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P I – 2–8 Early-life exposure to persistent organic pollutants and attention-deficit/hyperactivity disorder: a multi-pollutant assessment of a norwegian birth cohort
  1. Virissa Lenters1,
  2. Eliška Čechová2,
  3. Anton Kočan2,
  4. Juliette Legler3,
  5. Pim Leonards3,
  6. Joan Forns1,
  7. Nina Iszatt1,
  8. Hein Stigum4,
  9. Merete Eggesbø1
  1. 1Norwegian Institute of Public Health, Department of Environmental Exposure and Epidemiology, Oslo, Norway
  2. 2Masaryk University, Research Centre for Toxic Compounds in the Environment, Brno, Czech Republic
  3. 3VU University Amsterdam, Institute for Environmental Studies, Amsterdam, Netherlands
  4. 4Norwegian Institute of Public Health, Department of Non-Communicable Diseases, Oslo, Norway


Background/aim Numerous ubiquitous environmental chemicals are established or suspected neurotoxicants, and infants are exposed to a mixture of these during the critical period of brain maturation. Evidence for associations with the risk of attention-deficit/hyperactivity disorder (ADHD) is sparse. We investigated measured perinatal and estimated postnatal chemical exposure levels in relation to ADHD.

Methods We used a birth cohort of Norwegian mother–child pairs enrolled 2005–2009 (HUMIS-NoMIC). In a subset of 1199 oversampled for neurodevelopmental outcomes, 27 persistent organic pollutants were measured in maternal breastmilk samples (14 PCBs, 5 organochlorine pesticides, 6 brominated flame retardants, and 2 perfluoroalkyl substances). We modelled pre- and postnatal exposures using a pharmacokinetic model. ADHD (n=40) was identified based on an ICD-10 diagnosis of hyperkinetic disorder in the national patient registry by 2014 (median age of 10.3 years). To identify associations and adjust for co-exposure confounding, we used elastic net penalised logistic regression models, and then used multivariable logistic regression models to obtain effect estimates for the selected exposures.

Results Perfluorooctane sulfonate (PFOS) and β-hexachlorocyclohexane (β-HCH) were associated with increased odds and hexachlorobenzene (HCB) with decreased odds of ADHD diagnosis [confounder-adjusted odds ratio (OR) per interquartile range increase in breastmilk levels: 2.04 for PFOS; OR=1.64 for β-HCH; OR=0.36 for HCB]. Postnatal exposures showed similar results, whereas effect estimates for other chemicals were imprecise.

Conclusion In a multi-pollutant analysis of four classes of chemicals, early-life exposure to several persistent organic pollutants was associated with ADHD.

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