Joan Forns1, Hein Stigum2, Birgit Bjerre Høyer3,4, Isabelle Sioen5, Eva Sovcikova6, Nikola Nowack7, Maria-Jose Lopez-Espinosa8,9, Mònica Guxens9,10,11,12, Jesús Ibarluzea9,13,14,15, Matias Torrent11,16, Jürgen Wittsiepe17, Eva Govarts18, Tomas Trnovec19, Cecile Chevrier20, Gunnar Toft4, Martine Vrijheid9,10,11, Nina Iszatt1, Merete Eggesbø1. 1. Department of Environmental Exposure and Epidemiology, Norwegian Institute of Public Health, Oslo, Norway. 2. Department of Non-Communicable Diseases, Norwegian Institute of Public Health, Oslo, Norway. 3. Department of Occupational and Environmental Medicine, Bispebjerg University Hospital, Copenhagen, Denmark. 4. Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark. 5. Department of Food Technology, Safety and Health, Ghent University, Ghent, Belgium. 6. Department of Environmental Medicine, Faculty of Public Health, Slovak Medical University, Bratislava, Slovak Republic. 7. Department of Developmental Psychology, Ruhr University Bochum, Bochum, Germany. 8. Epidemiology and Environmental Health Joint Research Unit, FISABIO-Universitat Jaume I-Universitat de Valencia, Valencia, Spain. 9. Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, Barcelona, Spain. 10. ISGlobal, Center for Research in Environmental Epidemiology, Barcelona, Spain. 11. Pompeu Fabra University, Barcelona, Spain. 12. Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre-Sophia Children's Hospital, Rotterdam, the Netherlands. 13. Sub-Directorate for Public Health of Gipuzkoa, Department of Health of the Basque Country, San Sebastián, Spain. 14. BIODONOSTIA Health Research Institute, Basque Country, Spain. 15. Faculty of Psychology, University of the Basque Country, San Sebastian, Spain. 16. Menorca Health Area, Balearic Health Service (ib-salut), Menorca, Spain. 17. Department of Hygiene, Social and Environmental Medicine, Ruhr University Bochum, Bochum, Germany. 18. Unit Environmental Risk and Health, Flemish Institute for Technological Research (VITO), Mol, Belgium. 19. Faculty of Public Health, Department of Environmental Medicine, Slovak Medical University, Bratislava, Slovakia. 20. INSERM, UMR1085 IRSET, University Rennes 1, Rennes, France.
Abstract
Background: Attention-deficit/hyperactivity disorder (ADHD) is increasing worldwide for reasons largely unknown and environmental chemicals with neurotoxic properties, such as persistent organic pollutants (POPs), have been proposed to play a role. We investigated the association between prenatal and postnatal exposure to polychlorinated biphenyl-153 (PCB-153), p-p´-dichlorodiphenyldichloroethylene (p-p'-DDE) and hexachlorobenzene (HCB) and ADHD in childhood. Methods: We pooled seven European birth cohort studies encompassing 4437 mother-child pairs from the general population with concentrations of PCB-153, p-p´-DDE and HCB measured in cord blood, maternal blood or milk. We then calculated prenatal (birth) and postnatal (3, 6, 12 and 24 months) POP concentrations using a pharmacokinetic model. The operational definition of ADHD varied across cohorts and ranged from doctor diagnosis obtained from patient registries to maternal or teachers reports. We used multilevel (mixed) logistic regression models to estimate the associations between exposure to POPs at birth, 3, 6, 12 and 24 months and ADHD. Results: The global prevalence of ADHD in our study was 6%. The mean age at assessment of ADHD was 5.8 years (range: 3.8-9.5 years). We found no association between exposure to PCB-153, p-p´-DDE and HCB at any age point between birth and 24 months and ADHD, in the pooled analyses (pooled odds ratios ranging from 1.00 to 1.01). A number of sensitivity analyses gave basically the same results. Conclusions: In the largest study to date of 4437 children in seven European birth cohorts, we did not observe any association between either pre- or postnatal exposure (up to 24 months) to PCB-153, p-p´-DDE and HCB and the risk of ADHD before the age of 10 years.
Background: Attention-deficit/hyperactivity disorder (ADHD) is increasing worldwide for reasons largely unknown and environmental chemicals with neurotoxic properties, such as persistent organic pollutants (POPs), have been proposed to play a role. We investigated the association between prenatal and postnatal exposure to polychlorinated biphenyl-153 (PCB-153), p-p´-dichlorodiphenyldichloroethylene (p-p'-DDE) and hexachlorobenzene (HCB) and ADHD in childhood. Methods: We pooled seven European birth cohort studies encompassing 4437 mother-child pairs from the general population with concentrations of PCB-153, p-p´-DDE and HCB measured in cord blood, maternal blood or milk. We then calculated prenatal (birth) and postnatal (3, 6, 12 and 24 months) POP concentrations using a pharmacokinetic model. The operational definition of ADHD varied across cohorts and ranged from doctor diagnosis obtained from patient registries to maternal or teachers reports. We used multilevel (mixed) logistic regression models to estimate the associations between exposure to POPs at birth, 3, 6, 12 and 24 months and ADHD. Results: The global prevalence of ADHD in our study was 6%. The mean age at assessment of ADHD was 5.8 years (range: 3.8-9.5 years). We found no association between exposure to PCB-153, p-p´-DDE and HCB at any age point between birth and 24 months and ADHD, in the pooled analyses (pooled odds ratios ranging from 1.00 to 1.01). A number of sensitivity analyses gave basically the same results. Conclusions: In the largest study to date of 4437 children in seven European birth cohorts, we did not observe any association between either pre- or postnatal exposure (up to 24 months) to PCB-153, p-p´-DDE and HCB and the risk of ADHD before the age of 10 years.
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