HOME Study (Health Outcomes and Measures of the Environment Study)

Sponsor

National Institute of Environmental Health Sciences (NIEHS) (NIH)

Overall Status

Completed

CT.gov ID

NCT00129324

Collaborator

(none)

468

Enrollment

Location

Arms

185

Actual Duration (Months)

2.5

Patients Per Site Per Month

Study Details

Study Description

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 (PBDEs/PFCs), 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.

Condition or Disease	Intervention/Treatment	Phase
Environmental Exposures Child Development Lead and Injury Reduction	Procedure: Lead Hazard Control Intervention Procedure: Injury Hazard Control Intervention	N/A

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 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 Design

Study Type:

Interventional

Actual Enrollment :

468 participants

Allocation:

Randomized

Intervention Model:

Parallel Assignment

Masking:

Double (Investigator, Outcomes Assessor)

Primary Purpose:

Prevention

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 :

Mar 1, 2003

Actual Primary Completion Date :

Aug 1, 2018

Actual Study Completion Date :

Aug 1, 2018

Arms and Interventions

Arm	Intervention/Treatment
Other: 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.
Other: 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.

Arm

Intervention/Treatment

Other: 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.

Other: 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.

Outcome Measures

Primary Outcome Measures

Lead reduction intervention, blood lead concentrations & neurobehavioral outcomes [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 [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 [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