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δ-Aminolevulinic Acid Dehydratase Single Nucleotide Polymorphism 2 and Peptide Transporter 2*2 Haplotype May Differentially Mediate Lead Exposure in Male Children

  • Sobin, Christina1, 2, 3, 4
  • Parisi, Natali5
  • Schaub, Tanner5
  • Gutierrez, Marisela4
  • Ortega, Alma X.2
  • 1 University of Texas, Toxicology Project, Border Biomedical Research Center, El Paso, TX, USA , El Paso (United States)
  • 2 University of Texas, Department of Public Health Sciences, College of Health Sciences, El Paso, TX, USA , El Paso (United States)
  • 3 The Rockefeller University, Laboratory of Neuroendocrinology, New York, NY, USA , New York (United States)
  • 4 University of Texas, Laboratory of Neurocognitive Genetics and Developmental Neurocognition, Department of Psychology, El Paso, TX, USA , El Paso (United States)
  • 5 New Mexico State University, Chemical Analysis and Instrumentation Laboratory, College of Agricultural, Consumer and Environmental Sciences, Las Cruces, NM, USA , Las Cruces (United States)
Published Article
Archives of Environmental Contamination and Toxicology
Publication Date
Feb 16, 2011
DOI: 10.1007/s00244-011-9645-3
Springer Nature


Child low-level lead (Pb) exposure is an unresolved public health problem and an unaddressed child health disparity. Particularly in cases of low-level exposure, source removal can be impossible to accomplish, and the only practical strategy for reducing risk may be primary prevention. Genetic biomarkers of increased neurotoxic risk could help to identify small subgroups of children for early intervention. Previous studies have suggested that, by way of a distinct mechanism, δ-aminolevulinic acid dehydratase single nucleotide polymorphism 2 (ALAD2) and/or peptide transporter 2*2 haplotype (hPEPT2*2) increase Pb blood burden in children. Studies have not yet examined whether sex mediates the effects of genotype on blood Pb burden. Also, previous studies have not included blood iron (Fe) level in their analyses. Blood and cheek cell samples were obtained from 306 minority children, ages 5.1 to 12.9 years. 208Pb and 56Fe levels were determined with inductively coupled plasma–mass spectrometry. General linear model analyses were used to examine differences in Pb blood burden by genotype and sex while controlling for blood Fe level. The sample geometric mean Pb level was 2.75 μg/dl. Pb blood burden was differentially higher in ALAD2 heterozygous boys and hPEPT2*2 homozygous boys. These results suggest that the effect of ALAD2 and hPEPT2*2 on Pb blood burden may be sexually dimorphic. ALAD2 and hPEPT2*2 may be novel biomarkers of health and mental health risks in male children exposed to low levels of Pb.

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