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Backgraound <p>Dioxin-like polychlorinated biphenyls (DL-PCBs) are persistent organic pollutants with known endocrine-disrupting and developmental toxicity. Increasing evidence suggests that prenatal exposure to DL-PCBs may adversely affect fetal growth; however, few studies have examined congener-specific and mixture-level effects, and the underlying biological mechanisms remain unclear. This study aimed to assess the relationship between umbilical cord DL-PCB concentrations and key fetal growth indicators including birth weight (BW), birth length (BL), and head circumference (HC), and to explore whether mitochondrial dysfunction mediates these effects.</p> Methods <p>A total of 5421 mother–infant pairs were recruited between 2022 and 2024 from a multicenter birth cohort in China. Twelve WHO-designated DL-PCB congeners were quantified in umbilical cord blood using gas chromatography–mass spectrometry (GC-MS). We employed multivariable linear regression, sex-stratified models, Bayesian kernel machine regression, generalized weighted quantile sum (gWQS), quantile g-computation (g-comp), and mediation analysis to evaluate individual and mixture effects.</p> Results <p>Eight DL-PCBs, particularly PCB-77 and PCB-126, were significantly associated with reduced BW (ranging from − 26.52&#xa0;g to − 80.05&#xa0;g per IQR increase). PCB-77 and PCB-126 were also negatively associated with HC, while no DL-PCBs showed significant associations with BL. Although inverse associations appeared stronger in boys, sex interactions were not statistically significant. Mediation analysis revealed that mitochondrial DNA content partially mediated the relationship between several DL-PCBs (e.g., PCB-77, PCB-81, PCB-118, PCB-126) and BW, with up to 10.76% of the total effect explained. Mixture models confirmed negative associations with BW and HC, with g-comp estimating a 161.95&#xa0;g BW reduction per cumulative exposure unit. Bayesian kernel machine regression further identified PCB-77 and PCB-126 as dominant contributors.</p> Conclusion <p>These findings suggest that mitochondrial dysfunction may be a mechanistic pathway linking prenatal DL-PCB exposure to intrauterine growth restriction, especially reduced birth weight, highlighting potential developmental risks from environmental contamination.</p>

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Mitochondrial dysfunction as a potential pathway linking DL-PCB exposure to intrauterine growth retardation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月22日

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  • Huisheng Yao,
  • Chao Jiang,
  • Hongyan Zhang,
  • Si Si,
  • Xingqiang Li,
  • Yue Zhang

摘要

Backgraound

Dioxin-like polychlorinated biphenyls (DL-PCBs) are persistent organic pollutants with known endocrine-disrupting and developmental toxicity. Increasing evidence suggests that prenatal exposure to DL-PCBs may adversely affect fetal growth; however, few studies have examined congener-specific and mixture-level effects, and the underlying biological mechanisms remain unclear. This study aimed to assess the relationship between umbilical cord DL-PCB concentrations and key fetal growth indicators including birth weight (BW), birth length (BL), and head circumference (HC), and to explore whether mitochondrial dysfunction mediates these effects.

Methods

A total of 5421 mother–infant pairs were recruited between 2022 and 2024 from a multicenter birth cohort in China. Twelve WHO-designated DL-PCB congeners were quantified in umbilical cord blood using gas chromatography–mass spectrometry (GC-MS). We employed multivariable linear regression, sex-stratified models, Bayesian kernel machine regression, generalized weighted quantile sum (gWQS), quantile g-computation (g-comp), and mediation analysis to evaluate individual and mixture effects.

Results

Eight DL-PCBs, particularly PCB-77 and PCB-126, were significantly associated with reduced BW (ranging from − 26.52 g to − 80.05 g per IQR increase). PCB-77 and PCB-126 were also negatively associated with HC, while no DL-PCBs showed significant associations with BL. Although inverse associations appeared stronger in boys, sex interactions were not statistically significant. Mediation analysis revealed that mitochondrial DNA content partially mediated the relationship between several DL-PCBs (e.g., PCB-77, PCB-81, PCB-118, PCB-126) and BW, with up to 10.76% of the total effect explained. Mixture models confirmed negative associations with BW and HC, with g-comp estimating a 161.95 g BW reduction per cumulative exposure unit. Bayesian kernel machine regression further identified PCB-77 and PCB-126 as dominant contributors.

Conclusion

These findings suggest that mitochondrial dysfunction may be a mechanistic pathway linking prenatal DL-PCB exposure to intrauterine growth restriction, especially reduced birth weight, highlighting potential developmental risks from environmental contamination.