Smarter Decisions,
Better Care

UpToDate synthesizes the most recent medical information into evidence-based practical recommendations clinicians trust to make the right point-of-care decisions.

  • Rigorous editorial process: Evidence-based treatment recommendations
  • World-Renowned physician authors: over 5,100 physician authors and editors around the globe
  • Innovative technology: integrates into the workflow; access from EMRs

Choose from the list below to learn more about subscriptions for a:


Subscribers log in here


Childhood lead poisoning: Clinical manifestations and diagnosis

INTRODUCTION

Lead (Pb), a stable metallic element with an atomic number of 82 and atomic weight of 207, was first smelted around 4000 BC as a by-product of silver processing. The consequences of lead toxicity have been recognized for millennia and are thought to have contributed to the fall of the Roman Empire [1]. Complications of lead poisoning were first acknowledged in the United States in the early 20th century. Despite this knowledge, lead was included as an ingredient of gasoline in the 1920s and continued to be used in paint until the 1970s [2,3].

As lead was removed from gasoline and paint, the average blood lead level (BLL) in children decreased from 16 mcg/dL (0.77 micromol/L) to less than 3 mcg/dL (0.14 micromol/L) [4,5]. Residual lead from these and other products remains in the environment because elemental lead cannot be degraded. In many parts of the developing world, lead continues to be used in gasoline, pigment (eg, in paint, cosmetics, and crayons), pottery glaze, solder, cooking vessels, and even medications. These products occasionally are imported into the United States and are potential sources of lead exposure.

The clinical manifestations and diagnosis of lead toxicity will be reviewed here. Prevention and treatment of lead poisoning are discussed separately. (See "Childhood lead poisoning: Exposure and prevention" and "Childhood lead poisoning: Management".)

EPIDEMIOLOGY

The toxic lead level in the United States is determined by the Centers for Disease Control (CDC) based upon the current understanding of the complications caused by a given concentration of lead in the blood. Between 1970 and 2012, the toxic level or “reference value” was gradually decreased from 60 mcg/dL (2.9 micromol/L) to the 97.5th percentile of blood lead levels in US children (5 mcg/dL [0.24 micromol/L] as of 2012) (table 1). The decrease in 1991 was prompted by evidence of cognitive and behavioral effects of low-level lead toxicity [6,7] Changes in the definition of the toxic level have been accompanied by changes in policies for screening, treatment, and prevention [8]. Subsequently, a reference level corresponding to the 97.5th percentile of blood lead levels in US children (5 mcg/dL [0.24 micromol/L] as of 2012) has been adopted [9].

The prevalence of lead toxicity has decreased in the United States since the 1970s because of preschool screening programs, increased public awareness, and the removal of lead from gasoline and paint products. The prevalence of BLLs >10 mcg/dL (0.48 micromol/L) in American children between one and five years of age decreased from 88 to 4.4 percent between 1976 and 1994 [10], and to 0.8 percent for the period 2007 to 2010 [5,11]. Although the incidence and severity of lead poisoning in the United States are decreasing, an estimated 450,000 children in the United States were above the reference value of 5 mcg/dL (0.24 micromol/L) in 2012 [9].

                      

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Aug 2014. | This topic last updated: Jul 15, 2014.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2014 UpToDate, Inc.
References
Top
  1. Nriagu JO. Saturnine gout among Roman aristocrats. Did lead poisoning contribute to the fall of the Empire? N Engl J Med 1983; 308:660.
  2. Needleman HL. The removal of lead from gasoline: historical and personal reflections. Environ Res 2000; 84:20.
  3. Hernberg S. Lead poisoning in a historical perspective. Am J Ind Med 2000; 38:244.
  4. Annest JL. Trends in the blood lead levels of the US population. In: Lead Versus Health, Rutter M, Jones RR. (Eds), John Wiley and Sons, New York 1983. p.33.
  5. Centers for Disease Control and Prevention (CDC). Blood lead levels--United States, 1999-2002. MMWR Morb Mortal Wkly Rep 2005; 54:513.
  6. Bellinger D, Sloman J, Leviton A, et al. Low-level lead exposure and children's cognitive function in the preschool years. Pediatrics 1991; 87:219.
  7. Needleman HL, Schell A, Bellinger D, et al. The long-term effects of exposure to low doses of lead in childhood. An 11-year follow-up report. N Engl J Med 1990; 322:83.
  8. Centers for Disease Control and Prevention. Preventing lead poisoning in young children: a statement by the Centers for Disease Control, 1991.
  9. CDC response to Advisory Committee on Childhood Lead Poisoning Prevention Recommendations in "Low Level Lead Exposure Harms Children: A Renewed Call of Primary Prevention" http://www.cdc.gov/nceh/lead/ACCLPP/activities.htm (Accessed on May 17, 2012).
  10. 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 (NHANES). JAMA 1994; 272:284.
  11. Centers for Disease Control and Prevention (CDC). Blood lead levels in children aged 1-5 years - United States, 1999-2010. MMWR Morb Mortal Wkly Rep 2013; 62:245.
  12. Wright RO, Tsaih SW, Schwartz J, et al. Association between iron deficiency and blood lead level in a longitudinal analysis of children followed in an urban primary care clinic. J Pediatr 2003; 142:9.
  13. Agency for Toxic Substances and Disease Registry. Case Studies in Environmental Medicine (CSEM): Lead Toxicity Cover Page. www.atsdr.cdc.gov/csem/lead/pbcover_page2.html (Accessed on January 2, 2008).
  14. Raymond J, Wheeler W, Brown MJ. Lead screening and prevalence of blood lead levels in children aged 1--2 years --- child blood lead surveillance system, United States, 2002--2010 and national health and nutrition examination survey, United States, 1999--2010. MMWR Surveill Summ 2014; 63:36.
  15. Melman ST, Nimeh JW, Anbar RD. Prevalence of elevated blood lead levels in an inner-city pediatric clinic population. Environ Health Perspect 1998; 106:655.
  16. Centers for Disease Control and Prevention (CDC). Blood lead levels in young children--United States and selected states, 1996-1999. MMWR Morb Mortal Wkly Rep 2000; 49:1133.
  17. Centers for Disease Control and Prevention (CDC). Update: blood lead levels--United States, 1991-1994. MMWR Morb Mortal Wkly Rep 1997; 46:141.
  18. Geltman PL, Brown MJ, Cochran J. Lead poisoning among refugee children resettled in Massachusetts, 1995 to 1999. Pediatrics 2001; 108:158.
  19. Chung EK, Webb D, Clampet-Lundquist S, Campbell C. A comparison of elevated blood lead levels among children living in foster care, their siblings, and the general population. Pediatrics 2001; 107:E81.
  20. Centers for Disease Control and Prevention (CDC). Infant lead poisoning associated with use of tiro, an eye cosmetic from Nigeria--Boston, Massachusetts, 2011. MMWR Morb Mortal Wkly Rep 2012; 61:574.
  21. Alexander FW, Clayton BE, Delves HT. Mineral and trace-metal balances in children receiving normal and synthetic diets. Q J Med 1974; 43:89.
  22. Ziegler EE, Edwards BB, Jensen RL, et al. Absorption and retention of lead by infants. Pediatr Res 1978; 12:29.
  23. James HM, Hilburn ME, Blair JA. Effects of meals and meal times on uptake of lead from the gastrointestinal tract in humans. Hum Toxicol 1985; 4:401.
  24. Mahaffey KR. Environmental lead toxicity: nutrition as a component of intervention. Environ Health Perspect 1990; 89:75.
  25. Griffin TB, Coulston F, Wills H, Russell JC. Biologic effects of airborne particulate lead on continuously exposed rats and rhesus monkeys. Environ Qual Saf Suppl 1975; 2:202.
  26. Rabinowitz MB, Wetherill GW, Kopple JD. Kinetic analysis of lead metabolism in healthy humans. J Clin Invest 1976; 58:260.
  27. Griffin TB, Coulston F, Wills H, Russell JC. Clinical studies on men continuously exposed to airborne particulate lead. Environ Qual Saf Suppl 1975; 2:221.
  28. Hu H, Rabinowitz M, Smith D. Bone lead as a biological marker in epidemiologic studies of chronic toxicity: conceptual paradigms. Environ Health Perspect 1998; 106:1.
  29. Barry PS. A comparison of concentrations of lead in human tissues. Br J Ind Med 1975; 32:119.
  30. Lidsky TI, Schneider JS. Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain 2003; 126:5.
  31. Al-Modhefer AJ, Bradbury MW, Simons TJ. Observations on the chemical nature of lead in human blood serum. Clin Sci (Lond) 1991; 81:823.
  32. Johnson FM. The genetic effects of environmental lead. Mutat Res 1998; 410:123.
  33. Fox DA, Campbell ML, Blocker YS. Functional alterations and apoptotic cell death in the retina following developmental or adult lead exposure. Neurotoxicology 1997; 18:645.
  34. Fox DA, He L, Poblenz AT, et al. Lead-induced alterations in retinal cGMP phosphodiesterase trigger calcium overload, mitochondrial dysfunction and rod photoreceptor apoptosis. Toxicol Lett 1998; 102-103:359.
  35. He L, Poblenz AT, Medrano CJ, Fox DA. Lead and calcium produce rod photoreceptor cell apoptosis by opening the mitochondrial permeability transition pore. J Biol Chem 2000; 275:12175.
  36. Markovac J, Goldstein GW. Picomolar concentrations of lead stimulate brain protein kinase C. Nature 1988; 334:71.
  37. Johnston MV, Goldstein GW. Selective vulnerability of the developing brain to lead. Curr Opin Neurol 1998; 11:689.
  38. Srivastava D, Hurwitz RL, Fox DA. Lead- and calcium-mediated inhibition of bovine rod cGMP phosphodiesterase: interactions with magnesium. Toxicol Appl Pharmacol 1995; 134:43.
  39. Srivastava D, Fox DA, Hurwitz RL. Effects of magnesium on cyclic GMP hydrolysis by the bovine retinal rod cyclic GMP phosphodiesterase. Biochem J 1995; 308 ( Pt 2):653.
  40. Holtzman D, Hsu JS. Early effects of inorganic lead on immature rat brain mitochondrial respiration. Pediatr Res 1976; 10:70.
  41. Trope I, Lopez-Villegas D, Cecil KM, Lenkinski RE. Exposure to lead appears to selectively alter metabolism of cortical gray matter. Pediatrics 2001; 107:1437.
  42. Trope I, Lopez-Villegas D, Lenkinski RE. Magnetic resonance imaging and spectroscopy of regional brain structure in a 10-year-old boy with elevated blood lead levels. Pediatrics 1998; 101:E7.
  43. Cooper GP, Suszkiw JB, Manalis RS. Heavy metals: effects on synaptic transmission. Neurotoxicology 1984; 5:247.
  44. Zwart R, van Kleef RG, Van Hooft JA, et al. Cellular aspects of persistent neurotoxicants: effects of Pb2+ on neuronal nicotinic acetylcholine receptors. Neurotoxicology 1997; 18:709.
  45. Oortgiesen M, Leinders T, van Kleef RG, Vijverberg HP. Differential neurotoxicological effects of lead on voltage-dependent and receptor-operated ion channels. Neurotoxicology 1993; 14:87.
  46. Sirover MA, Loeb LA. Infidelity of DNA synthesis in vitro: screening for potential metal mutagens or carcinogens. Science 1976; 194:1434.
  47. Hoffman DJ, Niyogi SK. Metal mutagens and carcinogens affect RNA synthesis rates in a distinct manner. Science 1977; 198:513.
  48. Kobayashi N, Okamoto T. Effects of lead oxide on the induction of lung tumors in Syrian hamsters. J Natl Cancer Inst 1974; 52:1605.
  49. Kasprzak KS, Hoover KL, Poirier LA. Effects of dietary calcium acetate on lead subacetate carcinogenicity in kidneys of male Sprague-Dawley rats. Carcinogenesis 1985; 6:279.
  50. Buzard GS, Kasprzak KS. Possible roles of nitric oxide and redox cell signaling in metal-induced toxicity and carcinogenesis: a review. J Environ Pathol Toxicol Oncol 2000; 19:179.
  51. Koller LD, Kerkvliet NI, Exon JH. Neoplasia induced in male rats fed lead acetate, ethyl urea, and sodium nitrite. Toxicol Pathol 1985; 13:50.
  52. ZOLLINGER HU. [Renal adenoma and carcinoma produced by lead poisoning in rats, and relations to corresponding neoplastic formations in man]. Virchows Arch 1953; 323:694.
  53. Van Esch GJ, Kroes R. The induction of renal tumours by feeding basic lead acetate to mice and hamsters. Br J Cancer 1969; 23:765.
  54. DINGWALL-FORDYCE I, LANE RE. A FOLLOW-UP STUDY OF LEAD WORKERS. Br J Ind Med 1963; 20:313.
  55. Moore MR, Meredith PA. The carcinogenicity of lead. Arch Toxicol 1979; 42:87.
  56. Nelson DJ, Kiremidjian-Schumacher L, Stotzky G. Effects of cadmium, lead, and zinc on macrophage-mediated cytotoxicity toward tumor cells. Environ Res 1982; 28:154.
  57. Johnson DR, Foulkes EC, Hammond PB. The renal handling of delta-aminolevulinic acid in normal and lead-poisoning rabbits. Toxicol Appl Pharmacol 1976; 38:101.
  58. Hammond PB. Exposure of humans to lead. Annu Rev Pharmacol Toxicol 1977; 17:197.
  59. Campbell BC, Brodie MJ, Thompson GG, et al. Alterations in the activity of enzymes of haem biosynthesis in lead poisoning and acute hepatic prophyria. Clin Sci Mol Med 1977; 53:335.
  60. Rees DC, Duley JA, Marinaki AM. Pyrimidine 5' nucleotidase deficiency. Br J Haematol 2003; 120:375.
  61. Needleman HL. Lead poisoning. In: Oski's Pediatrics: Principles and Practice, 4th, McMillan JA, Feigin RD, DeAngelis C, Jones MD. (Eds), Lippincott Williams & Wilkins, Philadelphia 2006. p.767.
  62. Campbell TF, Needleman HL, Riess JA, Tobin MJ. Bone lead levels and language processing performance. Dev Neuropsychol 2000; 18:171.
  63. Liu J, Liu X, Wang W, et al. Blood lead concentrations and children’s behavioral and emotional problems: A cohort study. JAMA Pediatr 2014.
  64. Needleman HL, Riess JA, Tobin MJ, et al. Bone lead levels and delinquent behavior. JAMA 1996; 275:363.
  65. Mendelsohn AL, Dreyer BP, Fierman AH, et al. Low-level lead exposure and behavior in early childhood. Pediatrics 1998; 101:E10.
  66. Dietrich KN, Krafft KM, Bornschein RL, et al. Low-level fetal lead exposure effect on neurobehavioral development in early infancy. Pediatrics 1987; 80:721.
  67. Dietrich KN, Berger OG, Succop PA, et al. The developmental consequences of low to moderate prenatal and postnatal lead exposure: intellectual attainment in the Cincinnati Lead Study Cohort following school entry. Neurotoxicol Teratol 1993; 15:37.
  68. Baghurst PA, McMichael AJ, Wigg NR, et al. 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.
  69. Mendelsohn AL, Dreyer BP, Fierman AH, et al. Low-level lead exposure and cognitive development in early childhood. J Dev Behav Pediatr 1999; 20:425.
  70. Pocock SJ, Smith M, Baghurst P. Environmental lead and children's intelligence: a systematic review of the epidemiological evidence. BMJ 1994; 309:1189.
  71. Chen A, Cai B, Dietrich KN, et al. Lead exposure, IQ, and behavior in urban 5- to 7-year-olds: does lead affect behavior only by lowering IQ? Pediatrics 2007; 119:e650.
  72. Lanphear BP, Dietrich K, Auinger P, Cox C. Cognitive deficits associated with blood lead concentrations <10 microg/dL in US children and adolescents. Public Health Rep 2000; 115:521.
  73. Canfield RL, Henderson CR Jr, Cory-Slechta DA, et al. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med 2003; 348:1517.
  74. Lanphear BP, Hornung R, Khoury J, et al. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environ Health Perspect 2005; 113:894.
  75. Téllez-Rojo MM, Bellinger DC, Arroyo-Quiroz C, et al. Longitudinal associations between blood lead concentrations lower than 10 microg/dL and neurobehavioral development in environmentally exposed children in Mexico City. Pediatrics 2006; 118:e323.
  76. Gomaa A, Hu H, Bellinger D, et al. Maternal bone lead as an independent risk factor for fetal neurotoxicity: a prospective study. Pediatrics 2002; 110:110.
  77. Fergusson DM, Horwood LJ, Lynskey MT. Early dentine lead levels and educational outcomes at 18 years. J Child Psychol Psychiatry 1997; 38:471.
  78. Finkelstein Y, Markowitz ME, Rosen JF. Low-level lead-induced neurotoxicity in children: an update on central nervous system effects. Brain Res Brain Res Rev 1998; 27:168.
  79. Bellinger D, Leviton A, Waternaux C, et al. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. N Engl J Med 1987; 316:1037.
  80. Schroeder SR, Hawk B, Otto DA, et al. Separating the effects of lead and social factors on IQ. Environ Res 1985; 38:144.
  81. Ruff HA, Bijur PE, Markowitz M, et al. Declining blood lead levels and cognitive changes in moderately lead-poisoned children. JAMA 1993; 269:1641.
  82. Soong WT, Chao KY, Jang CS, Wang JD. Long-term effect of increased lead absorption on intelligence of children. Arch Environ Health 1999; 54:297.
  83. Bellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study. Pediatrics 1992; 90:855.
  84. Ruff HA. Population-based data and the development of individual children: the case of low to moderate lead levels and intelligence. J Dev Behav Pediatr 1999; 20:42.
  85. Osman K, Pawlas K, Schütz A, et al. Lead exposure and hearing effects in children in Katowice, Poland. Environ Res 1999; 80:1.
  86. CHISOLM JJ Jr, HARRISON HE. The exposure of children to lead. Pediatrics 1956; 18:943.
  87. Erenberg G, Rinsler SS, Fish BG. Lead neuropathy and sickle cell disease. Pediatrics 1974; 54:438.
  88. Anku VD, Harris JW. Peripheral neuropathy and lead poisoning in a child with sickle-cell anemia. Case report and review of the literature. J Pediatr 1974; 85:337.
  89. Imbus CE, Warner J, Smith E, et al. Peripheral neuropathy in lead-intoxicated sickle cell patients. Muscle Nerve 1978; 1:168.
  90. Feldman RG, Hayes MK, Younes R, Aldrich FD. Lead neuropathy in adults and children. Arch Neurol 1977; 34:481.
  91. Schwartz J, Landrigan PJ, Feldman RG, et al. Threshold effect in lead-induced peripheral neuropathy. J Pediatr 1988; 112:12.
  92. Suarez CR, Black LE 3rd, Hurley RM. Elevated lead levels in a patient with sickle cell disease and inappropriate secretion of antidiuretic hormone. Pediatr Emerg Care 1992; 8:88.
  93. MYERSON RM, EISENHAUER JH. Atrioventricular conduction defects in lead poisoning. Am J Cardiol 1963; 11:409.
  94. Lubran MM. Lead toxicity and heme biosynthesis. Ann Clin Lab Sci 1980; 10:402.
  95. Meredith PA, Moore MR, Goldberg A. Erythrocyte delta-aminolaevulinic acid dehydratase activity and blood protoporphyrin concentrations as indices of lead exposure and altered haem biosynthesis. Clin Sci (Lond) 1979; 56:61.
  96. Hammad TA, Sexton M, Langenberg P. Relationship between blood lead and dietary iron intake in preschool children. A cross-sectional study. Ann Epidemiol 1996; 6:30.
  97. Clark M, Royal J, Seeler R. Interaction of iron deficiency and lead and the hematologic findings in children with severe lead poisoning. Pediatrics 1988; 81:247.
  98. Bhambhani K, Aronow R. Lead poisoning and thalassemia trait or iron deficiency. The value of the red blood cell distribution width. Am J Dis Child 1990; 144:1231.
  99. Rosen JF, Chesney RW, Hamstra A, et al. Reduction in 1,25-dihydroxyvitamin D in children with increased lead absorption. N Engl J Med 1980; 302:1128.
  100. Selevan SG, Rice DC, Hogan KA, et al. Blood lead concentration and delayed puberty in girls. N Engl J Med 2003; 348:1527.
  101. Tong S, Baghurst PA, Sawyer MG, et al. Declining blood lead levels and changes in cognitive function during childhood: the Port Pirie Cohort Study. JAMA 1998; 280:1915.
  102. Rosen JF, Mushak P. Primary prevention of childhood lead poisoning--the only solution. N Engl J Med 2001; 344:1470.
  103. Rogan WJ, Dietrich KN, Ware JH, et al. The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead. N Engl J Med 2001; 344:1421.
  104. Lewendon G, Kinra S, Nelder R, Cronin T. Should children with developmental and behavioural problems be routinely screened for lead? Arch Dis Child 2001; 85:286.
  105. Gordon RA, Roberts G, Amin Z, et al. Aggressive approach in the treatment of acute lead encephalopathy with an extraordinarily high concentration of lead. Arch Pediatr Adolesc Med 1998; 152:1100.
  106. Chisolm JJ Jr. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatr 1968; 73:1.
  107. Chisolm JJ Jr. The continuing hazard of lead exposure and its effects in children. Neurotoxicology 1984; 5:23.
  108. Rajkumar S, Geibel V, Devanagondi B, et al. The diagnostic significance of free erythrocyte protoporphyrin and the FEP/hemoglobin ratio in plumbism. N Y State J Med 1987; 87:542.
  109. Carraccio CL, Bergman GE, Daley BP. Combined iron deficiency and lead poisoning in children. Effect on FEP levels. Clin Pediatr (Phila) 1987; 26:644.
  110. Piomelli S. The diagnostic utility of measurements of erythrocyte porphyrins. Hematol Oncol Clin North Am 1987; 1:419.
  111. McElvaine MD, Orbach HG, Binder S, et al. Evaluation of the erythrocyte protoporphyrin test as a screen for elevated blood lead levels. J Pediatr 1991; 119:548.
  112. Tehranifar P, Leighton J, Auchincloss AH, et al. Immigration and risk of childhood lead poisoning: findings from a case control study of New York City children. Am J Public Health 2008; 98:92.
  113. Parsons PJ, Reilly AA, Esernio-Jenssen D. Screening children exposed to lead: an assessment of the capillary blood lead fingerstick test. Clin Chem 1997; 43:302.
  114. Screening for elevated blood lead levels. American Academy of Pediatrics Committee on Environmental Health. Pediatrics 1998; 101:1072.
  115. Binns HJ, Campbell C, Brown MJ, Centers for Disease Control and Prevention Advisory Committee on Childhood Lead Poisoning Prevention. Interpreting and managing blood lead levels of less than 10 microg/dL in children and reducing childhood exposure to lead: recommendations of the Centers for Disease Control and Prevention Advisory Committee on Childhood Lead Poisoning Prevention. Pediatrics 2007; 120:e1285.
  116. Roberts, JR, Reigart, JR. Medical Assessment and Interventions. In: Managing Elevated Blood Lead Levels Among Young children: Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Centers for Disease Control and Prevention, Atlanta, GA, 2002.
  117. Porru S, Alessio L. The use of chelating agents in occupational lead poisoning. Occup Med (Lond) 1996; 46:41.
  118. Kulshrestha MK. Lead poisoning diagnosed by abdominal X-rays. J Toxicol Clin Toxicol 1996; 34:107.
  119. Woolf DA, Riach IC, Derweesh A, Vyas H. Lead lines in young infants with acute lead encephalopathy: a reliable diagnostic test. J Trop Pediatr 1990; 36:90.