Advertisement

Medical Toxicology

, Volume 1, Issue 6, pp 387–410 | Cite as

Lead Intoxication

  • L. S. Ibels
  • C. A. Pollock
Toxicology Management Review

Summary

Lead intoxication was recognised as early as 2000 BC and the widespread use of lead has been a cause of endemic chronic plumbism in several societies throughout history. In the twentieth century, lead intoxication is still a common problem. In children it is largely due to ingestion of pica and environmental exposure, whereas adult groups at greatest risk are the industrially exposed: thus, screening of these workers should be undertaken at regular intervals. The clinical features of lead intoxication are nonspecific and often go unrecognised. The early manifestations are largely neuropsychiatric, followed by more significant disturbances of the central and peripheral nervous systems, symptomatic gastrointestinal, musculoskeletal, haematological and endocrine abnormalities. The association of lead poisoning with renal disease is well documented and must be considered, particularly if there is associated hypertension and/or gout.

Blood lead concentrations are an unreliable predictor of body lead stores as they are indicative only of recent exposure. Haematological parameters have been used to assess those at risk of toxicity, but although more reliable than blood concentrations, they also fail to predict those patients at risk of toxicity. The recommended assessment for patients with suspected lead intoxication is a calcium disodium edetate chelation test, which is a sensitive marker for assessing body stores and subsequent intoxication. In children the dosage should be 50 mg/kg up to 1000mg, and in adults 1000mg administered intravenously or 2000mg intramuscularly in divided doses 12 hours apart with subsequent 72 hour urinary lead estimations. Lead excretion levels greater than 350 μg/72 hours should be considered as suggestive of intoxication, particularly if supported by historical, clinical or biochemical evidence of lead exposure. Treatment of patients with positive chelation tests involves symptomatic treatment and a course of chelation therapy utilising calcium disodium edetate in doses similar to those used for testing, and in the more severely intoxicated patient, the addition of dimercaprol in doses of 75 mg/m2 every 4 hours to a total of 300 mg/m2/day. The safety of these treatment regimens is well documented.

Keywords

Gout Lead Exposure Blood Lead Level Lead Poisoning Lead Toxicity 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Albahary C, Truhaut R, Boudene C, Desoille H. Le depistage de l’impregnation saturnine par un test de mobilisation du plomb. Presse Medicale 69: 2121–2123, 1961PubMedGoogle Scholar
  2. Aono H, Araki S. The effects of calcium EDTA injection on lead, zinc, copper, and ALAD in erythrocyte, plasma and urine in lead exposed workers: a 24 hour observation. International Archives of Occupational and Environmental Health 55: 13–18, 1984PubMedGoogle Scholar
  3. Araki S, Murata K, Aono H. A comparison of the diminution of rates of lead in blood and lead mobilised by calcium EDTA after termination of occupational exposure: a long term observation in two lead workers. Journal of Toxicology — Clinical Toxicology 20: 475–486, 1983PubMedGoogle Scholar
  4. Baker EL, Goyer RA, Fowler BA, et al. Occupational lead exposure: nephropathy and renal cancer. American Journal of Industrial Medicine 1: 139–148, 1980PubMedGoogle Scholar
  5. Bakerman S. Lead poisoning. Clinical Chemistry 23: 1–9, 1983Google Scholar
  6. Ball GV, Sorenson LB. Pathogenesis of hyperuricaemia in saturnine gout. New England Journal of Medicine 280: 1199–1202, 1969PubMedGoogle Scholar
  7. Batuman V, Landy E, Maesaka JK, Wedeen RP. Contribution of lead to hypertension with renal impairment. New England Journal of Medicine 309: 17–21, 1983PubMedGoogle Scholar
  8. Batuman V, Maesaka JK, Haddad B, Tepper L. The role of lead in gout nephropathy. New England Journal of Medicine 304: 520–523, 1981PubMedGoogle Scholar
  9. Beattie AD, Moore MR, Goldberg A. Tetraethyl lead poisoning. Lancet 2: 12–15, 1972PubMedGoogle Scholar
  10. Beattie AD, Mullin PH, Baxter RH, Moore MR. Acute lead poisoning: an individual case of hepatitis. Scottish Medical Journal 24: 318–321, 1979PubMedGoogle Scholar
  11. Beevers DG, Erskine E, Robertson M, et al. Blood lead and hypertension. Lancet 2: 1–3, 1976PubMedGoogle Scholar
  12. Belknap EL. EDTA in the treatment of lead poisoning. Industrial Medicine and Surgery 21: 305, 1952PubMedGoogle Scholar
  13. Benson MD, Price J. Cerebellar calcification and lead. Journal of Neurology, Neurosurgery and Psychiatry 48: 814–815, 1985Google Scholar
  14. Brownie CF, Aronson AL. Comparative effects of calcium ethylene diamine tetra acetic acid (EDTA), Zn EDTA and Zn Ca EDTA in mobilizing lead. Toxicology and Applied Pharmacology 75: 167–172, 1984PubMedGoogle Scholar
  15. Braunstein GD, Dahlgren J, Loriaux L. Hypogonadism in chronically lead exposed men. Infertility 1: 33, 1978PubMedGoogle Scholar
  16. Campbell BC, Beattie AD, Moore MR, et al. Renal insufficiency associated with excessive lead exposure. British Medical Journal 1: 482–485, 1977PubMedGoogle Scholar
  17. Chisolm JJ. The use of chelating agents in the treatment of acute and chronic lead intoxication in children. Journal of Paediatrics 73: 1–38, 1968Google Scholar
  18. Chisolm JJ, Barrett MB, Harrison MV. Indicators of internal dose of lead in relationship to derangement of heme synthesis. Johns Hopkins Medical Journal 137: 6–12, 1975PubMedGoogle Scholar
  19. Chisolm JJ, Mellits E, Barrett MB. Interrelationships among blood lead concentration, quantitative daily ALA-U and urinary lead output following calcium EDTA. In Nordberg (Ed.) Effects and dose-response relationships of toxic metals, pp. 4–423, Elsevier, Amsterdam, 1976Google Scholar
  20. Chisolm JJ, Thomas DJ. Use of 2,3-dimercaptopropane-1-sulfonate in treatment of lead poisoning in children. Journal of Pharmacology and Experimental Therapeutics 235: 665–669, 1985PubMedGoogle Scholar
  21. Center for Disease Control. Preventing lead poisoning in young children. Journal of Paediatrics 93: 709–720, 1978Google Scholar
  22. Choie DD, Richter GW. Effects of lead on the kidney function. In Singhal & Thomas (Eds) Lead toxicity, pp. 187–212, Urban and Schwartzenberg, Baltimore/Munich, 1980Google Scholar
  23. Cramer K, Goyer R, Jagenburg R, et al. Renal ultrastructure, renal function and parameters of lead toxicity in workers with different periods of lead exposure. British Journal of Industrial Medicine 31: 113–127, 1974PubMedGoogle Scholar
  24. Craswell PW, Price J, Boyle PD, et al. Chronic renal failure with gout: a marker of chronic lead poisoning. Kidney International 26: 319–323, 1984PubMedGoogle Scholar
  25. Cullen MR, Robins JM, Eskenzai B. Adult inorganic lead intoxication: presentation of thirty-one new cases and a review of recent advances in the literature. Medicine 62: 221–247, 1983PubMedGoogle Scholar
  26. David OJ, Katz S, Arcoleo CG. Chelation therapy in children as treatment of sequelae in severe lead toxicity. Archives of Environmental Health 40: 109–113, 1985PubMedGoogle Scholar
  27. Department of Health & Social Security Working Party on lead in the environment. Lead and Health, HMSO, London, 1980Google Scholar
  28. Di Maio VJ, Garriott J. A fatal case of lead poisoning due to a retained bullet. Veterinary and Human Toxicology 22: 390–391, 1980Google Scholar
  29. Editorial. Diagnosis of inorganic lead poisoning: a statement. British Medical Journal 4: 501, 1968Google Scholar
  30. Editorial. Lead. It’s everywhere. Emergency Medicine 17(11): 60–91, 1985Google Scholar
  31. Emmerson BT. Chronic lead nephropathy. Kidney International 4: 1–5, 1973PubMedGoogle Scholar
  32. Emmerson BT. Chronic lead nephropathy. The diagnostic use of calcium EDTA and the association with gout. Australian and New Zealand Journal of Medicine 12: 310–324, 1963Google Scholar
  33. Emmerson BT. The renal excretion of urate in chronic lead nephropathy. Australian Annals of Medicine 14: 295–303, 1965Google Scholar
  34. Emmerson BT, Mirosch E, Douglas JB. The relative contributions of tubular reabsorption and secretion to urate excretion in lead nephropathy. Australian and New Zealand Journal of Medicine 4: 353–362, 1971Google Scholar
  35. Emmerson BT, Thiele BR. Calcium versenate in the diagnosis of chronic lead nephropathy. Medical Journal of Australia 1: 243–248, 1960Google Scholar
  36. Fahim MS, Fahim Z, Hall DG. Effects of subtoxic lead levels on pregnant women in the State of Missouri. Research Communications in Chemical Pathology and Pharmacology 13: 309–313, 1976PubMedGoogle Scholar
  37. Farkas WR, Stanawitz T, Schneider M. Saturnine gout: lead induced formation of guanine crystals. Science 199: 786–787, 1978PubMedGoogle Scholar
  38. Feldman RG, Hayes MK, Younes R, Aldrich FD. Lead nephropathy in adults and children. Archives of Neurology 34: 481–488, 1977PubMedGoogle Scholar
  39. Fell GS. Lead toxicity: problems of definition and laboratory evaluation. Annals of Clinical Biochemistry 21: 453–460, 1984PubMedGoogle Scholar
  40. Foreman M, Trujillo TT. The metabolism of C14 labelled ethylene diamine tetra acetate in human beings. Journal of Laboratory and Clinical Medicine 43: 566–571, 1984Google Scholar
  41. Fortenberry JD. Gasoline sniffing. American Journal of Medicine 79: 740–744, 1985PubMedGoogle Scholar
  42. Gonzales JJ, Werk EE, Thrasher K, et al. Renin-aldosterone system and potassium levels in chronic lead intoxication. Southern Medical Journal 72: 433–436, 440, 1979Google Scholar
  43. Gordon NC, Brown S, Khosla VM. Lead poisoning: a comprehensive review and report of a case. Oral Surgery 47: 500–512, 1979Google Scholar
  44. Goyer RA, Wilson MH. Lead induced inclusion bodies: results of ethylene diamine tetra-acetate acid treatment. Journal of Laboratory Investigations 32: 149–156, 1965Google Scholar
  45. Graef JW, Kopito L, Schwachman H. Lead intoxication in children: diagnosis and treatment. Postgraduate Medicine 50: 133–138, 1971PubMedGoogle Scholar
  46. Grandjean P. Widening perspectives of lead toxicity: a review of health effects of lead exposure in adults. Environmental Research 17: 303–321, 1978PubMedGoogle Scholar
  47. Granick JL, Sassa S, Kappas A. Some biological and clinical aspects of lead intoxication. Advances in Clinical Chemistry 20: 287–339, 1978PubMedGoogle Scholar
  48. Graziano JH. Role of 2,3 dimercaptosuccinic acid in the treatment of heavy metal poisoning. Medical Toxicology 1: 155–161, 1986PubMedGoogle Scholar
  49. Haenninen H, Hernberg S, Mantere P, et al. Psychological performance of subjects with low exposure to lead. Journal of Occupational Medicine 20: 683–689, 1978PubMedGoogle Scholar
  50. Hammond PB, Lerner SI, Gartside PS, et al. The relationship of biological exposure to the health status of workers in a secondary lead smelter. Journal of Occupational Medicine 22: 475–484, 1980PubMedGoogle Scholar
  51. Hansen JPB, Dossing M, Palver PE. Chelation of lead body burden (by calcium-disodium EDTA) and block lead concentration in man. Journal of Occupational Medicine 23: 39–43, 1981PubMedGoogle Scholar
  52. Health and Safety Commission. Control of Lead at Work. Her Majestys Stationery Office, London, 1980Google Scholar
  53. Henderson DA. A follow-up of cases of plumbism in children. Australasian Annals of Medicine 3: 219–224, 1954PubMedGoogle Scholar
  54. Henderson DA, Inglis JA. The lead content of bone in chronic Bright’s disease. Australasian Annals of Medicine 6: 145–154, 1957PubMedGoogle Scholar
  55. Hong CD, Hanenson IB, Lerner S, et al. Occupational exposure to lead: effects on renal function. Kidney International 18: 489–494, 1980PubMedGoogle Scholar
  56. Ishihara N, Shiojima S, Hasegawa K. Lead and zinc concentration in plasma, erythrocytes and urine in relation to ALA-D: activity after intravenous infusion of Ca-EDTA. British Journal of Industrial Medicine 41: 235–240, 1984PubMedGoogle Scholar
  57. Lancranjan F, Popsesui HI, Gavanescu O, et al. Reproductive ability of workmen occupationally exposed to lead. Archives of Environmental Health 30: 396–401, 1975PubMedGoogle Scholar
  58. Lead, alloys and inorganic compounds. Encyclopaedia of occupational health and safety, 33rd ed., pp. 1200–1209, ILO, Geneva, 1983Google Scholar
  59. Leckie WJH, Thomsett SL. The diagnostic and therapeutic use of edathamil calcium disodium (EDTA versene) in excessive inorganic lead absorption. Quarterly Journal of Medicine 105: 65–82, 1978Google Scholar
  60. Lilis R, Valciukas JA, Malkin J, Weber J-P. Effects of low-level lead arsenic exposure on copper smelter workers. Archives of Environmental Health 40: 34–48, 1985Google Scholar
  61. Lilis R, Fischbein A, Valciukas JA, et al. Kidney function and lead; relationship in several occupational groups with different levels of exposure. American Journal of Industrial Medicine 1: 405–412, 1980PubMedGoogle Scholar
  62. Lin-Fu JS. Lead poisoning in children: what price shall we pay? Children Today 8: 9–13, 36, 1979PubMedGoogle Scholar
  63. Mahaffey KR, Annest JL, Roberts J, Murphy RS. National estimates of blood lead levels: United States, 1976–1980. Association with selected demographic and socioeconomic factors. New England Journal of Medicine 20: 50–53, 1970Google Scholar
  64. Malcolm D. The effects of lead on the kidney. Transactions of the Society of Occupational Medicine 20: 50–53, 1970PubMedGoogle Scholar
  65. Markowitz ME, Rosen JH. Assessment of lead stores in children: validation of an eight hour CaNa2 EDTA provocative test. Journal of Paediatrics 104: 337–341, 1984Google Scholar
  66. Moore MR. Lead, ethanol and delta-aminolevulinate dehydratase. Biochemical Journal 129: 43P-44P, 1972Google Scholar
  67. Morgan JM, Hartley MW, Miller RE. Nephropathy in chronic lead poisoning. Archives of Internal Medicine 118: 17–29, 1966PubMedGoogle Scholar
  68. National Academy of Sciences, Commission on Natural Resources. Lead in the Human Environment, National Academy of Sciences, Washington DC, 1980Google Scholar
  69. Needleman HL, Gunnoe C, Leviton A, et al. Deficits in psychological and classroom performance of children with elevated dentine lead levels. New England Journal of Medicine 300: 688–695, 1979Google Scholar
  70. Neri LC, Johansen H, Hewitt D. Health effects of low-level occupational exposure to lead: the trial, British Columbia study. Archives of Environmental Health 38: 180–189, 1983PubMedGoogle Scholar
  71. Nriagu JO. Saturnine gout among Roman aristocrats: did lead poisoning contribute to the fall of the Empire? New England Journal of Medicine 308: 660–663, 1983PubMedGoogle Scholar
  72. Oliver T. Lead poisoning. Paul B. Hoeber Inc., New York, 1914Google Scholar
  73. Perlstein MA, Attala R. Neurologic sequelae of plumbism in children. Clinical Paediatrics 5: 292–298, 1966Google Scholar
  74. Piomelli S, Graziano J. Laboratory diagnosis of lead poisoning. Pediatric Clinics of North America 27: 843–853, 1980PubMedGoogle Scholar
  75. Piomelli S, Rosen JF, Chisholm JJ, Graef JW. Management of childhood lead poisoning. Journal of Paediatrics 105: 523–532, 1984Google Scholar
  76. Pocock SJ, Shaper AG, Ashby D, et al. Blood lead concentration, blood pressure and renal function. British Medical Journal 289: 872–874, 1984PubMedGoogle Scholar
  77. Pollock CA, Ibels LS. Lead intoxication in industry. Medical Journal of Australia, in press, 1986aGoogle Scholar
  78. Pollock CA, Ibels LS. Lead intoxication in industry. Medical Journal of Australia 145: 53, 1986aPubMedGoogle Scholar
  79. Prerovska I, Teisinger J. Excretion of lead and its biological activity several years after termination of exposure. British Journal of Industrial Medicine 27: 352–355, 1970PubMedGoogle Scholar
  80. Rabinowitz MB, Wetherill GW, Kopple JD. Kinetic analysis of lead metabolism in healthy humans. Journal of Clinical Investigations 58: 260–270, 1976Google Scholar
  81. Radosevic Z, Saric M, Beritic T, et al. The kidney in lead poisoning. British Journal of Industrial Medicine 18: 222–230, 1961PubMedGoogle Scholar
  82. Ramires-Cervantes B, Embree JW, Hine CH, et al. Health assessment of employees with different body burdens of lead. Journal of Occupational Medicine 20: 610–671, 1978Google Scholar
  83. Repko JD, Morgan BB, Nicholson J. Behavioral effects of occupational exposure to lead. Publication No. (NIOSH) 75–164, US Department of Health, Education and Welfare, Washington DC, 1975Google Scholar
  84. Reynolds P, Knapp M, Baraf H, Holmes E. Moonshine and lead: relationship to the pathogenesis of hyperuricaemia in gout. Arthritis and Rheumatism 9: 1057–1064, 1983Google Scholar
  85. Rosen JF, Chesney RW, Hanstra A, et al. Reduction in 1,25 dihydroxy vitamin D in children with increased lead absorption. New England Journal of Medicine 302: 1128–1131, 1980PubMedGoogle Scholar
  86. Sachs HK, Blanksma LA, Murray EF, et al. Ambulatory treatment of lead poisoning: Report of 1,155 cases. Pediatrics 46: 389–396, 1970PubMedGoogle Scholar
  87. Saenger P, Rosen J, Markowitz M. Diagnostic significance of edetate disodium calcium testing in children with increased lead absorption. American Journal of Diseases in Children 136: 312–315, 1982Google Scholar
  88. Salvini M. Mobilizzazione del piombo mediante iniezione di EDTA e diagnosi di saturnismo [Meeting]. Folia Medica (Napoli) 38: 168–169, 1955Google Scholar
  89. Sanstead HH, Michelakis AM, Temple TE. Lead intoxication: its effects on the renin-aldosterone response to sodium deprivation. Archives of Environmental Health 20: 356–381, 1970Google Scholar
  90. Singerman A. Clinical signs versus biochemical effects of toxic metals. In Nordberg GF (Ed.) Effects and dose-response relationships of toxic metals, pp. 207–255, Elsevier, Amsterdam, 1976Google Scholar
  91. Smith HD, King LR, Margolin EG. Treatment of lead encephalopathy. American Journal of Diseases in Children 109: 322–324, 1965Google Scholar
  92. Talbott JM, Terplan KL. The kidney in gout. Medicine 38: 405–467, 1960Google Scholar
  93. Teisinger J, Srbova J. The value of mobilization of lead by calcium ethylene-diamine-tetra-acetate in the diagnosis of lead poisoning. British Journal of Industrial Medicine 16: 148–152, 1959PubMedGoogle Scholar
  94. Tepper LB. Renal function subsequent to childhood plumbism. Archives of Environmental Health 7: 82–91, 1963Google Scholar
  95. US Department of Labor, Occupational Safety and Health Administration. Occupational exposure to lead: final standard. Federal Register No. 14: 52952–53014, 1978Google Scholar
  96. Wedeen RP. Blood lead levels, dietary calcium and hypertension. Annals of Internal Medicine 102: 403–404, 1985PubMedGoogle Scholar
  97. Wedeen RP. Lead and the gouty kidney. American Journal of Kidney Disease 2: 559–563, 1983Google Scholar
  98. Wedeen RP. Occupational renal disease. American Journal of Kidney Disease 3: 241–257, 1984Google Scholar
  99. Wedeen RP. The role of lead in renal failure. Clinical and Experimental Dialysis and Apheresis 6: 113–146, 1982PubMedGoogle Scholar
  100. Wedeen RP, Batuman V, Landy E. The safety of the EDTA mobilization test. Environmental Research 30: 58–62, 1983PubMedGoogle Scholar
  101. Wedeen RP, Maesaka JK, Weiner B, et al. Occupational lead nephropathy. American Journal of Medicine 59: 630–641, 1975PubMedGoogle Scholar
  102. Wedeen RP, Mallick DK, Batuman V. Detection and treatment of occupational lead nephropathy. Archives of Internal Medicine 139: 52–57, 1979Google Scholar
  103. Whitfield CL, Ch’ien LT, Whitehead JD. Lead encephalopathy in adults. American Journal of Medicine 52: 289–298, 1972PubMedGoogle Scholar
  104. World Health Organisation. Environmental Health Criteria. 3. Lead, WHO, Geneva, 1977Google Scholar
  105. World Health Organisation Technical Report Series 410: urban air pollution with particular reference to motor vehicles, 1969Google Scholar
  106. Wright LF, Saylor RP, Cecere FA. Occult lead intoxication in patients with gout and kidney disease. Journal of Rheumatology 11: 517–520, 1984PubMedGoogle Scholar
  107. Yu T. Lead nephropathy and gout. American Journal of Kidney Disease 11: 555–558, 1983Google Scholar
  108. Yule W, Landsdown R, Millar IB, Urbanowicz MA. The relationship between blood lead concentration, intelligence and attainment in a school population: a pilot study. Developmental Medicine and Child Neurology 23: 567–576, 1981PubMedGoogle Scholar
  109. Zambrano A, Rossi L, Mantovano S. II calcio disordieo versenato nella diagnosi di saturnismo professionale. Folia Medica (Napoli) 38: 1248–1255, 1955Google Scholar
  110. Zelhuis RL. Second international workshop: permissible levels for occupational exposure to inorganic lead. International Archives of Occupational and Environmental Health 39: 59–72, 1977Google Scholar
  111. Ziegler EE, Edwards BB, Jensen RL, Mahaffey KR, Fomon SJ. Absorption and retention of lead by infants. Pediatric Research 12: 29–34, 1978PubMedGoogle Scholar

Copyright information

© ADIS Press Limited 1986

Authors and Affiliations

  • L. S. Ibels
    • 1
  • C. A. Pollock
    • 1
  1. 1.Department of Renal MedicineRoyal North Shore HospitalSt LeonardsAustralia

Personalised recommendations