Association between aminolevulinate dehydrogenase genotype and blood lead levels in Taiwan

J Occup Environ Med. 2000 Feb;42(2):151-5. doi: 10.1097/00043764-200002000-00009.

Abstract

This study was designed to evaluate the association between the aminolevulinate dehydrogenase (ALAD) genotype and blood lead levels in a general population environmentally exposed to lead. This study population of 660 subjects was secondarily sampled from the 3000 random samples of Taiwanese general population to study the distribution of blood lead levels in the Taiwanese population. A simple assay based on the polymerase chain reaction-restriction fragment length polymorphism technique was used to determine the genotype of the ALAD gene. This study found that most of the Taiwanese population was ALAD 1-1 (95.4%). Only 4.6% (30 subjects) of population were found to be 1-2 or 2-2. It has been hypothesized that the ALAD2 allele is associated with increased absorption of lead. This study found that individuals with ALAD2 alleles had 20% higher blood lead levels than persons with ALAD1 alleles (7.83 +/- 5.95 vs 6.51 +/- 5.03 micrograms/dL). However, the difference was not statistically significant, even after adjustment for other risk factors of environmental exposure. The result supports the previous finding that individuals with ALAD2 allele had higher blood lead levels. The small sample size and large amount of variation in our study may account for the insignificant association.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asian Continental Ancestry Group / genetics*
  • Base Sequence
  • Environmental Exposure / adverse effects*
  • Ethnic Groups
  • Female
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Lead / adverse effects
  • Lead / blood*
  • Lead Poisoning / genetics*
  • Male
  • Molecular Sequence Data
  • Polymerase Chain Reaction
  • Porphobilinogen Synthase / genetics*
  • Sampling Studies
  • Sensitivity and Specificity
  • Taiwan

Substances

  • Lead
  • Porphobilinogen Synthase