Awardee OrganizationUNIVERSITY OF SOUTHERN CALIFORNIA
Description
Abstract Text
PROJECT SUMMARY/ABSTRACT--PROJECT 1
Depression is the leading cause of mental health-related morbidity worldwide, affecting approximately 300 million
people annually. Depression is nearly twice as prevalent among women than men and multiple individual and
psychosocial risk factors are associated with risk of depression. Hispanic women in the US have unique risk
factors for depression and other mental health disorders relative to non-Hispanic women including overcoming
stress associated with acculturation as well as lower awareness and utilization of mental health care services.
Traffic-related and ambient air pollutants are potentially modifiable environmental exposures that are known to
disproportionately impact health disparity populations and have increasingly been implicated in risk of
depression. Pregnancy is a period of dynamic biological and hormonal fluctuations designed to support fetal
development that may increase susceptibility to environmental insults and effects on later depression. Despite
growing evidence of the impact of prenatal air pollution on depressive symptoms in the first few months
postpartum, there have been no studies on whether exposures during this critical period may increase long-term
risk of maternal depression. Understanding biological mechanisms that mediate downstream effects of
environmental exposures may lead to improved treatment approaches and reductions in morbidity associated
with depression. As primary regulators of gene expression, epigenetic mechanisms, such as microRNA (miRNA),
may be important mediators of air pollution effects on depression. MiRNA regulate numerous cellular processes,
including neuroendocrine and inflammatory pathways important in depression pathophysiology. We will
investigate these mechanisms and the following specific aims in 500 women in the first four postpartum years in
the MADRES pregnancy cohort—an ongoing cohort of predominantly Hispanic, socioeconomically-
disadvantaged women in urban Los Angeles. We will (1) investigate the association of prenatal exposures to
traffic-related and regional air pollution with symptoms of maternal depression in the first four years postpartum
and examine whether these associations vary by prenatal psychosocial stressors and acculturation factors; (2)
evaluate whether there is a sustained response at 2 and 4 years postpartum between prenatal air pollution
exposures and neuroendocrine (cortisol, norepinephrine and epinephrine) and pro-inflammatory markers (IL-6
and CRP) known to be associated with depression; and (3) determine the role of neuroendocrine and
inflammatory-related miRNA in prenatal air pollution-related associations in maternal depression in the first four
years postpartum and test whether they mediate associations between prenatal air pollution and maternal
depression as well as examine the functional relevance of these miRNA. Results from this study may improve
policy and treatment approaches to reduce the burden of depression among health disparity populations.
Public Health Relevance Statement
Data not available.
NIH Spending Category
No NIH Spending Category available.
Project Terms
AcculturationAdolescenceAffectAir PollutantsAir PollutionAnimalsAwarenessBiologicalBrainCell PhysiologyChronic stressCountryDevelopmentDiseaseEnvironmental ExposureEnvironmental Risk FactorEpigenetic ProcessEpinephrineExposure toFetal DevelopmentFunctional disorderGene ExpressionGene TargetingGenetic Predisposition to DiseaseHispanicHormonalHormonesHumanHydrocortisoneIndividualInflammatoryInterleukin-6LanguageLos AngelesMajor Depressive DisorderMediatingMediatorMental DepressionMental HealthMental Health ServicesMental disordersMicroRNAsMorbidity - disease rateNeurosecretory SystemsNorepinephrineNot Hispanic or LatinoPathway interactionsPersonsPoliciesPopulationPostpartum DepressionPostpartum PeriodPredispositionPregnancyRecording of previous eventsRecurrenceRegulator GenesReproductive PeriodsRiskRisk FactorsRoleSocial statusStressStressful EventSubgroupSymptomsTestingVictimizationWomanambient air pollutioncohortcopingcritical periodcytokinedepressive symptomsdesigndisadvantaged womenenvironmental stressorfine particleshealth care servicehealth disparity populationsimprovedinflammatory markermaternal depressionmaternal riskmenmiddle agemodifiable riskneighborhood disadvantageneuroinflammationperceived stresspreferenceprenatalprenatal exposurepsychosocialpsychosocial stressorspublic health prioritiesresponsesocialsocial disparitiessocial stressorsocioeconomic disadvantage
National Institute on Minority Health and Health Disparities
CFDA Code
DUNS Number
072933393
UEI
G88KLJR3KYT5
Project Start Date
01-September-2015
Project End Date
31-March-2026
Budget Start Date
01-April-2024
Budget End Date
31-March-2025
Project Funding Information for 2024
Total Funding
$259,293
Direct Costs
$153,983
Indirect Costs
$105,310
Year
Funding IC
FY Total Cost by IC
2024
National Institute on Minority Health and Health Disparities
$259,293
Year
Funding IC
FY Total Cost by IC
Sub Projects
No Sub Projects information available for 5P50MD015705-10 5883
Publications
Publications are associated with projects, but cannot be identified with any particular year of the project or fiscal year of funding. This is due to the continuous and cumulative nature of knowledge generation across the life of a project and the sometimes long and variable publishing timeline. Similarly, for multi-component projects, publications are associated with the parent core project and not with individual sub-projects.
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Outcomes
The Project Outcomes shown here are displayed verbatim as submitted by the Principal Investigator (PI) for this award. Any opinions, findings, and conclusions or recommendations expressed are those of the PI and do not necessarily reflect the views of the National Institutes of Health. NIH has not endorsed the content below.
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