Awardee Classifications
Public/State Controlled Institution Of Higher Education
Awarding Office
75AGNA NIH AGGREGATE FINANCIAL ASSISTANCE DATA AWARDING OFFICE
Funding Office
75NA00 NIH OFFICE OF THE DIRECTOR
Awardee UEI
TX2DAGQPENZ5
Awardee CAGE
1CBG4
Performance District
CA-04
Senators
Dianne Feinstein
Alejandro Padilla
Alejandro Padilla
Budget Funding
Federal Account | Budget Subfunction | Object Class | Total | Percentage |
---|---|---|---|---|
Office of the Director, National Institutes of Health, Health and Human Services (075-0846) | Health research and training | Grants, subsidies, and contributions (41.0) | $1,273,600 | 100% |
Modified: 6/20/24