Ignite Creation Date:
2024-05-05 @ 11:47 AM
Last Modification Date:
2024-10-26 @ 9:13 AM
Study NCT ID:
NCT00129324
Status:
COMPLETED
Last Update Posted:
2020-03-06
First Post:
2005-08-10
Brief Title:
HOME Study Health Outcomes and Measures of the Environment Study
Sponsor:
National Institute of Environmental Health Sciences NIEHS
Organization:
National Institute of Environmental Health Sciences NIEHS
Study Overview
Official Title:
Neurobehavioral Effects of Prevalent Neurotoxicants in Children A Cohort Study of the Cincinnati Center for Childrens Environmental Health
Status:
COMPLETED
Status Verified Date:
2020-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The goal of the HOME Study is to quantify the impact of low-level fetal and early childhood exposures to environmental toxicants including lead mercury and other metals pesticides polychlorinated biphenyls PCBs persistent organic pollutants PBDEsPFCs phthalates phenols environmental tobacco smoke and alcohol on child development neurobehavior health and growth The HOME Study will also evaluate meconium as a biomarker for fetal exposure and test the effectiveness of home repairs to control lead hazards and injuries in early childhood
Detailed Description:
This study aims to examine the effects of low-level exposures to prevalent neurotoxicants on health growth and neurobehavior among a representative sample of children Pregnant women were enrolled in the project around 16 weeks of gestation In the first phase of the study we followed children resulting from the pregnancy through the age of 36 months The second phase extended follow-up through 72 months Phase 3 extended follow-up to 8 years range 75-10 with comprehensive neurobehavioral assessments Phase 4 will allow follow-up at 12 years range 11-13 and includes measures of health growth and body composition behavior and mental health and neuroimaging To address the potential adverse health risks of environmental chemicals including persistent pollutants such as PBDEs and PFCs and other non-persistent chemicals on fetal infant and child neurobehavior the investigators are systematically examining their associations with endocrine function cognition learning and memory motor skills attention and executive function and behavior from age 1 to 75-10 years The investigators are also examining exposures at different developmental stages in utero at 16 weeks of gestation early childhood school age preadolescence using stored biological samples and measure child neurobehavior at 1 2 3 4 5 8 and 12 years This longitudinal study will allow the investigators to determine the dose response windows of susceptibility and persistence of the association The investigators are also examining the contribution of PBDE exposures from house dust in a subset of children who have complete sets of samples of maternal serum and child serum collected from annual visits along with extensive measures of mouthing behaviors
Hypotheses from the four phases of the study are as follows
1 In utero exposures measured by survey alcohol and ETS maternal and cord blood lead and mercury maternal and cord serum ETS and urine pesticides are less predictive of in utero effects of prevalent toxicants including cognition behavior problems and growth compared with the same toxicants in meconium
2 Prenatal and postnatal exposures to prevalent pesticides and ETS are associated with adverse neurobehavioral effects and growth delay in children
3 Higher lead exposure measured during pregnancy and early childhood using maternal blood cord blood meconium and childrens blood will be associated with lower IQ scores and more behavioral problems for children with a maximal blood lead level 5 mgdL
4 Children in the lead treatment arm will have blood lead that is 27 mgdL lower higher IQ scores greater growth velocity and fewer behavioral problems than children in the control group
5 Levels of lead in dust soil and water will be significantly lower for housing units in the lead treatment arm compared with the injury control arm at 36 and 48 month home visits
6 A multifactorial housing intervention will reduce residential injury by 30 percent among children in the injury treatment arm compared with those in the lead treatment arm
7 Prenatal and Postnatal exposures to PBDEs and PFCs are associated with altered thyroid hormone levels and deficits in infant and child neurobehavior
8 With increasing child age PBDE exposure from household dust becomes a stronger predictor of child serum PBDE concentration than exposure from placenta or breast milk
9 Developmental PBDE and PFC exposures are associated with internalizing symptoms
10 Developmental PBDE and PFC exposures are associated with adverse changes in anatomical structure neurochemistry organization of white matter tracts and connectivity of neural networks
11 PFAS affect the gene expression and function of several biological pathways that program the fetusinfant towards a thrifty phenotype This leads to accelerated early childhood growth increased fat mass and features of metabolic syndrome
Hypotheses from the four phases of the study are as follows
1 In utero exposures measured by survey alcohol and ETS maternal and cord blood lead and mercury maternal and cord serum ETS and urine pesticides are less predictive of in utero effects of prevalent toxicants including cognition behavior problems and growth compared with the same toxicants in meconium
2 Prenatal and postnatal exposures to prevalent pesticides and ETS are associated with adverse neurobehavioral effects and growth delay in children
3 Higher lead exposure measured during pregnancy and early childhood using maternal blood cord blood meconium and childrens blood will be associated with lower IQ scores and more behavioral problems for children with a maximal blood lead level 5 mgdL
4 Children in the lead treatment arm will have blood lead that is 27 mgdL lower higher IQ scores greater growth velocity and fewer behavioral problems than children in the control group
5 Levels of lead in dust soil and water will be significantly lower for housing units in the lead treatment arm compared with the injury control arm at 36 and 48 month home visits
6 A multifactorial housing intervention will reduce residential injury by 30 percent among children in the injury treatment arm compared with those in the lead treatment arm
7 Prenatal and Postnatal exposures to PBDEs and PFCs are associated with altered thyroid hormone levels and deficits in infant and child neurobehavior
8 With increasing child age PBDE exposure from household dust becomes a stronger predictor of child serum PBDE concentration than exposure from placenta or breast milk
9 Developmental PBDE and PFC exposures are associated with internalizing symptoms
10 Developmental PBDE and PFC exposures are associated with adverse changes in anatomical structure neurochemistry organization of white matter tracts and connectivity of neural networks
11 PFAS affect the gene expression and function of several biological pathways that program the fetusinfant towards a thrifty phenotype This leads to accelerated early childhood growth increased fat mass and features of metabolic syndrome
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| MDLTS0008-18 | OTHER_GRANT | HUD | httpsreporternihgovquickSearchR01ES030078 |
| R01ES014575 | NIH | None | None |
| P01ES011261 | NIH | None | None |
| R01ES020349 | NIH | None | None |
| R01ES015517 | NIH | None | None |
| R01ES025214 | NIH | None | None |
| R01ES027224 | NIH | None | None |
| R01ES028277 | NIH | None | None |
| R01ES024381 | NIH | None | None |
| R01ES026903 | NIH | None | None |
| R01ES030078 | NIH | None | None |