Air pollution, a critical global public health concern, significantly impacts neurodevelopment, with children particularly vulnerable due to immature defenses and high ventilation rates. Epidemiological studies highlight robust associations between air pollution—most notably fine particulate matter (PM2.5), nitrogen dioxide (NO₂), and coarse particles—and increased risks of neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), across sensitive windows from pregnancy to early childhood. Neuroimaging evidence reveals structural and functional brain alterations, such as reduced cortical thickness, white matter microstructural deficits (e.g., lower fractional anisotropy), and disrupted connectivity, aligning with NDD-related pathologies. Animal models further elucidate underlying mechanisms, including microglial activation, astrocyte reactivity, glutamate excitotoxicity, and white matter damage (e.g., ventriculomegaly, myelination abnormalities), which link exposure to NDD-like behavioral deficits (e.g., repetitive behaviors, social impairments). Collectively, these findings emphasize the need to characterize pollutant-specific effects and sensitive exposure windows to safeguard pediatric brain health.

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Air Pollution and Neurodevelopment

  • Hui-Xian Zeng,
  • Xiao-Wen Zeng,
  • Guang-Hui Dong

摘要

Air pollution, a critical global public health concern, significantly impacts neurodevelopment, with children particularly vulnerable due to immature defenses and high ventilation rates. Epidemiological studies highlight robust associations between air pollution—most notably fine particulate matter (PM2.5), nitrogen dioxide (NO₂), and coarse particles—and increased risks of neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), across sensitive windows from pregnancy to early childhood. Neuroimaging evidence reveals structural and functional brain alterations, such as reduced cortical thickness, white matter microstructural deficits (e.g., lower fractional anisotropy), and disrupted connectivity, aligning with NDD-related pathologies. Animal models further elucidate underlying mechanisms, including microglial activation, astrocyte reactivity, glutamate excitotoxicity, and white matter damage (e.g., ventriculomegaly, myelination abnormalities), which link exposure to NDD-like behavioral deficits (e.g., repetitive behaviors, social impairments). Collectively, these findings emphasize the need to characterize pollutant-specific effects and sensitive exposure windows to safeguard pediatric brain health.