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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
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Perinatal maternal lead exposure induces intergenerational neurotoxicity via mitochondrial dysfunction and mediation

Lin Zhang1, An-Xin Lu2, Ling Li3

  • 1Deprtment of Labor Health and Environmental Hygiene, School of Public Health, Lanzhou University, Lanzhou 730000, China; Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.

Journal of Hazardous Materials
|November 18, 2025
PubMed

Insights

Maternal lead exposure, especially from bone stores, harms children

Area of Science:

  • Environmental Health
  • Neurotoxicology
  • Endocrinology

Background:

  • Perinatal maternal lead (Pb) exposure is a significant source of early childhood Pb exposure.
  • Endogenous skeletal Pb mobilization during pregnancy is a key contributor to this exposure.
  • Pb exposure is linked to neurodevelopmental deficits and thyroid dysfunction.

Purpose of the Study:

  • To investigate the intergenerational effects of maternal skeletal Pb mobilization on offspring neurodevelopment.
  • To explore the role of the thyroid-astrocytic mitochondrial axis in Pb-induced neurotoxicity.
  • To examine sex-specific differences in Pb exposure effects on neurodevelopment and thyroid function.

Main Methods:

  • Utilized a rat model of maternal skeletal Pb mobilization.
  • Assessed offspring neurotoxicity, astrocytic mitochondrial injury, and maternal-offspring thyroid function.
  • Conducted mediation analysis to determine the role of maternal thyroid hormones (THs).
  • Analyzed cord blood Pb levels, THs, and infant motor skills in a human cohort (298 mother-child pairs).

Main Results:

  • Maternal Pb exposure induced offspring neurotoxicity, astrocytic mitochondrial injury, and maternal-offspring thyroid dysfunction.
  • Maternal THs mediated Pb-induced intergenerational neurotoxicity.
  • In humans, cord blood Pb correlated with fine motor scores in girls and disrupted TH levels in infants (notably TT4 in boys).
  • TSH and FT4 levels showed negative correlations with infant motor domains, particularly in boys.

Conclusions:

  • The 'thyroid-astrocytic mitochondrial axis' is a critical pathway for intergenerational neurotoxicity from perinatal maternal Pb exposure.
  • Endogenous Pb mobilization poses a significant risk for neurodevelopmental outcomes.
  • Findings reveal significant sex-specific differences in Pb neurotoxicity and thyroid disruption.

Keywords:
Bone lead mobilizationIntergenerational neurotoxicityMediation analysisPerinatal lead exposureThyroid-mitochondrial axis

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