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HuGENet Reviews

δ-Aminolevulinic Acid Dehydratase (ALAD) Genotype and Lead Toxicity
Samir N. Kelada1,4, Erin Shelton2, Rachel B. Kaufmann3, and Muin J. Khoury1

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 REFERENCES

  1. Wetmur JG, Bishop DF, Cantelmo C, et al. Human delta-aminolevulinate dehydratase: nucleotide sequence of a full-length cDNA clone. Proc Natl Acad Sci USA 1986;83:7703-7.
  2. Jaffe EK. The porphobilinogen synthase family of metalloenzymes. Acta Crystallogr D Biol Crystallogr 2000;56(Pt 2):115-28.
  3. Wetmur JG. Influence of the common human delta-aminolevulinate dehydratase polymorphism on lead body burden. Environ Health Perspect 1994;102 Suppl 3:215-9. 
  4. Battistuzzi G, Petrucci R, Silvagni L, et al. delta-Aminolevulinate dehydrase: a new genetic polymorphism in man. Ann Hum Genet 1981; 45:223-9. 
  5. Wetmur JG, Kaya AH, Plewinska M, et al. Molecular characterization of the human delta-aminolevulinate dehydratase2 (ALAD2) allele: implications for molecular screening of individuals for genetic susceptibility to lead poisoning. Am J Hum Genet 1991;49:167-74. 
  6. Fleming DE, Chettle DR, Wetmur JG, et al. Effect of the delta-aminolevulinate dehydratase polymorphism on the accumulation of lead in bone and blood in lead smelter workers. Environ Res 1998;77(1):49-61. 
  7. Alexander BH, Checkoway H, Costa-Mallen P, et al. Interaction of blood lead and delta-aminolevulinic acid dehydratase genotype on markers of heme synthesis and sperm production in lead smelter workers. Environ Health Perspect 1998;106(4):213-6. 
  8. Goedde HW, Rothhammer F, Benkmann HG, et al. Ecogenetic studies in Atacameno Indians. Hum Genet 1984;67(3):343-6. 
  9. Eiberg H, Mohr J, Nielsen LS. delta-Aminolevulinate dehydrase: synteny with ABO-AK1-ORM (and assignment to chromosome 9). Clin Genet 1983;23(2):150-4. 
  10. Juli E, Scheil HG, Gunther A. [Gene frequency of delta-aminolevulinate dehydratase (E.C. 4.2.1.24) in a West German population]. Anthropol Anz 1983;41(4):309-11. 
  11. Benkmann H-G, Bogdanski P, Goedde HW. Polymorphism of delta-aminolevulinic acid dehydratase in various populations. Hum Hered 1983;33:62-4. 
  12. Scheil HG, Scheffrahn W. [Gene frequencies of the enzymes ALADH, GOT2, GPT, PGM3, SAHH and UMPK in a Swiss population]. Anthropol Anz 1987;45(3):255-60. 
  13. Kapotis C, Tsomi A, Babionitakis A, et al. The genetic polymorphism of aminolevulinate dehydratase (ALADH) in Greece. Hum Hered 1998;48(3):155-7. 
  14. Ben-Ezzer J, Oelsner H, Szeinberg A. Genetic polymorphism of delta-aminolevulinate dehydrase in several population groups in Israel. Hum Hered 1987;37(4):229-32. 
  15. Petrucci R, Leonardi A, Battistuzzi G. The genetic polymorphism of human delta-Aminolevulinate dehydratase in Italy. Hum Genet 1982;60:289-90.
  16. Komatsu N, Ose Y, Kido A, et al. Distribution of ALADH Types in Yamanashi Prefecture. Jpn J Legal Med 1987;41(1):1-3. 
  17. Sakai T, Morita Y, Araki T, et al. Relationship Between Delta-Aminolevulinic Acid Dehydratase Genotypes and Heme Precursors in Lead Workers. Am J Ind Med 2000;38:355-60. 
  18. Raczek E. Polymorphism of delta-aminolevulinate dehydratase in the upper Silesian population, Poland. Hum Hered 1994;44(3):172-4. 
  19. Amorim A, Rocha J, Santos MT. Distribution of ACP1, AK1 and ALAD polymorphisms in northern Portugal. Gene Geogr 1994;8(2):147-50. 
  20. Roychoudhury AK, Nei M. Human polymorphic genes: world distribution. New York, NY: Oxford University Press, 1988:54. 
  21. Garcia-Orad A, Aguirre AI, Mazon LI, et al. Polymorphism of delta-aminolevulinic acid dehydratase in Basque populations. Hum Hered 1987;37(5):321-2. 
  22. Caeiro B, Rey D. Genetic heterogeneity of delta-aminolevulinate dehydrase and phosphoglycolate phosphatase in north-west Spain. Hum Hered 1985;35(1):21-4. 
  23. Hsieh LL, Liou SH, Chen YH, et al. Association between aminolevulinate dehydrogenase genotype and blood lead levels in Taiwan. J Occup Environ Med 2000;42(2):151-5. 
  24. Smith CM, Wang X, Hu H, et al. A polymorphism in the d-aminolevulinic acid dehydratase gene may modify the pharmacokinetics and toxicity of lead. Environ Health Perspect 1995;103:248-253. 
  25. Astrin KH, Bishop DF, Wetmur JG, et al. delta-Aminolevulinic acid dehydratase isozymes and lead toxicity. Ann NY Acad Sci 1987;514:23-9. 
  26. Wetmur JG, Lehnert G, Desnick RJ. The delta-aminolevulinate dehydratase polymorphism: higher blood lead levels in lead workers and environmentally exposed children with the 1-2 and 2-2 isozymes. Environ Res 1991;56(2):109-19. 
  27. Mahaffey K, McKinney J, Reigart JR. Lead and compounds. In: Lippmann M, ed. Environmental toxicants, human exposures and their health effects, 2nd ed. New York, NY: John Wiley and Sons, 2000: 481-521. 
  28. Goyer RA. Toxic Effects of Metals. In: Klaassen CD, ed. Casarett & Doull’s Toxicology, the basic science of poisons, 5th ed. New York, NY: McGraw-Hill, 1996: 691-736. 
  29. National Research Council (NRC). Measuring lead exposure in infants, children, and other sensitive populations. Washington, DC: NRC, 1990. 
  30. Lin-Fu JS. Vulnerability of children to lead exposure and toxicity: Part one. N Eng J Med 1973;289:1229-33. 
  31.  Ziegler EE, Edwards BB, Jensen RL, et al. Absorption and retention of lead by infants. Ped Res 1978; 12:29-34. 
  32. Mahaffey KR. Nutrition and lead: Strategies for public health. Environ Health Perspect 1995; 103 (Suppl 6):191-6. 
  33. National Institute of Occupational Health and Safety (NIOSH). Protecting workers exposed to lead-based paint hazards, a report to Congress. Cincinnati, OH: NIOSH, 1997. 
  34. Osterlow JF, Sharp DS, Hata B. Quality Control Data for Low Blood Lead Concentrations by Three Methods Used in Clinical Studies. J Analyt Toxicol 1990;14:8-11. 
  35. McElvaine MD, Orbach HG, Binder S, et al. Evaluation of erythrocyte protoporphyrin test as a screen for elevated blood lead levels, Chicago, Illinois, 1988-1989. J Pediatr 1991;119(4):548-550. 
  36. Schutz, AS, Skervfing J, Christoffersson JO. Chelatable level versus lead in human trabecular and compact bone. Sci Total Environ 1987;68:45-59.
  37. Pirkle JL, Kaufmann RB, Brody DJ, et al. Exposure of the U.S. population to lead, 1991-1994. Environ Health Perspect 1998;11:745-50. 
  38. Lanphear BP, Byrd RS, Auinger P, et al. Community characteristics associated with children’s blood lead levels. Pediatrics 1998;101:264-71. 
  39. Sargent JD, Brown MJ, Freeman JL, et al. Childhood lead poisoning in Massachusetts communities: Its association with sociodemographic and housing characteristics. Am J Pub Health 1995; 85:528-34. 
  40. Baghurst, PA, McMichael AJ, Wigg NR. Environmental exposure to lead and children’s intelligence at the age of seven years. The Port Pirie Cohort Study. N Engl J Med 1992; 327:1279-84. 
  41. Friscancho AR, Ryan AS. Decreased stature associated with moderate blood lead concentrations in Mexican-American children. Am J Clin Nutr 1991;54:516-19. 
  42. Otto DA and Fox DA. Auditory and visual dysfunction following lead exposure. Neurotox 1993;14(2-3):191-207. 
  43. Banks EC, Ferretti LE, Shucard DW. Effects of low level lead exposure on cognitive function in children: a review of behavioral, neuropsychological and behavioral evidence. Neurotox 1997;18(1):237-81. 
  44. Bellinger D, Dietrich KN. Low-level lead exposure and cognitive function in children. Pediatr Ann 1994;23(11):600-5. 
  45. Lanphear BP, Dietrich KN, Auinger P, et al. Subclinical lead toxicity in U.S. children and adolescents. Ped Res 2000;152A. 
  46. Schwartz J. Low-level lead exposure and children’s IQ: a meta-analysis and search for a threshold. Environ Res 1994;65:42-55. 
  47. Centers for Disease Control (CDC). Screening young children for lead poisoning: guidance for state and local public health officials.  Atlanta: CDC, 1997. 
  48. Lanphear BP. The paradox of lead poisoning prevention. Science 1998;1617-18. 
  49. Pirkle JL, Brody DJ, Gunter EW, et al. The decline in blood lead levels in the United States. The National Health and Nutrition Examination Surveys. J Amer Med Assoc 1994;272(4):284-91. 
  50. CDC. Adult blood lead epidemiology and surveillance – United States, second and third quarters, 1998, and annual 1994-1997. Morbidity and Mortality Weekly Report 1999; 48(10):213-6. 
  51. Kappas A, Sassa S, Galbraith RA, et al. The porphyrias. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The metabolic and molecular basis of inherited disease, 7th ed. New York:McGraw-Hill, 1995;2103-59. 
  52. Chisolm JJ Jr, Thomas DJ, Hamill TG. Erythrocyte porphobilinogen synthase activity as an indicator of lead exposure in children. Clin Chem 1985;31:601-605. 
  53. Rogan WJ, Reigart JR, Gladen BC. Association of aminolevulinate dehydratase levels and ferrochelatase inhibition in childhood lead exposure. J Pediatr 1986;109:60-64. 
  54. Jaffe EK, Bagla S, Michini PA. Reevaluation of a sensitive indicator of early lead exposure. Measurement of porphobilinogen synthase in blood. Biol Trace Element Res 1991;28:223-31. 
  55. Warren MJ, Cooper JB, Wood SP, et al. Lead poisoning, haem synthesis and 5-aminolaevulinic acid dehydratase. Trends Biochem Sci 1998;23(6):217-21. 
  56. Muller WE, Snyder SH. delta-Aminolevulinic acid: influences on synaptic GABA receptor binding may explain CNS symptoms of porphyria. Ann Neurol 1977;2:340-42. 
  57. Brennan MJ, Cantrill RC. delta-Aminolaevulinic acid is a potent agonist for GABA autoreceptors. Nature 1979;280:514-15. 
  58. Ziemsen B, Angerer J, Lehnert G, et al. Polymorphism of delta-aminolevulinic acid dehydratase in lead-exposed workers. Int Arch Occup Environ Health 1986;58:245-47. 
  59. Schwartz BS, Lee BK, Stewart W, et al. Associations of d-aminolevulinic acid dehydratase genotype with plant, exposure duration, and blood lead and zinc protoporphyrin levels in Korean lead workers. Am J Epidemiol 1995;142:738-45. 
  60. Bergdahl IA, Gerhardsson L, Schutz A, et al. Delta-aminolevulinic acid dehydratase polymorphism: influence on lead levels and kidney function in humans. Arch Environ Health 1997;52(2):91-6. 
  61. Schwartz BS, Lee BK, Stewart W, et al. delta-Aminolevulinic acid dehydratase genotype modifies four hour urinary lead excretion after oral administration of dimercaptosuccinic acid. Occup Environ Med 1997;54(4):241-6. 
  62. Schwartz BS, Lee BK, Stewart W, et al. Associations of subtypes of hemoglobin with delta-aminolevulinic acid dehydratase genotype and dimercaptosuccinic acid-chelatable lead levels. Arch Environ Health 1997;52:97-103. 
  63. Sithisarankul P, Schwartz BS, Lee BK, et al. Aminolevulinic acid dehydratase genotype mediates plasma levels of the neurotoxin, 5-aminolevulinic acid, in lead-exposed workers. Am J Ind Med 1997;32:15-20. 
  64. Schwartz BS, Lee B-L, Lee G-S, et al. Associations of Blood Lead, Dimercaptosuccinic Acid-Chelatable Lead, and Tibia Lead with Polymorphisms in the Vitamin D Receptor and d-Aminolevulinic Acid Dehydratase Genes. Environ Health Perspect 2000;108(10):949-54. 
  65. Bergdahl IA, Grubb A, Schutz A, et al. Lead binding to delta-aminolevulinic acid dehydratase (ALAD) in human erythrocytes. Pharmacol Toxicol 1997;81(4):153-8. 
  66. Bellinger D, Hu H, Titlebaum L, et al. Attentional correlates of dentin and bone lead levels in adolescents. Arch Environ Health 1994;49:98-105. 
  67. Doss M, Laubenthal F, Stoeppler M. Lead poisoning in inherited d-aminolevulinic acid dehydratase deficiency. Int Arch Occup Environ Health 1984;54:55-63. 
  68. Mahaffey KR, Gartside PS, Glueck CJ. Blood lead levels and dietary calcium intake in 1-11-year-old children: the Second National Health and Nutrition Examination Survey, 1976-1980. Pediatrics 1986;78:257-62. 
  69. Blake KCH, Mann M. Effect of calcium and phosphorus on the gastrointestinal absorption of 203 Pb in man. Environ Res 1983;30:188-94. 
  70. Cooper GS, Umbach DM. Are vitamin D receptor polymorphisms associated with bone mineral density? A meta-analysis. J Bone Miner Res 1996;11:1841-49. 
  71. Schwartz BS, Stewart WF, Kelsey K, et al. Associations of tibial lead levels with BsmI polymorphisms in the vitamin D receptor in former organolead manufacturing workers. Environ Health Perspect 2000;108(3):199-203. 
  72. Mahaffey-Six K, Goyer RA. Experimental enhancement of lead toxicity by low dietary calcium. J Lab Clin Med 1972;76:933-42. 
  73. Barton JC, Patton MA, Edwards CQ, et al. Blood lead concentrations in hereditary hemochromatosis. J Lab Clin Med 1994; 124(2):193-8. 
  74. Åkesson A, Stål P, Vahter M. Phlebotomy increases cadmium uptake in hemochromatosis. Environ Health Perspect 2000 Apr;108(4):289-91. 
  75. Fujita, H, Sato K, Sano S. Increase in the amount of erythrocyte d-aminolevulinate dehydratase in workers with moderate lead exposure. Int Arch Occup Environ Health 1982; 50:287-97. 
  76. Boudene C, Despaux-Pages N, Comoy E, et al. Immunological and enzymatic studies of erythrocytic d-aminolevulinate dehydratase. Comparison of results obtained in normal and lead-exposed subjects. Int Arch Occup Environ Health 1984;55: 57-96.
Page last reviewed: July 1, 2001 (archived document)
Page last updated: November 2, 2007
Content Source: CDC's Office of Public Health Genomics