HOME Study (Health Outcomes and Measures of the Environment Study)
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|ClinicalTrials.gov Identifier: NCT00129324|
Recruitment Status : Completed
First Posted : August 11, 2005
Last Update Posted : March 6, 2020
|Condition or disease||Intervention/treatment||Phase|
|Environmental Exposures Child Development Lead and Injury Reduction||Procedure: Lead Hazard Control Intervention Procedure: Injury Hazard Control Intervention||Not Applicable|
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 7.5-10) 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 7.5-10 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:
- 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.
- Prenatal and postnatal exposures to prevalent pesticides and ETS are associated with adverse neurobehavioral effects, and growth delay in children.
- Higher lead exposure, measured during pregnancy and early childhood using maternal blood, cord blood, meconium and children's blood, will be associated with lower IQ scores and more behavioral problems for children with a maximal blood lead level < 5 mg/dL.
- Children in the lead treatment arm will have: blood lead that is 2.7 mg/dL lower, higher IQ scores, greater growth velocity, and fewer behavioral problems than children in the control group.
- 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.
- 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.
- Prenatal and Postnatal exposures to PBDEs and PFCs are associated with altered thyroid hormone levels and deficits in infant and child neurobehavior
- 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.
- Developmental PBDE and PFC exposures are associated with internalizing symptoms.
- Developmental PBDE and PFC exposures are associated with adverse changes in anatomical structure, neurochemistry, organization of white matter tracts, and connectivity of neural networks.
- PFAS affect the gene expression and function of several biological pathways that program the fetus/infant towards a 'thrifty phenotype'. This leads to accelerated early childhood growth, increased fat mass, and features of metabolic syndrome.
|Study Type :||Interventional (Clinical Trial)|
|Actual Enrollment :||468 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Double (Investigator, Outcomes Assessor)|
|Official Title:||Neurobehavioral Effects of Prevalent Neurotoxicants in Children: A Cohort Study of the Cincinnati Center for Children's Environmental Health|
|Actual Study Start Date :||March 2003|
|Actual Primary Completion Date :||August 2018|
|Actual Study Completion Date :||August 2018|
Lead Reduction Arm
random assignment to receive lead hazard control intervention. Assessing lead hazards in the home. Reducing lead hazards by cleaning, painting, covering, and/or replacing/repairing interior and exterior components of the home.
Procedure: Lead Hazard Control Intervention
Prior to their child's birth, participants randomized to Lead Reduction Group received lead hazard reduction controls to reduce residential exposure to lead.
Injury Reduction Arm
random assignment to receive injury hazard control intervention. Assessing home for potential injury hazards. Controlling hazards by 1) installing safety equipment such as stairway gates, cabinet locks, smoke & CO detectors, etc. 2) removing the hazards from the reach of a child and/or 3) restricting access to the hazards.
Procedure: Injury Hazard Control Intervention
Between 3 and 6 months of age, participants randomized to Injury Reduction Arm received injury hazard controls to reduce the number of residential injuries.
- Lead reduction intervention, blood lead concentrations & neurobehavioral outcomes [ Time Frame: 16wk & 26wk gestation, birth, annually at 1y-12y ]Testing the efficacy of lead reduction controls in the homes of participants. Examining the effects of low level blood lead concentration on child development and neurobehavior. Measures of blood lead concentration were taken from mothers prenatally at approximately 16 and 26 weeks gestation, from cord blood at birth, and annually from participating children from 1 - 10 years of age.
- Exposure to environmental chemicals and their effects on child health, neurobehavior and development [ Time Frame: 16wk & 26wk gestation, birth, 4wk postnatal, annually years 1-12. ]Addressing potential adverse health risks of environmental chemicals (persistent organic pollutants, metals, cotinine, pesticides, flame retardants, BPA, and phthalates) on fetal, infant, and child neurobehavior. Examining their associations with endocrine function, body composition (DXA), neuroimaging (MRI/fMRI), cognition, learning and memory, motor skills, attention and executive function, behavior, and mental health. Also examining exposures at different developmental stages and measuring child neurobehavior.
- Injury prevention measures and household injuries [ Time Frame: Postnatally up to age 5 years ]Test the efficacy of injury reduction controls in the homes of study participants. Assessed homes for potential injury hazards and installed child safety equipment. Collected parent report of injury events and validated the events against injuries tracked in the Hamilton County Injury Surveillance System
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00129324
|United States, Ohio|
|Cincinnati Children's Environmental Health Center|
|Cincinnati, Ohio, United States, 45229|
|Principal Investigator:||Kimberly Yolton, PhD||Children's Hospital Medical Center, Cincinnati|