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<p>Lead (Pb), a toxic metal, accumulates to trigger inflammation via excess free radicals and Nuclear transcription factor kappa B (NF-κB) activation, causing neuroendocrine dysfunction. However, human studies on Pb's inflammatory effects disrupting endogenous melatonin secretion remain scarce. We explored links between Pb exposure, inflammation, and endogenous melatonin in healthy children. We conducted demographic surveys and physical exams in 213 children (108 from Guiyu electronic waste (e-waste) recycling area, 105 from Haojiang reference). Circulating melatonin was assessed via urinary 6-sulfatoxymelatonin (aMT6s), with blood measurements of Pb, inflammatory cells, and 7 serum cytokines. Blood Pb levels were significantly elevated in exposed versus reference groups, correlating with hygiene practices and living conditions. Exposed children showed higher urinary aMT6s, neutrophil/monocyte counts, and serum interleukin (IL)-2, IL-8, IL-13, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α levels. After adjusting for age, gender, body mass index (BMI), head circumference, milk consumption, and e-waste proximity (&lt; 50&#xa0;m), increased Pb exposure associated with elevated aMT6s, monocytes, and IL-13. Additionally, multiple analyses revealed that the first quartile of blood Pb levels was associated with the fourth quartile of head circumference, height, and weight. The fourth quartile of blood Pb and urinary aMT6s was associated with the first quartile of head circumference, height, and weight. Our findings suggest that environmental Pb exposure increases endogenous melatonin levels and leads to growth retardation in children by inducing an immune-inflammatory response.</p> Graphical Abstract <p></p>

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High Urinary aMT6s Concentrations are Linked to Lead-Induced Inflammation in Children

  • 期刊论文

  • 发表日期：

    2025年3月25日

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  • Qiong Luo,
  • Xia Huo,
  • Zihan Chen,
  • Yu Huang,
  • Jiangxia Yang,
  • Weiqiu Li,
  • Xijin Xu

摘要

Lead (Pb), a toxic metal, accumulates to trigger inflammation via excess free radicals and Nuclear transcription factor kappa B (NF-κB) activation, causing neuroendocrine dysfunction. However, human studies on Pb's inflammatory effects disrupting endogenous melatonin secretion remain scarce. We explored links between Pb exposure, inflammation, and endogenous melatonin in healthy children. We conducted demographic surveys and physical exams in 213 children (108 from Guiyu electronic waste (e-waste) recycling area, 105 from Haojiang reference). Circulating melatonin was assessed via urinary 6-sulfatoxymelatonin (aMT6s), with blood measurements of Pb, inflammatory cells, and 7 serum cytokines. Blood Pb levels were significantly elevated in exposed versus reference groups, correlating with hygiene practices and living conditions. Exposed children showed higher urinary aMT6s, neutrophil/monocyte counts, and serum interleukin (IL)-2, IL-8, IL-13, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α levels. After adjusting for age, gender, body mass index (BMI), head circumference, milk consumption, and e-waste proximity (< 50 m), increased Pb exposure associated with elevated aMT6s, monocytes, and IL-13. Additionally, multiple analyses revealed that the first quartile of blood Pb levels was associated with the fourth quartile of head circumference, height, and weight. The fourth quartile of blood Pb and urinary aMT6s was associated with the first quartile of head circumference, height, and weight. Our findings suggest that environmental Pb exposure increases endogenous melatonin levels and leads to growth retardation in children by inducing an immune-inflammatory response.

Graphical Abstract