title: Lack of association of delta-aminolevulinic acid dehydratase genotype with cytogenetic damage in lead workers.
abstract: OBJECTIVE
  The objective of this study was to evaluate the correlations of genetic polymorphism of genotypes delta-aminolevulinic acid dehydratase (ALAD), blood lead levels (BLLs), zinc protoporphyrin (ZPP), sister chromatid exchanges (SCEs), and high SCE frequency cells (HFCs) in lead workers.
  
  
  METHODS
  Three groups of lead workers were included in the study: high lead exposure group (26 workers), low lead exposure group (31 workers) and control group (30 controls who lived in an area uncontaminated by lead). Blood samples were taken from all subjects and analyzed for lead levels, ALAD genotype and SCE levels.
  
  
  RESULTS
  Occupationally exposed workers had significantly higher BLLs, ZPP and hemoglobin levels than the controls. There were no differences among the three groups regarding percentages of ALAD 1-1 and ALAD 1-2 genotypes, but the ALAD 2-2 genotype was not detected in any of the three groups. There were no significant differences among the three groups for BLLs, ZPP and hemoglobin levels based on ALAD 1-1 and ALAD 1-2. Average SCE values in the high lead exposure group were significantly greater than those in the control group (6.2 vs 5.2 SCEs/cell, P < 0.05). HFC analysis revealed a significantly higher HFC percentage (53.9%) in the high lead exposure group than in the low lead exposure group (16.1%) and the control group (10%). There appeared to be an interaction effect on HFC percentages between smoking and lead exposure. When multiple regression analysis was used, the factors that affected SCE levels were lead exposure and smoking, but ALAD genotypes did not have any significant effect.
  
  
  CONCLUSIONS
  A significant association existed between both SCE and HFC levels and lead exposure. However, different ALAD genotypes were not found to be associated with levels of blood lead and ZPP in the three groups.
authors.affiliation: Institute of Environmental Health, China Medical University, 91 Hsueh-Shin Road, Taichung, Taiwan.
authors.forename: Fang-Yang
authors.initials: FY
authors.lastname: Wu
authors.forename: Pao-Wen
authors.initials: PW
authors.lastname: Chang
authors.forename: Chin-Ching
authors.initials: CC
authors.lastname: Wu
authors.forename: Jim-Shoung
authors.initials: JS
authors.lastname: Lai
authors.forename: Hsien-Wen
authors.initials: HW
authors.lastname: Kuo
mesh_terms: D000328:Adult; D003582:Cytogenetics; D005260:Female; D005838:Genotype; D006801:Humans; D007854:Lead / Q000097:blood / Q000633:toxicity*; D016014:Linear Models; D008297:Male; D008669:Metallurgy; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects* / Q000032:analysis; D010087:Oxides / Q000097:blood / Q000633:toxicity*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000187:drug effects; D000623:Porphobilinogen Synthase / Q000097:blood / Q000235:genetics*; D011524:Protoporphyrins / Q000097:blood / Q000235:genetics; D012307:Risk Factors; D012854:Sister Chromatid Exchange / Q000187:drug effects* / Q000235:genetics; D011795:Surveys and Questionnaires; D013624:Taiwan / Q000453:epidemiology; D000078329:Workforce
chemical_list: D010087:Oxides; D011524:Protoporphyrins; C017803:zinc protoporphyrin; D007854:Lead; C047365:lead oxide; D000623:Porphobilinogen Synthase