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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTE3NDc1Mi10cmVhdG1lbnQ=\nDrugs & Diseases > Neurology\nLead Toxicity Treatment & Management\nAuthor: Pranay Kathuria, MD, FACP, FASN, FNKF; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS more...\nLead Toxicity\nSections Lead Toxicity\nPlain Radiography\nCT and MRI\nDietary Measures\nAntidotes\nThe most important step in treatment is to prevent further exposure to lead. Accurate assessment of environmental and occupational exposure is essential. Modifying children’s behavior to decrease hand-to-mouth activity is beneficial.\nThe US Occupational Safety and Health Administration (OSHA) has recommendations for occupational lead exposure. Under these guidelines, the permissible exposure limit is 50 µg/m3 for an 8-hour, time-weighted average. Workers with blood lead levels (BLLs) of 60 µg/dL or higher must be removed from the workplace. Additionally, employees should be removed from the workplace if the average of their last 3 BLLs is 50 µg/dL or higher. Individuals with BLLs of 40 µg/dL or higher must undergo medical evaluation.\nCommunity-wide preventive actions are recommended when children are found to have BLLs of 10 µg/dL or higher. With BLLs of 15-19 µg/dL, nutritional and educational interventions are recommended. With BLLs of 20 µg/dL or higher, medical evaluations and environmental interventions are recommended.\nMedical treatment (ie, chelation therapy) is but one element of a comprehensive treatment plan for exposure to lead; removal of the source of lead exposure is more important. The interventions described below relate to chelation therapy for the most severe cases of lead poisoning. Chelation is of only transient benefit in the patient whose source of lead exposure has not been identified and removed.\nChelation therapy, especially in the setting of encephalopathy, can be complicated. If appropriate facilities for treatment are not available, consider transfer to an institution that is capable of managing an encephalopathic patient and also has a provider experienced in lead poisoning and chelation therapy. Ideally, children should be treated in specialized pediatric intensive care units.\nChelation agents\nSuccimer is a water-soluble, oral chelating agent that is appropriate for use with BLLs higher than 45 µg/dL. [22, 31] In a retrospective study from Nigeria, chelation therapy using dimercaptosuccinic acid (DMSA) lowered blood lead levels in children with severe lead poisoning. [32]\nD-penicillamine is a second-line oral chelating agent, although it is not approved by the US Food and Drug Administration (FDA) for use in lead poisoning.\nEdetate (EDTA) calcium disodium (CaNa2 EDTA) is a parenteral chelating agent. It should never be used as the sole agent in patients manifesting with lead encephalopathy, because it does not cross the blood-brain barrier and can potentially lead to exacerbation of lead encephalopathy; dimercaprol, which does cross the blood-brain barrier, should be administered first. Life-threatening hypocalcemia has been reported when disodium EDTA was inadvertently substituted for CaNa2 EDTA.\nDimercaprol (also referred to as British antilewisite [BAL]) is another parenteral chelating agent recommended as an agent of first choice for patients with lead encephalopathy. With high BLLs (ie, > 100 µg/dL), it is used in conjunction with CaNa2 EDTA.\nAcute lead poisoning and nephropathy\nIn the acute setting, if suggestive radiopacities are observed on a plain radiograph of the abdomen, gastric lavage, cathartics, or whole bowel irrigation may be used to limit lead absorption.\nWith acute lead poisoning, the indications for chelation therapy are well defined. Institute chelation therapy in children with BLLs of 45 µg/dL or higher. Treat children whose BLLs are 70 µg/dL or higher as medical emergencies.\nSuccimer and penicillamine may be given orally. Penicillamine may be used when blood lead levels are 25-40 µg/dL, especially with a negative CaNa2 EDTA mobilization test result. Succimer may be an alternative; its main indication is in persons whose BLLs are 45 µg/dL or higher.\nIntravenous (IV) therapy is preferable for persons with BLLs of 70 µg/dL or higher. Use the combination of dimercaprol and CaNa2 EDTA with BLLs of 70 µg/dL or higher and in the presence of lead encephalopathy.\nIn adults, consider chelation therapy for patients with blood lead levels BLLs of 70 µg/dL or higher. Also consider chelation therapy in symptomatic adults with BLLs exceeding 50 µg/dL. Available chelation agents for adults are dimercaprol and CaNa2 EDTA; penicillamine and succimer do not have US Food and Drug Administration (FDA) approval for this application, although they are effective treatments.\nChelation therapy reverses Fanconi syndrome, transient hypertension, and tubular structural changes observed on histopathology findings.\nChronic lead nephropathy\nPatients with chronic lead nephropathy, in the absence of marked interstitial fibrosis and with only minimal impairment in kidney function, may respond to chelation therapy.\nExtremely limited data are available regarding the benefits of chelation therapy with documented lead nephropathy. In 1979, Wedeen et al treated patients with occupational lead nephropathy and found a 20% improvement in the GFR in 4 of 8 patients given EDTA 3 times a week for 6-50 months. [33] The reported improvements in kidney function could be from reversal of acute-on-chronic lead nephropathy.\nLin and coworkers from Taiwan performed 3 well-designed studies addressing populations of patients with high-normal BLLs and chronic kidney disease. [34, 35, 36]\nThe first of these studies included 32 subjects with chronic kidney disease (serum creatinine level [SCr] of 1.5-4 mg/dL) and mildly elevated body lead burden (lead excretion value of 150-600 µg with the 3-D CaNa2 EDTA lead mobilization test). Subjects were randomly assigned to receive EDTA chelation therapy or placebo weekly for 2 months and were followed for an additional 12 months. The reciprocal of serum creatinine (1/SCr) versus time data suggested that using chelation may slow the progression of renal disease.\nThe second study described the results of chelation therapy in 36 subjects (24 study group subjects and 12 controls) with serum creatinine values of 1.5-4 mg/dL and high-normal bone lead burden. This time, chelation therapy with CaNa2 EDTA was administered weekly for 3 months. In the treated group, creatinine clearance improved by as much as 10.2% at 1 year, whereas in the control group, kidney function declined by as much as 11%.\nThe third study included 202 subjects who were followed for 2 years. In this study, 64 patients with a high-normal body lead burden (urinary lead excretion > 80 µg and < 600 µg after 1 g of CaNa2 EDTA infusion) and SCr lower than 4.2 mg/dL were randomized to chelation or placebo.\nIn the initial 3 months, the chelation group received 1 g of CaNa2 EDTA every week, and the controls received placebo. In the ensuing 24 months, repeated chelation therapy was administered weekly to patients with a high-normal lead burden unless, on repeated testing, the body lead burden fell below 60 µg.\nThe glomerular filtration ate (GFR) increased by 11.9% (+3.4 mL/min) in the chelation group at the end of the initial 3 months, whereas it fell by 3.6% (-1 mL/min) in the control group. Thereafter, no further improvement in the GFR was observed in these patients. At the end of 27 months, the mean change in GFR was +2.1 mL/min in the chelation group and -6 mL/min in the control group over the 27-month study.\nThese studies suggest that in patients with an increased lead burden, chelation with small doses of CaNa2 EDTA at longer intervals might be safe for treating chronic kidney disease. However, repeated and chronic exposure to CaNa2 EDTA may create its own nephrotoxicity; therefore, use caution when deciding to institute chelation therapy. Exclude other causes of kidney disease, and define an endpoint of therapy, such as normalization of the CaNa2 EDTA test results or improvement in kidney function.\nSupplementary measures\nClosely monitor cardiovascular and mental status in patients with lead poisoning. Maintain an adequate urine output. Assess renal and hepatic functions.\nDiphenhydramine may help alleviate the adverse effects of dimercaprol. Iron supplementation should be avoided in patients receiving dimercaprol chelation therapy because dimercaprol forms a complex with iron, leading to toxicity.\nThe diet should be adequate in energy (caloric) intake and replete in calcium, zinc, and iron. Data from the Normative Aging Study suggest that low dietary intake of vitamin D may increase accumulation of lead in bones, whereas low dietary intake of vitamin C and iron may increase lead levels in blood in subjects who range in age from middle-aged to elderly.\nSimilar data associate calcium and iron deficiency with lead absorption in children. Although no studies have specifically addressed treatment of lead exposure with calcium and iron supplementation, it is a logical therapy to help limit the absorption of lead.\nThe 2010 Healthy People objective to eliminate childhood lead poisoning can be achieved through primary prevention. Pediatricians and family practitioners provide a fundamental role with anticipatory guidance about potential sources of lead exposure and its hazards for the development of children.\nA successful primary prevention should focus on the 2 main exposure sources for children in the United States: lead in housing and nonessential uses of lead in certain products, such as imported and domestically manufactured toys, eating and drinking utensils, cosmetics, and traditional medicines.\nEnvironmental measures for prevention of lead toxicity include abatement of lead paint usage, removal of lead from gasoline, and removal of lead solder from cans. Lead abatement in dwellings must be performed by skilled and experienced workers.\nFor adults, occupational measures focus on engineering controls, such as isolation by containment and local exhaust systems, personal protective equipment (eg, respirators), and good work practices. Workers should be educated regarding the health risks of lead and sources that may cause poisoning.\nOSHA standards should be followed in the workplace. These standards for permissible exposure limit lead in the workplace to a maximum of 50 µg/m3 of air averaged over an 8-hour period. Medical surveillance is indicated when workers are exposed to lead levels exceeding 30 µg/m3 for more than 30 days a year (regardless of respiratory protection).\nEfforts to prevent lead poisoning have focused primarily on secondary prevention because the cost of primary prevention in the form of environmental inspection and abatement of all homes and other sources of lead is prohibitive. This focus does not reflect the true importance of primary prevention.\nSecondary prevention focuses on the early detection of lead poisoning. The CDC has devised screening criteria to determine which children are at high risk for lead poisoning; screening of BLLs should be carried out according to these criteria (see Workup). Medical evaluation, treatment, and environmental and public health follow-up are essential in individuals with elevated BLLs.\nConsultation with a toxicologist and a nephrologist is appropriate. Medical toxicology services can typically be located by contacting a local poison center.\nAll occupational exposures must be reported to OSHA. The local or county health departments responsible for monitoring children with lead toxicity, should be informed about patients with elevated lead levels or those undergoing medical treatment, so that they may initiate appropriate environmental evaluation and lead abatement.\nMany local health departments have programs for appropriate lead screening of children, in cooperation with local pediatricians. Stressing the need for screening in any patient at risk (because of housing, industrial, ethnic, recreational concerns) is important. Repairs of older homes must be done carefully to avoid lead exposure. Proper lead abatement in older homes prevents future exposure to lead and, thus, prevents further lead poisoning.\nAll patients treated for lead poisoning require extensive outpatient follow-up. The intent of such follow-up is to avoid further exposure to lead and to maintain lead levels in the acceptable range.\nAfter chelation, the blood lead level should be rechecked in 7-21 days to determine whether repeat chelation therapy is required. Chelation therapy, either oral or intravenous, may be continued in an outpatient setting if indicated. Carefully monitor kidney and liver function during therapy.\nAssess the source of lead. Involvement of the local health department can assist in this regard. Do not discharge patients from the hospital until they can go to a lead-free environment. Children in particular should not be allowed to return to a lead-contaminated environment; if they are exposed to more lead, their lead levels will rapidly rise again.\nThere is a general belief, probably incorrect, that once chelation is terminated, BLLs will rebound rapidly. Numerous publications have discussed the effect of lead stored in bone. [37, 38, 39, 40, 41, 18] In the light of the known kinetics of lead in the body and the reports of expected decreases in lead level over time, this would not appear to be expected, because the half-life of lead in bone is measured in years. Thus, significant elevations in BLL after termination of chelation should be considered probable reexposure.\nMurata K, Iwata T, Dakeishi M, Karita K. Lead toxicity: does the critical level of lead resulting in adverse effects differ between adults and children?. J Occup Health. 2009. 51(1):1-12. [Medline].\nBerg R. Lead in adults: the lesser concern rears its head. J Environ Health. 2009 Dec. 72(5):8-13. [Medline].\nRebelo FM, Caldas ED. Arsenic, lead, mercury and cadmium: Toxicity, levels in breast milk and the risks for breastfed infants. Environ Res. 2016 Nov. 151:671-688. [Medline].\nCanfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med. 2003 Apr 17. 348(16):1517-26. [Medline].\nBellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study. Pediatrics. 1992 Dec. 90(6):855-61. [Medline].\nChen A, Dietrich KN, Ware JH, Radcliffe J, Rogan WJ. IQ and blood lead from 2 to 7 years of age: are the effects in older children the residual of high blood lead concentrations in 2-year-olds?. Environ Health Perspect. 2005 May. 113(5):597-601. [Medline]. [Full Text].\nHornung R, Lanphear B, Dietrich K. Response to: \"What is the meaning of non-linear dose-response relationships between blood lead concentration and IQ?\". Neurotoxicology. 2006 Jul. 27(4):635. [Medline].\nLanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, et al. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environ Health Perspect. 2005 Jul. 113(7):894-9. [Medline]. [Full Text].\nFlora G, Gupta D, Tiwari A. Toxicity of lead: A review with recent updates. Interdiscip Toxicol. 2012 Jun. 5 (2):47-58. [Medline].\nHerman SS, Geraldine M, Venkatesh T. Influence of minerals on lead-induced alterations in liver function in rats exposed to long-term lead exposure. J of Hazardous Materials. In press.\nElevated Lead in D.C. Drinking Water - A Study of Potential Causative Events, Final Summary Report. EPA; August 2007:[Full Text].\nOnuah, F and Abrak, I. At Least 28 Children Killed by Lead Poisoning in Nigeria. Medscape Medical News. Available at http://www.medscape.com/viewarticle/844746. May 18, 2015; Accessed: September 22, 2015.\nHolstege CP, Ferguson JD, Wolf CE, Baer AB, Poklis A. Analysis of moonshine for contaminants. J Toxicol Clin Toxicol. 2004. 42(5):597-601. [Medline].\nCristante AF, de Souza FI, Barros Filho TE, Oliveira RP, Marcon RM. Lead poisoning by intradiscal firearm bullet: a case report. Spine (Phila Pa 1976). 2010 Feb 15. 35(4):E140-3. [Medline].\nNorman EH, Bordley WC, Hertz-Picciotto I, Newton DA. Rural-urban blood lead differences in North Carolina children. Pediatrics. 1994 Jul. 94(1):59-64. [Medline].\nJones RL, Homa DM, Meyer PA, Brody DJ, Caldwell KL, Pirkle JL, et al. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 years, 1988-2004. Pediatrics. 2009 Mar. 123(3):e376-85. [Medline].\nCDC. US Department of Health and Human Services, National Institute for Occupational Safety and Health; 2013. Adult Blood Lead Epidemiology and Surveillance (ABLES). [Full Text].\nGuérin O, Carré N, Garnier R. [Determining factors in lowering blood lead levels below the poisoning threshold in Greater Paris (1992-2006)]. Rev Epidemiol Sante Publique. 2010 Jun. 58(3):181-7. [Medline].\nEvans M, Fored CM, Nise G, Bellocco R, Nyrén O, Elinder CG. Occupational lead exposure and severe CKD: a population-based case-control and prospective observational cohort study in Sweden. Am J Kidney Dis. 2010 Mar. 55(3):497-506. [Medline].\nMorgan BW, Todd KH, Moore B. Elevated blood lead levels in urban moonshine drinkers. Ann Emerg Med. 2001 Jan. 37(1):51-4. [Medline].\nDietrich KN, Berger OG, Succop PA. Lead exposure and the motor developmental status of urban six-year-old children in the Cincinnati Prospective Study. Pediatrics. 1993 Feb. 91(2):301-7. [Medline].\nFluri F, Balestra G, Christ M, Marsch S, Fuhr P, Rüegg S. Stimulus-induced rhythmic, periodic or ictal discharges (SIRPIDs) elicited by stimulating exclusively the ophthalmic nerve. Clin Neurophysiol. 2008 Aug. 119(8):1934-8. [Medline].\nLead exposure in children: prevention, detection, and management. Pediatrics. 2005 Oct. 116(4):1036-46. [Medline].\nAmerican Academy of Pediatrics Committee on Environmental Health. Lead. In:. Handbook of Pediatric Environmental Health. American Academy of Pediatrics. Elk Grove, IL: AAP; 1999:131-43.:\nCDC. Preventing Lead Poisoning in Young Children. DC, United States Department of Health and Human Services:1991:[Full Text].\nCDC. Screening Young Children for Lead Poisoning. Guidance for State and Local Public Health Officials. . Atlanta, GA: United States Department of Health and Human Services; 1997:[Full Text].\nTreatment guidelines for lead exposure in children. American Academy of Pediatrics Committee on Drugs. Pediatrics. 1995 Jul. 96(1 Pt 1):155-60. [Medline].\nCarton JA, Maradona JA, Arribas JM. Acute-subacute lead poisoning. Clinical findings and comparative study of diagnostic tests. Arch Intern Med. 1987 Apr. 147(4):697-703. [Medline].\nDietrich KN, Ware JH, Salganik M, Radcliffe J, Rogan WJ, Rhoads GG, et al. Effect of chelation therapy on the neuropsychological and behavioral development of lead-exposed children after school entry. Pediatrics. 2004 Jul. 114(1):19-26. [Medline].\nAtre AL, Shinde PR, Shinde SN, Wadia RS, Nanivadekar AA, Vaid SJ, et al. Pre- and posttreatment MR imaging findings in lead encephalopathy. AJNR Am J Neuroradiol. 2006 Apr. 27(4):902-3. [Medline].\nRogan WJ, Dietrich KN, Ware JH, Dockery DW, Salganik M, Radcliffe J, et al. The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead. N Engl J Med. 2001 May 10. 344(19):1421-6. [Medline].\nThurtle N, Greig J, Cooney L, Amitai Y, Ariti C, Brown MJ, et al. Description of 3,180 courses of chelation with dimercaptosuccinic acid in children ≤ 5 y with severe lead poisoning in Zamfara, Northern Nigeria: a retrospective analysis of programme data. PLoS Med. 2014 Oct. 11 (10):e1001739. [Medline].\nWedeen RP, Malik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med. 1979 Jan. 139(1):53-7. [Medline].\nLin 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 Jan 5. 130(1):7-13. [Medline].\nLin JL, Lin-Tan DT, Hsu KH, Yu CC. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes. N Engl J Med. 2003 Jan 23. 348(4):277-86. [Medline].\nLin JL, Tan DT, Hsu KH, Yu CC. Environmental lead exposure and progressive renal insufficiency. Arch Intern Med. 2001 Jan 22. 161(2):264-71. [Medline].\nMushak P. Lead remediation and changes in human lead exposure: some physiological and biokinetic dimensions. Sci Total Environ. 2003 Feb 15. 303(1-2):35-50. [Medline].\nRoberts JR, Reigart JR, Ebeling M, Hulsey TC. Time required for blood lead levels to decline in nonchelated children. J Toxicol Clin Toxicol. 2001. 39(2):153-60. [Medline].\nRust SW, Kumar P, Burgoon DA, Niemuth NA, Schultz BD. Influence of bone-lead stores on the observed effectiveness of lead hazard intervention. Environ Res. 1999 Oct. 81(3):175-84. [Medline].\nRabinowitz MB. Toxicokinetics of bone lead. Environ Health Perspect. 1991 Feb. 91:33-7. [Medline]. [Full Text].\nRabinowitz MB, Wetherill GW, Kopple JD. Kinetic analysis of lead metabolism in healthy humans. J Clin Invest. 1976 Aug. 58(2):260-70. [Medline]. [Full Text].\nFadrowski JJ, Navas-Acien A, Tellez-Plaza M, Guallar E, Weaver VM, Furth SL. Blood lead level and kidney function in US adolescents: The Third National Health and Nutrition Examination Survey. Arch Intern Med. 2010 Jan 11. 170(1):75-82. [Medline].\nCenters for Disease Control and Prevention. Adult blood lead epidemiology and surveillance--United States, 2005-2007. MMWR Morb Mortal Wkly Rep. 2009 Apr 17. 58(14):365-9. [Medline].\nPeripheral smear taken from 8-year-old Pakistani girl who presented with acute hemolytic anemia and lead level of 125 µg/dL.\nGrowth arrest lines, also known as lead lines, in bones of child who recovered from lead poisoning.\nLead line on gingival border of adult with lead poisoning.\nWrist drop in adult with lead poisoning and renal failure.\nAbdominal flat plate showing multiple radiopaque foreign bodies, including paint chips and earring.\nKidney biopsy results from patient with chronic lead nephropathy show nonspecific tubular atrophy and interstitial fibrosis. Note absence of interstitial infiltrate. Single glomerulus included in section is normal. Image courtesy of Vecihi Batuman, MD, FACP.\nPranay Kathuria, MD, FACP, FASN, FNKF Professor of Medicine, Director, Division of Nephrology and Hypertension, Program Director of Nephrology Fellowship, University of Oklahoma School of Community Medicine\nPranay Kathuria, MD, FACP, FASN, FNKF is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Hypertension, American Society of Nephrology, National Kidney Foundation\nAdam K Rowden, DO Assistant Professor of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University; Director, Division of Toxicology, Department of Emergency Medicine, Albert Einstein Medical Center; Consulting Toxicologist, Children's Hospital of Philadelphia\nAdam K Rowden, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Osteopathic Emergency Physicians, American Osteopathic Association, Society for Academic Emergency Medicine\nRika Nagakuni O'Malley, MD Instructor, Department of Emergency Medicine, Thomas Jefferson University Hospital\nNicholas Lorenzo, MD, MHA, CPE Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc\nNicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association for Physician Leadership\nTarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital\nTarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine\nDavid A Griesemer, MD, Professor, Departments of Neuroscience and Pediatrics, Medical University of South Carolina\nDavid A Griesemer, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Neurology, American Epilepsy Society, Child Neurology Society, and Society for Neuroscience\nChristopher P Holstege, MD Associate Professor of Emergency Medicine and Pediatrics, University of Virginia School of Medicine; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Center; Associate Medical Toxicology Fellowship Director, Veterans Affairs Department of Health\nChristopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, European Association of Poisons Centres and Clinical Toxicologists, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society\nJ Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine\nJ Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine\nJonathan S Rutchik, MD, MPH Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco\nJonathan S Rutchik, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Occupational and Environmental Medicine, and Society of Toxicology\nFrancisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; 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