Prenatal eksponering for miljøgifter og risiko for ADHD
To investigate if prenatal exposure to environmental toxicants disrupts normal fetal brain development, acting through thyroid and epigenetic mechanisms.
About the project
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Project period: 01.07.2012 - 31.12.2026 (Active)
- Coordinating Institution: Norwegian Institute of Public Health
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Project Manager:
- Gro Dehli Andersen, Norwegian Institute of Public Health
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Project Participants:
- Heidi Aase, Child Health and Development
- Rachel Nethery, University of North Carolina at Chapel Hill
- Amrit Kaur Sakhi, Infection Control
- Kjell Vegard Fjeldheim Weyde, Child Health and Development
- Deborah Gordon Hirtz, University of Vermont
- Esra Susser, Columbia University in the City of New York
- Mady Hornig, Columbia University in the City of New York
- R. Thomas Zoeller, University of Massachusetts at Amherst
- Kristin Romvig Øvergaard, Oslo University Hospital
- Ragnhild Eek Brandlistuen, Norwegian Institute of Public Health
- Per Minor Magnus, Centre for Fertility and Health
- Tiril Cecilie Borge, Child Health and Development
- Ida Henriette Caspersen, Infection Control
- Line Småstuen Haug, Infection Control
- Cathrine Thomsen, Infection Control
- Yankai Xia, Nanjing Medical University
- Ian Lipkin, Columbia University in the City of New York
- Guro Lillemoen Andersen, Norwegian University of Science and Technology
Summary
AIM: To investigate if prenatal exposure to environmental toxicants disrupts normal fetal brain development, acting through thyroid and epigenetic mechanisms.
Secondary aims
1. Investigate the general and differential effects of maternal toxicant levels during pregnancy on neurodevelopmental outcomes in the child: cognitive functions and diagnoses of ADHD, ASD, CP and epilepsy, including sub-phenotypes of these disorders (WP1)
2. Assess complex mixture effects of maternal levels of organic and inorganic neurotoxicants (perfluoroalkyl substances (PFAS) and metals) on neurodevelopmental outcome variables in children (WP2)
3. Investigate the relations between maternal neurotoxicant levels, neonatal thyroid hormone status, neonatal DNA methylationpatterns, and neurodevelopmental outcomes later in childhood (WP3)