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Blood lead levels and serum insulin-like growth factor 1 concentrations in peripubertal boys

Abby F Fleisch1, Jane S Burns, Paige L Williams

  • 1Department of Endocrinology, Children's Hospital Boston, Boston, Massachusetts, USA.

Environmental Health Perspectives
|May 2, 2013
PubMed

Insights

Childhood lead exposure, measured by blood lead levels (BLLs), is linked to lower insulin-like growth factor 1 (IGF-1) in boys. This suggests lead may impact growth by affecting the hypothalamic-pituitary-growth axis.

Area of Science:

  • Environmental Health
  • Pediatric Endocrinology
  • Toxicology

Background:

  • Childhood lead exposure is a known risk factor for growth delay.
  • The specific relationship between blood lead levels (BLLs) and insulin-like growth factor 1 (IGF-1) in low-level exposure scenarios remains under-characterized in large cohorts.

Purpose of the Study:

  • To investigate the association between baseline blood lead levels (BLLs) and serum insulin-like growth factor 1 (IGF-1) concentrations in a cohort of boys.
  • To determine if lead exposure impacts growth markers in children with low-level exposure.

Main Methods:

  • Recruited 394 boys aged 8-9 years from an industrial Russian town.
  • Employed linear regression models to assess the association between baseline BLLs and serum IGF-1 at ages 10-11 and 12-13 years.
  • Adjusted for demographic, socioeconomic, and pubertal status covariates.

Main Results:

  • A median BLL of 3 μg/dL was observed at baseline; 86% of boys were prepubertal.
  • Higher BLLs were significantly associated with lower mean serum IGF-1 concentrations at follow-up (e.g., -29.2 ng/mL difference for BLLs ≥ 5 μg/dL vs. < 5 μg/dL).
  • The inverse association between BLLs and IGF-1 was more pronounced in mid-pubertal boys and showed a dose-response relationship across different BLL categories.

Conclusions:

  • Elevated blood lead levels in peripubertal boys with low-level exposure are associated with reduced serum IGF-1.
  • Lead exposure may contribute to growth delay through potential inhibition of the hypothalamic-pituitary-growth axis.
Abstract

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