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<p>Air pollution is a ubiquitous neurotoxicant linked to altered structural brain connectivity. Sleep may offer neuroprotection through its roles in brain waste clearance and immune regulation. Using Fitbit-derived sleep data and multi-shell diffusion MRI from 2178 children (ages 10–13) in the ABCD Study®, we examined whether sleep moderated associations between prenatal and childhood exposure to PM<sub>2.5</sub>, NO<sub>2</sub>, and O<sub>3</sub> and white matter microstructure. Restriction spectrum imaging yielded restricted normalized isotropic (RNI) and directional (RND) metrics, averaged across tracts. Pollution exposure was estimated at prenatal and childhood (ages 9–10) residences. Linear mixed-effects models tested sleep-by-pollution interactions on RNI/RND. Childhood NO<sub>2</sub> and prenatal O<sub>3</sub> interacted with sleep duration and efficiency, respectively, to influence RND. Among children with similar pollutant exposure, those with longer sleep duration and higher sleep efficiency had lower RND than peers with poorer sleep. This suggests that healthy sleep may buffer adverse effects of air pollution on white matter integrity.</p>

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Sleep moderates how prenatal and childhood pollutant exposure impacts white matter microstructural integrity in adolescence

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月4日

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  • Devyn L. Cotter,
  • Orsolya Kiss,
  • Hedyeh Ahmadi,
  • Alethea V. de Jesus,
  • Joel Schwartz,
  • Fiona C. Baker,
  • Daniel A. Hackman,
  • Megan M. Herting

摘要

Air pollution is a ubiquitous neurotoxicant linked to altered structural brain connectivity. Sleep may offer neuroprotection through its roles in brain waste clearance and immune regulation. Using Fitbit-derived sleep data and multi-shell diffusion MRI from 2178 children (ages 10–13) in the ABCD Study®, we examined whether sleep moderated associations between prenatal and childhood exposure to PM2.5, NO2, and O3 and white matter microstructure. Restriction spectrum imaging yielded restricted normalized isotropic (RNI) and directional (RND) metrics, averaged across tracts. Pollution exposure was estimated at prenatal and childhood (ages 9–10) residences. Linear mixed-effects models tested sleep-by-pollution interactions on RNI/RND. Childhood NO2 and prenatal O3 interacted with sleep duration and efficiency, respectively, to influence RND. Among children with similar pollutant exposure, those with longer sleep duration and higher sleep efficiency had lower RND than peers with poorer sleep. This suggests that healthy sleep may buffer adverse effects of air pollution on white matter integrity.