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Adult lead poisoning

Rose H Goldman, MD, MPH
Howard Hu, ScD, MD
Section Editor
Joann G Elmore, MD, MPH
Deputy Editor
Lee Park, MD, MPH


Lead poisoning can present with nonspecific signs and symptoms such as abdominal pain, constipation, irritability, difficulty concentrating, and anemia. Clinicians need to consider this diagnosis and know the appropriate tests to order for documenting exposure and assessing for early health effects. It is also now well-established that chronic exposure to modest levels of lead, too low to trigger symptoms, can increase risk for hypertension and accelerated future cognitive and renal decline in adults.

Clinicians need to know how to play a proactive role in early detection and prevention by screening patients known to work in occupations with possible lead exposure, and what actions to take when excessive exposure is found. The costs and consequences of lead poisoning can be entirely prevented by eliminating and decreasing sources of exposures and by early recognition of elevated lead levels or lead poisoning.

Some of the clinical conditions related to lead poisoning and issues related to lead poisoning in children are presented separately. (See "Sideroblastic anemias: Diagnosis and management" and "Lead nephropathy and lead-related nephrotoxicity".)


The true extent of adult lead poisoning in the United States (US) is difficult to measure because of limited data. One source of data is the Centers for Disease Control's (CDC's) Adult Blood Lead Epidemiology and Surveillance (ABLES) program that monitors laboratory reported elevated blood lead levels (BLLs) among adults in 41 states [1]. An elevated BLL had previously been defined as greater than or equal to 25 mcg/dL (1.21 micromol/L), but in 2009 ABLES updated its definition to >10mcg/dL (0.48 micromol/L) [1]. This is consistent with the decrease in BLLs in the US population and newer research demonstrating adverse health effects at lower levels [2]. (See 'Management' below.)

The ABLES surveillance results have indicated an overall decrease in the US prevalence of elevated BLLs from 14.0 per 100,000 in 1994 to 5.7 in 2012 [3]. Ninety-four percent of the adults with an identified exposure source were exposed at work [4]. These work exposures occurred mainly in battery manufacturing, lead and zinc ore mining, and painting and paper hanging industry subsectors. Despite these improvements, there are still thousands of adults in the US with high BLLs (>40 mcg/dL [1.93 micromol/L]) [5].


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  1. Centers for Disease Control (CDC) and Prevention. Adult blood lead epidemiology and surveillance (ABLES). http://www.cdc.gov/niosh/topics/ables/description.html (Accessed on March 06, 2016).
  2. National Toxicology Program. Health effects of low-level lead evaluation. Research Triangle Park, NC: US Department of Health and Human Services; 2012. http://ntp.niehs.nih.gov/pubhealth/hat/noms/lead/index.html (Accessed on March 06, 2016).
  3. Centers for Disease Control and Prevention (CDC). Elevated blood lead levels among employed adults--United States, 1994-2012. MMWR Morb Mortal Wkly Rep 2015; 62:52.
  4. Centers for Disease Control and Prevention (CDC). Adult blood lead epidemiology and surveillance--United States, 2005-2007. MMWR Morb Mortal Wkly Rep 2009; 58:365.
  5. Centers for Disease Control and Prevention (CDC). Very high blood lead levels among adults - United States, 2002-2011. MMWR Morb Mortal Wkly Rep 2013; 62:967.
  6. Centers for Disease Control and Prevention (CDC). Blood lead levels--United States, 1999-2002. MMWR Morb Mortal Wkly Rep 2005; 54:513.
  7. Centers for Disease Control (CDC) and Prevention. Fourth national report on human exposure to environmental chemicals. February 2015. http://www.cdc.gov/biomonitoring/pdf/FourthReport_UpdatedTables_Feb2015.pdf (Accessed on March 06, 2016).
  8. Kosnett MJ, Wedeen RP, Rothenberg SJ, et al. Recommendations for medical management of adult lead exposure. Environ Health Perspect 2007; 115:463.
  9. US Department of Health and Human Services. Occupational safety and health, Objective 20-7: Reduce the proportion of adults who have elevated blood lead concentrations. Healthy People 2010 midcourse review. Washington DC: US Department of Health and Human Services: 2007: 20-18. Available at: http://healthypeople.gov/2020/topicsobjectives2020/objectiveslist.aspx?topicId=12 (Accessed on July 20, 2011).
  10. ATSDR. Toxicological Profile for Lead. US Department of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, Atlanta, GA 2007. Available at: http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=96&tid=22 (Accessed on March 06, 2016).
  11. Fischbein A, Hu H. Occupational and environmental exposure to lead. In: Environmental and Occupational Medicine, Rom WN, Markowitz SB (Eds), Lippincott Williams & Wilkins, Philadelphia 2007. p.958.
  12. Warren C. Brush with Death: A Social History of Lead Poisoning, The Johns Hopkins University Press, Baltimore 2000. p.32.
  13. Centers for Disease Control (CDC). Blood-lead levels in U.S. population. MMWR Morb Mortal Wkly Rep 1982; 31:132.
  14. Haefliger P, Mathieu-Nolf M, Lociciro S, et al. Mass lead intoxication from informal used lead-acid battery recycling in dakar, senegal. Environ Health Perspect 2009; 117:1535.
  15. Moszynski P. Lead poisoning in Nigeria causes "unprecedented" emergency. BMJ 2010; 341:c4031.
  16. Gottesfeld P, Pokhrel AK. Review: Lead exposure in battery manufacturing and recycling in developing countries and among children in nearby communities. J Occup Environ Hyg 2011; 8:520.
  17. Dooyema CA, Neri A, Lo YC, et al. Outbreak of fatal childhood lead poisoning related to artisanal gold mining in northwestern Nigeria, 2010. Environ Health Perspect 2012; 120:601.
  18. Burton A. Massive childhood lead poisoning: the price of Nigerian gold. Environ Health Perspect 2012; 120:A165.
  19. Levin SM, Goldberg M. Clinical evaluation and management of lead-exposed construction workers. Am J Ind Med 2000; 37:23.
  20. Clark CS, Rampal KG, Thuppil V, et al. The lead content of currently available new residential paint in several Asian countries. Environ Res 2006; 102:9.
  21. Rabito FA, Iqbal S, Perry S, et al. Environmental lead after Hurricane Katrina: implications for future populations. Environ Health Perspect 2012; 120:180.
  22. Centers for Disease Control and Prevention (CDC). Potential risk for lead exposure in dental offices. MMWR Morb Mortal Wkly Rep 2001; 50:873.
  23. Morgan BW, Barnes L, Parramore CS, Kaufmann RB. Elevated blood lead levels associated with the consumption of moonshine among emergency department patients in Atlanta, Georgia. Ann Emerg Med 2003; 42:351.
  24. Busse F, Omidi L, Timper K, et al. Lead poisoning due to adulterated marijuana. N Engl J Med 2008; 358:1641.
  25. National Research Council. Potential Health Risks to DOD Firing-Range Personnel from Recurrent Lead Exposure, The National Academies Press, Washington, DC 2013.
  26. Beaucham C, Page E, Alarcon WA, et al. Indoor firing ranges and elevated blood lead levels - United States, 2002-2013. MMWR Morb Mortal Wkly Rep 2014; 63:347.
  27. Centers for Disease Control and Prevention (CDC). Lead poisoning associated with ayurvedic medications--five states, 2000-2003. MMWR Morb Mortal Wkly Rep 2004; 53:582.
  28. Saper RB, Kales SN, Paquin J, et al. Heavy metal content of ayurvedic herbal medicine products. JAMA 2004; 292:2868.
  29. Frith D, Yeung K, Thrush S, et al. Lead poisoning--a differential diagnosis for abdominal pain. Lancet 2005; 366:2146.
  30. Saper RB, Phillips RS, Sehgal A, et al. Lead, mercury, and arsenic in US- and Indian-manufactured Ayurvedic medicines sold via the Internet. JAMA 2008; 300:915.
  31. Centers for Disease Control and Prevention (CDC). Childhood lead poisoning from commercially manufactured French ceramic dinnerware--New York City, 2003. MMWR Morb Mortal Wkly Rep 2004; 53:584.
  32. Centers for Disease Control and Prevention (CDC). Lead poisoning in pregnant women who used Ayurvedic medications from India--New York City, 2011-2012. MMWR Morb Mortal Wkly Rep 2012; 61:641.
  33. Centers for Disease Control and Prevention (CDC). Lead poisoning associated with use of litargirio--Rhode Island, 2003. MMWR Morb Mortal Wkly Rep 2005; 54:227.
  34. 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.
  35. Buettner C, Mukamal KJ, Gardiner P, et al. Herbal supplement use and blood lead levels of United States adults. J Gen Intern Med 2009; 24:1175.
  36. Rabinowitz MB. Toxicokinetics of bone lead. Environ Health Perspect 1991; 91:33.
  37. Hryhorczuk DO, Rabinowitz MB, Hessl SM, et al. Elimination kinetics of blood lead in workers with chronic lead intoxication. Am J Ind Med 1985; 8:33.
  38. Goldman RH, White R, Kales SN, Hu H. Lead poisoning from mobilization of bone stores during thyrotoxicosis. Am J Ind Med 1994; 25:417.
  39. Riess ML, Halm JK. Lead poisoning in an adult: lead mobilization by pregnancy? J Gen Intern Med 2007; 22:1212.
  40. Gulson BL, Mahaffey KR, Jameson CW, et al. Mobilization of lead from the skeleton during the postnatal period is larger than during pregnancy. J Lab Clin Med 1998; 131:324.
  41. Valentine WN, Paglia DE, Fink K, Madokoro G. Lead poisoning: association with hemolytic anemia, basophilic stippling, erythrocyte pyrimidine 5'-nucleotidase deficiency, and intraerythrocytic accumulation of pyrimidines. J Clin Invest 1976; 58:926.
  42. Struzyńska L, Walski M, Gadamski R, et al. Lead-induced abnormalities in blood-brain barrier permeability in experimental chronic toxicity. Mol Chem Neuropathol 1997; 31:207.
  43. Wright RO, Schwartz J, Wright RJ, et al. Biomarkers of lead exposure and DNA methylation within retrotransposons. Environ Health Perspect 2010; 118:790.
  44. Li C, Yang X, Xu M, et al. Epigenetic marker (LINE-1 promoter) methylation level was associated with occupational lead exposure. Clin Toxicol (Phila) 2013; 51:225.
  45. Wu Y, Liu Y, Ni N, et al. High lead exposure is associated with telomere length shortening in Chinese battery manufacturing plant workers. Occup Environ Med 2012; 69:557.
  46. Ni Z, Hou S, Barton CH, Vaziri ND. Lead exposure raises superoxide and hydrogen peroxide in human endothelial and vascular smooth muscle cells. Kidney Int 2004; 66:2329.
  47. Wang FT, Hu H, Schwartz J, et al. Modifying effects of the HFE polymorphisms on the association between lead burden and cognitive decline. Environ Health Perspect 2007; 115:1210.
  48. Rajan P, Kelsey KT, Schwartz JD, et al. Interaction of the delta-aminolevulinic acid dehydratase polymorphism and lead burden on cognitive function: the VA normative aging study. J Occup Environ Med 2008; 50:1053.
  49. Leroyer A, Leleu B, Dehon B, et al. Influence of delta-aminolevulinic acid dehydratase gene polymorphism on selected lead exposure biomarkers in a cohort of ex-smelter workers. J Toxicol Environ Health A 2013; 76:895.
  50. Feldman RG. Urban lead mining: lead intoxication among deleaders. N Engl J Med 1978; 298:1143.
  51. Cullen MR, Robins JM, Eskenazi B. Adult inorganic lead intoxication: presentation of 31 new cases and a review of recent advances in the literature. Medicine (Baltimore) 1983; 62:221.
  52. Friedman LS, Simmons LH, Goldman RH, Sohani AR. Case records of the Massachusetts General Hospital. Case 12-2014. A 59-year-old man with fatigue, abdominal pain, anemia, and abnormal liver function. N Engl J Med 2014; 370:1542.
  53. Cheson BD, Rom WN, Webber RC. Basophilic stippling of red blood cells: a nonspecific finding of multiple etiology. Am J Ind Med 1984; 5:327.
  54. Thomson RM, Parry GJ. Neuropathies associated with excessive exposure to lead. Muscle Nerve 2006; 33:732.
  55. Nawrot TS, Thijs L, Den Hond EM, et al. An epidemiological re-appraisal of the association between blood pressure and blood lead: a meta-analysis. J Hum Hypertens 2002; 16:123.
  56. Navas-Acien A, Guallar E, Silbergeld EK, Rothenberg SJ. Lead exposure and cardiovascular disease--a systematic review. Environ Health Perspect 2007; 115:472.
  57. Nash D, Magder L, Lustberg M, et al. Blood lead, blood pressure, and hypertension in perimenopausal and postmenopausal women. JAMA 2003; 289:1523.
  58. Hu H, Aro A, Payton M, et al. The relationship of bone and blood lead to hypertension. The Normative Aging Study. JAMA 1996; 275:1171.
  59. Martin D, Glass TA, Bandeen-Roche K, et al. Association of blood lead and tibia lead with blood pressure and hypertension in a community sample of older adults. Am J Epidemiol 2006; 163:467.
  60. Korrick SA, Hunter DJ, Rotnitzky A, et al. Lead and hypertension in a sample of middle-aged women. Am J Public Health 1999; 89:330.
  61. Lustberg M, Silbergeld E. Blood lead levels and mortality. Arch Intern Med 2002; 162:2443.
  62. Menke A, Muntner P, Batuman V, et al. Blood lead below 0.48 micromol/L (10 microg/dL) and mortality among US adults. Circulation 2006; 114:1388.
  63. Schober SE, Mirel LB, Graubard BI, et al. Blood lead levels and death from all causes, cardiovascular disease, and cancer: results from the NHANES III mortality study. Environ Health Perspect 2006; 114:1538.
  64. Weisskopf MG, Jain N, Nie H, et al. A prospective study of bone lead concentration and death from all causes, cardiovascular diseases, and cancer in the Department of Veterans Affairs Normative Aging Study. Circulation 2009; 120:1056.
  65. Perlstein T, Weuve J, Schwartz J, et al. Cumulative community-level lead exposure and pulse pressure: the normative aging study. Environ Health Perspect 2007; 115:1696.
  66. Poręba R, Gać P, Poręba M, et al. Relationship between occupational exposure to lead and local arterial stiffness and left ventricular diastolic function in individuals with arterial hypertension. Toxicol Appl Pharmacol 2011; 254:342.
  67. Khalil N, Morrow LA, Needleman H, et al. Association of cumulative lead and neurocognitive function in an occupational cohort. Neuropsychology 2009; 23:10.
  68. Balbus-Kornfeld JM, Stewart W, Bolla KI, Schwartz BS. Cumulative exposure to inorganic lead and neurobehavioural test performance in adults: an epidemiological review. Occup Environ Med 1995; 52:2.
  69. Weisskopf MG, Wright RO, Schwartz J, et al. Cumulative lead exposure and prospective change in cognition among elderly men: the VA Normative Aging Study. Am J Epidemiol 2004; 160:1184.
  70. Shih RA, Glass TA, Bandeen-Roche K, et al. Environmental lead exposure and cognitive function in community-dwelling older adults. Neurology 2006; 67:1556.
  71. Rajan P, Kelsey KT, Schwartz JD, et al. Lead burden and psychiatric symptoms and the modifying influence of the delta-aminolevulinic acid dehydratase (ALAD) polymorphism: the VA Normative Aging Study. Am J Epidemiol 2007; 166:1400.
  72. Eum KD, Korrick SA, Weuve J, et al. Relation of cumulative low-level lead exposure to depressive and phobic anxiety symptom scores in middle-age and elderly women. Environ Health Perspect 2012; 120:817.
  73. Cheng Y, Schwartz J, Vokonas PS, et al. Electrocardiographic conduction disturbances in association with low-level lead exposure (the Normative Aging Study). Am J Cardiol 1998; 82:594.
  74. Park SK, Elmarsafawy S, Mukherjee B, et al. Cumulative lead exposure and age-related hearing loss: the VA Normative Aging Study. Hear Res 2010; 269:48.
  75. Stewart WF, Schwartz BS, Davatzikos C, et al. Past adult lead exposure is linked to neurodegeneration measured by brain MRI. Neurology 2006; 66:1476.
  76. Weisskopf MG, Hu H, Sparrow D, et al. Proton magnetic resonance spectroscopic evidence of glial effects of cumulative lead exposure in the adult human hippocampus. Environ Health Perspect 2007; 115:519.
  77. Shih RA, Hu H, Weisskopf MG, Schwartz BS. Cumulative lead dose and cognitive function in adults: a review of studies that measured both blood lead and bone lead. Environ Health Perspect 2007; 115:483.
  78. Weisskopf MG, Weuve J, Nie H, et al. Association of cumulative lead exposure with Parkinson's disease. Environ Health Perspect 2010; 118:1609.
  79. Weuve J, Press DZ, Grodstein F, et al. Cumulative exposure to lead and cognition in persons with Parkinson's disease. Mov Disord 2013; 28:176.
  80. Taylor CM, Golding J, Emond AM. Adverse effects of maternal lead levels on birth outcomes in the ALSPAC study: a prospective birth cohort study. BJOG 2015; 122:322.
  81. González-Cossío T, Peterson KE, Sanín LH, et al. Decrease in birth weight in relation to maternal bone-lead burden. Pediatrics 1997; 100:856.
  82. 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.
  83. 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.
  84. Rothenberg SJ, Kondrashov V, Manalo M, et al. Increases in hypertension and blood pressure during pregnancy with increased bone lead levels. Am J Epidemiol 2002; 156:1079.
  85. Hu H, Téllez-Rojo MM, Bellinger D, et al. Fetal lead exposure at each stage of pregnancy as a predictor of infant mental development. Environ Health Perspect 2006; 114:1730.
  86. Lancranjan I, Popescu HI, GAvănescu O, et al. Reproductive ability of workmen occupationally exposed to lead. Arch Environ Health 1975; 30:396.
  87. Alexander BH, Checkoway H, van Netten C, et al. Semen quality of men employed at a lead smelter. Occup Environ Med 1996; 53:411.
  88. Robins TG, Bornman MS, Ehrlich RI, et al. Semen quality and fertility of men employed in a South African lead acid battery plant. Am J Ind Med 1997; 32:369.
  89. Ng TP, Goh HH, Ng YL, et al. Male endocrine functions in workers with moderate exposure to lead. Br J Ind Med 1991; 48:485.
  90. Schaumberg DA, Mendes F, Balaram M, et al. Accumulated lead exposure and risk of age-related cataract in men. JAMA 2004; 292:2750.
  91. Arora M, Weuve J, Weisskopf MG, et al. Cumulative lead exposure and tooth loss in men: the normative aging study. Environ Health Perspect 2009; 117:1531.
  92. Krishnan E, Lingala B, Bhalla V. Low-level lead exposure and the prevalence of gout: an observational study. Ann Intern Med 2012; 157:233.
  93. National Toxicology Program (NTP), US Department of Health and Human Services. Report on Carcinogens, 13th ed. Lead and Lead Compounds (CAS No. 7439-92-1 [Lead]). http://ntp.niehs.nih.gov/ntp/roc/twelfth/profiles/Lead.pdf (Accessed on March 06, 2016).
  94. White RF, Diamond R, Proctor S, et al. Residual cognitive deficits 50 years after lead poisoning during childhood. Br J Ind Med 1993; 50:613.
  95. Hu H. A 50-year follow-up of childhood plumbism. Hypertension, renal function, and hemoglobin levels among survivors. Am J Dis Child 1991; 145:681.
  96. Hu H. Knowledge of diagnosis and reproductive history among survivors of childhood plumbism. Am J Public Health 1991; 81:1070.
  97. Bain BJ. Lead poisoning. Am J Hematol 2014; 89:1141.
  98. US Department of. Occupational exposure to lead. Fed Reg 1978; :43.
  99. U.S. Department of Labor, Occupational Safety and Health Administration. 29 CFR Part 1926: Lead exposure in construction; interim final rule. Fed Reg 1993; :58.
  100. Taylor L, Jones RL, Ashley K, et al. Comparison of capillary earlobe and venous blood monitoring for occupational lead surveillance. J Lab Clin Med 2004; 143:217.
  101. 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.
  102. Hu H, Shih R, Rothenberg S, Schwartz BS. The epidemiology of lead toxicity in adults: measuring dose and consideration of other methodologic issues. Environ Health Perspect 2007; 115:455.
  103. Hu H. Bone lead as a new biologic marker of lead dose: recent findings and implications for public health. Environ Health Perspect 1998; 106 Suppl 4:961.
  104. Barbosa F Jr, Tanus-Santos JE, Gerlach RF, Parsons PJ. A critical review of biomarkers used for monitoring human exposure to lead: advantages, limitations, and future needs. Environ Health Perspect 2005; 113:1669.
  105. Park SK, Mukherjee B, Xia X, et al. Bone lead level prediction models and their application to examine the relationship of lead exposure and hypertension in the Third National Health and Nutrition Examination Survey. J Occup Environ Med 2009; 51:1422.
  106. Chia SE, Chia HP, Ong CN, Jeyaratnam J. Cumulative blood lead levels and neurobehavioral test performance. Neurotoxicology 1997; 18:793.
  107. American College of Occupational and Environmental Medicine. Recommendation to OSHA Regarding Blood Lead Levels. 2010. Available at: http://www.acoem.org/BloodLeadLevels.aspx (Accessed on March 02, 2014).
  108. Ettinger, AS, Gurthrie Wengrovitz, A (Eds). Guidelines for the identification and management of lead exposure in pregnant and lactating women. National Center for Environmental Health/Agency for Toxic Substances and Disease Registry; Centers for Disease Control and Prevention, Atlanta, GA, 2010 available at http://www.cdc.gov/nceh/lead/publications/LeadandPregnancy2010.pdf.
  109. Centers for Disease Control and Prevention (CDC). Adult blood lead epidemiology and surveillance--United States, 2003-2004. MMWR Morb Mortal Wkly Rep 2006; 55:876.
  110. Association for Occupational and Environmental Clinics: Medical management guidelines for lead exposed adults. Available at: www.aoec.org/documents/positions/MMG_FINAL.pdf (Accessed on July 20, 2011).
  111. Kosnett MJ. Lead. In: Critical Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient, Brent J, Phillips SD, Wallace KL, et al. (Eds), Elsevier Mosby, 2005. p.821.
  112. Grandjean P, Jacobsen IA, Jørgensen PJ. Chronic lead poisoning treated with dimercaptosuccinic acid. Pharmacol Toxicol 1991; 68:266.
  113. Lin JL, Ho HH, Yu CC. Chelation therapy for patients with elevated body lead burden and progressive renal insufficiency. A randomized, controlled trial. Ann Intern Med 1999; 130:7.
  114. Porru S, Alessio L. The use of chelating agents in occupational lead poisoning. Occup Med (Lond) 1996; 46:41.
  115. Bradberry S, Sheehan T, Vale A. Use of oral dimercaptosuccinic acid (succimer) in adult patients with inorganic lead poisoning. QJM 2009; 102:721.
  116. Charlton N, Wallace KL. American College of Medical Toxicology Position Statement on post-chelator challenge urinary metal testing. http://www.acmt.net/zine_service.html (Accessed on March 06, 2016).
  117. Simon JA, Hudes ES. Relationship of ascorbic acid to blood lead levels. JAMA 1999; 281:2289.
  118. 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.
  119. Rischitelli G, Nygren P, Bougatsos C, et al. Screening for elevated lead levels in childhood and pregnancy: an updated summary of evidence for the US Preventive Services Task Force. Pediatrics 2006; 118:e1867.