Lead Toxicity

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Continuing Education Activity

Lead became a common occupational toxin with the birth of the Industrial Revolution, by the end of the 19-century childhood lead poisoning secondary to exposure to lead-based paints was beginning to be recognized. As the 20 century progressed, so did the appreciation for increasingly subtle and even subclinical manifestations of lead toxicity. Today, healthcare providers and public health officials must grapple with the mounting evidence implicating lead as a potent neurotoxin with measurable negative effects on cognition at vanishingly low blood lead concentrations in the face of the difficulties surrounding the feasibility of completely eliminating lead from children’s environment. This activity reviews the etiology, presentation, evaluation, and management/prevention of lead toxicity, and reviews the role of the interprofessional team in evaluating, diagnosing, and managing the condition.


  • Describe the toxicokinetics and pathophysiology of lead toxicity, including the effects of long-term exposure.
  • Review the components of a good history and examination for suspected lead toxicity.
  • Summarize the strategies for the treatment and management of lead toxicity, including prevention strategies.
  • Explain the importance of improving care coordination among the interprofessional team to enhance the delivery of care for patients with lead toxicity.


Humans have been using lead for a variety of applications since millennia, and concomitant with this use has developed an ancient recognition of the adverse effects of lead on the human body. As early as the second century BCE, physicians understood the link between lead exposure and neurocognitive disease,[1] and some scholars have wondered whether the extensive use of sapa, a syrup of unfermented grape juice reduced in a leaded vessel and used as a preservative for wine, may have contributed to the downfall of the Roman Empire.[2] Though lead became a common occupational toxin with the birth of the Industrial Revolution, by the end of the 19-century childhood lead poisoning secondary to exposure to lead-based paints was beginning to be recognized.[1] As the 20 century progressed, so did the appreciation for increasingly subtle and even subclinical manifestations of lead toxicity. Today, healthcare providers and public health officials must grapple with the mounting evidence implicating lead as a potent neurotoxin with measurable negative effects on cognition at vanishingly low blood lead concentrations in the face of the difficulties surrounding the feasibility of completely eliminating lead from children’s environment.


Because lead is not biodegradable, it demonstrates remarkable environmental persistence.[3] Despite the fact that the amount of lead in paint intended for use in or on residential buildings, furniture, or children’s toys in the United States has been restricted to 0.06% since 1978 and was further reduced to 0.009% in 2008, lead-based paint continues to be a major source of lead exposure in young children.[4] This is partially due to the fact that several million young children in the United States live in older homes in which lead-based paint was previously used, and as this old paint ages, it peels, flakes, and crumbles into dust that settles on the interior surfaces of homes and in the soil surrounding the exterior of the home.[5] The dust and soil containing these tiny paint particles inevitably make their way into children’s mouths as a result of normal childhood exploratory hand-to-mouth behavior.

Another ubiquitous potential source of lead is tap water, typically secondary to the presence of lead in plumbing. Though the US Environmental Protection Agency (EPA) banned the use of lead in pipes and solder used for plumbing in 1986, up to 10 million homes are still thought to be served by lead service lines.[4][5] In many countries outside the United States where leaded gasoline is still available, lead-contaminated air from emissions is a major source of exposure. This is because the emissions contaminate soil used to grow the food supply, and even though leaded gasoline was phased out of the US in the 1970s, the lead content in the soil in urban areas with historically high leaded gasoline emissions remains elevated.[4]

A variety of occupations and hobbies may expose adults to lead, and working parents may inadvertently bring lead home where they can expose their children second-hand. Some of the highest risk occupations and hobbies include metal welding, battery manufacturing, and recycling, shipbuilding and shipbreaking, firing range use or instruction as well as bullet salvaging, lead smelting and refining, painting and construction work, and pipefitting and plumbing.[4][6] Finally, a variety of other less ubiquitous exposures have nonetheless been implicated in both children and adults with elevated lead concentrations, including contaminated pewter and ceramic dining ware, imported spices and cosmetics, folk remedies, and ingestion of lead foreign bodies and retained leaded bullets.[4][7]


Approximately 535000 children between 1 and 5 years of age have an elevated blood lead concentration, defined by the Advisory Committee on Childhood Lead Poisoning Prevention of the Centers for Disease Control and Prevention (CDC) as greater than or equal to 5mcg/dL based on the 97.5 percentile of blood lead concentrations in the most recent National Health and Nutrition Examination Survey (NHANES) dataset.[4][8] Prevalence rates of children under 1 year of age with elevated blood lead concentrations are consistently lower than those in the 1 to 4 year age group, likely because lead is a cumulative toxin and because young children are more mobile and overall have more hand-to-mouth behavior compared to infants. In 2014 (the most recent data published by the CDC), for example, there were 444.5 per 100000 children aged 1 to 4 years in the US with a blood lead concentration of 5 to 9 mcg/dL, compared to 148.5 per 100000 children under 1 year of age in the US with a blood lead concentration in that same range. Rates of blood lead concentrations over 10mcg/dL are much lower: in 2014, 50.66 per 100000 children ages 1 to 4 years and 19.9 per 100000 children under 1 year of age had a blood lead concentration greater than 10mcg/dL.[8] In general, the rates of adults with elevated blood lead levels also tend to be relatively low; in 2013, 20.4 per 100 000 employed adults (defined as at least 16 years old) had a blood lead concentration over 10mcg/dL.[9]


Broadly speaking, lead interacts with human physiology in two significant ways: it has a strong affinity for sulfhydryl groups and electron donor groups in general, such that lead ends up bound to and affecting a wide range of proteins. Because of its similarity to other divalent cations like calcium and zinc, it interferes with the vast array of cellular mechanisms that are regulated by and mediated by these cations.[3] Because of the ubiquity of electron donor groups and divalent cations throughout the human body, the pathophysiology of lead toxicity is quite complex and involves virtually every organ system.

From a neurologic perspective, lead is thought to undermine the normal synaptic pruning process in young brains, likely underlying the cognitive and behavioral changes seen in young children with excessive lead exposure.[10] Peripheral neuropathy is a common manifestation of chronic lead toxicity in adults, but the mechanism underlying its development is poorly understood. The most severe neurologic manifestations of lead toxicity such as seizures and coma occur in acute lead encephalopathy, which is thought to be at least in part secondary to lead-induced cerebral microvascular changes leading to cerebral edema and resultant increased intracranial pressure.[11]

From a hematologic perspective, lead causes anemia by interfering with the function of several enzymes involved in heme synthesis as well as enzymes involved in maintaining erythrocyte cell membrane integrity, which leads to decreased production and increased destruction of erythrocytes, respectively.[3] The classic appearance of basophilic stippling is thought to represent clumps of degraded RNA, which is normally cleared by an enzyme known as pyrimidine-5’-nucleotidase that is inhibited by lead.[12]

From a renal perspective, lead can induce a global proximal tubule dysfunction leading to a Fanconi-like syndrome, and lead also competes with uric acid for excretion in the distal tubule, leading to higher blood concentrations of urate, which ultimately gets deposited as urate crystals in joints and is the mechanism underlying so-called “saturnine gout.” Lead is also known to be associated with the development of hypertension and subsequent cardiovascular disease; the mechanism is likely multifactorial and may involve increasing serum renin concentrations and activity as well as the development of neuropathy of the peripheral autonomic nervous system.[3][13] Lead also has a multitude of effects on the endocrine system, including impairing thyroid function, growth and skeletal development, and reproduction. Finally, though the mechanism remains poorly understood, lead is very clearly associated with GI symptoms such as abdominal pain, constipation, and anorexia.[3]


An important feature of the toxicokinetics of lead is the differential absorption, distribution, metabolism, and elimination of lead in young children compared to adults. In both adults and children, lead is primarily absorbed via the lung (inhalation) and GI tract (ingestion). While pulmonary absorption is reasonably efficient in both age groups (about 40%), children inhale more air relative to their body size than adults do, placing them at proportionally higher risk. Children generally absorb about 40 to 50% of the lead they ingest, while adults only absorb about 10 to 15%. The GI absorption of lead is also higher in those individuals with concomitant iron, calcium, or zinc deficiency, which tend to plague young children more often than adults.[14][15] Rarely, lead absorption may occur from the soft tissues in cases of embedded lead foreign bodies, such as retained lead bullets.[7] Of note, lead readily crosses the placenta.[16]

Once the lead is absorbed, it binds to red blood cells and distributes into two major compartments: the bone and the soft tissues. The soft tissue compartment includes the liver, kidneys, bone marrow, and brain, and is relatively labile compared to the more stable bone compartment. In adults, nearly the entire body burden of lead; about 85 to 95% - is stored in the stable bone compartment, whereas only about 70% of the body burden of lead storage is in bone in children. Children are thus again at greater risk of developing manifestations of lead toxicity because more of their lead body burden is stored in metabolically active sites, rather than in relatively inert bone.[3][17] A portion of the absorbed lead does not get incorporated into either of these compartments and ultimately gets excreted via the urine and bile; the excreted fraction is higher in adults than children, again putting children at greater risk of toxicity.[18]

History and Physical

The clinical manifestations of lead toxicity vary depending on the dose and chronicity of exposure. In the US, hundreds of thousands of children have elevated blood lead concentrations, but the vast majority of them are asymptomatic, meaning they have no overt clinical or laboratory findings that would indicate toxicity aside from the lead concentration itself. The primary concern in this group is that multiple meta-analyses have demonstrated that, even at low blood lead concentrations, there is an inverse relationship between blood lead concentrations and intelligence quotient (IQ) scores and markers of academic achievement. Especially worrisome is the finding that the dose-response curve is steeper at lower blood lead concentrations, meaning that the number of IQ points lost per unit increase in blood lead concentration is higher in the 1 to 10mcg/dL lead range than in the 10 to 20mcg/dL range.[19][20]

As the dose and duration of exposure increase children may develop nonspecific signs and symptoms often dismissed as typical toddlerhood maladies, such as irritability (tantrums), constipation and abdominal pain (often attributed to poor dietary choices or lack of fiber), and anorexia (often perceived as picky eating). Adults also demonstrate similar nonspecific signs and symptoms, and because of the likely longer duration of exposure, may additionally develop hypertension, associated cardiovascular disease, and adverse effects on fertility. As concentrations continue to increase in adults, many of them will go on to develop further evidence of toxicity such as peripheral neuropathy and arthritis secondary to saturnine gout.[3][21]

Eventually, if lead exposure continues, patients develop much more dramatic features of severe plumbism. In children, acute lead encephalopathy characteristically presents as unusual behavior, developmental regression, ataxia, vomiting, seizures, and at times, cerebral edema and resultant increased intracranial pressure, coma, and death. Generally, this syndrome occurs in children with extremely elevated blood lead concentrations (above 70 to 100 mcg/dL). Adults with extremely high blood lead concentrations also demonstrate similar neurologic findings, including encephalopathy, confusion, headaches, seizures, and obtundation. Generally, such severe lead toxicity does not occur in adults from occupational exposures but rather from unusual exposures such as large ingestions of contaminated folk remedies or contaminated moonshine.[3][10][11][21]


Pediatric screening guidelines for lead varies from state to state because the prevalence of lead toxicity tends to be higher in older urban areas, but regardless, the Early Periodic Screening, Diagnosis, and Treatment (EPSDT) component of Medicaid requires that all children with Medicaid obtain screening at 12 and 24 months. It also requires all children between 3 and 5 years of age to be screened if they have not previously had screening.[22] Also, the Occupational Safety and Health Administration (OSHA) requires employers to implement medical surveillance (i.e., lead screening) for any employee who may suffer exposure to airborne lead in concentrations exceeding 30 mg/minute averaged over eight hours for more than 30 days per year.[23] Screening is generally done with capillary blood because it is faster and more convenient to obtain, but any elevated result from capillary blood (i.e., over 5 mcg/dL) should have confirmation with a whole blood venous sample. In patients with a confirmed elevated whole blood venous lead, additional screening labs aimed at assessing the iron status and anemia are necessary, and an abdominal X-ray should be a consideration if the patient may have ingested a lead-containing foreign body (such as paint chips, a bullet, or a fishing weight, for example). As with all patients in whom the toxin-mediated disease is suspected, the evaluation should include a thorough history and physical exam. In the case of lead exposure, in particular, a detailed exposure history should be sought, with specific attention paid to occupation and hobbies (of the patient, in the case of an adult, or parents/caregivers, in the case of a child), home environment (for example, the age of the home, any recent renovations or repairs) and food and water sources.[4][23]

Treatment / Management

The most aspect of management in a patient with an elevated blood lead concentration is identifying the source of lead and removing it from the patient’s environment. Many county and state health departments employ individuals who can assess the home environments of children found to have elevated blood lead concentrations and assist in identifying the likely source. Patients with ingested foreign bodies should be monitored for the passage of the foreign body and should receive laxatives or cathartics if required to assist the object in passing, and those who have had massive ingestions may warrant whole bowel irrigation. Surgery should be a consideration for those with retained lead bullets. Additionally, optimizing the patient’s nutritional status is paramount, with particular attention to ensuring adequate iron, calcium, and zinc intake. Those who are found to have decreased iron stores should also begin iron therapy to replete their stores.[4][23]

Children with a blood lead concentration higher than 45mcg/dL, adults with a blood lead concentration of over 70 to 100 mcg/dL, or any patient with lead encephalopathy (which is usually accompanied by a markedly elevated blood lead concentration) should undergo chelation therapy under the direction of a medical toxicologist.[4][23] A variety of chelating agents alone or in combination can be used depending on the severity of clinical presentation and the patient’s blood lead concentration, including succimer, calcium disodium ethylenediaminetetraacetic acid (EDTA), and British anti-Lewisite (BAL, also known as dimercaprol). It is critical to understand that chelators are slow and inefficient in their ability to reduce the total body burden of lead and in some situations can potentially be harmful because they can mobilize lead from the relatively stable bone compartment to the relatively labile soft tissue compartment, where more acute toxicity occurs.[24] As such, aggressive supportive care for severely symptomatic patients is paramount even during the administration of chelation therapy.

Differential Diagnosis

As discussed in previous sections, the vast majority of individuals with elevated blood lead concentrations will have no clinical manifestations of plumbism. Those with mild symptoms often get misdiagnosed because their symptoms are so nonspecific. As such, lead toxicity should merit consideration in the differential of children presenting with behavioral problems (the so-called “difficult child”) as well as those presenting with nonspecific GI complaints such as constipation, abdominal pain, or picky eating. Realistically, these types of complaints are so common in toddlerhood that relatively few are likely secondary to lead, but blood testing for lead is so simple that it should not be overlooked, particularly because these symptoms can be the harbinger of much more severe toxicity if the child continues to be exposed to lead. Similarly, many children with anemia secondary to lead toxicity are also at risk for iron deficiency anemia, and lead’s role in precipitating anemia may easily be overlooked. Adults with peripheral neuropathy may present with symptoms mimicking carpal tunnel syndrome, and the underlying etiology in those with saturnine gout may not be appreciated, especially if the patient is an older male with a high purine diet (the prototypical patient who develops gout unrelated to lead toxicity). Patients with severe plumbism and especially those with lead encephalopathy may clinically look like patients with infectious or autoimmune encephalitis; again, though these cases are rare, blood lead testing is so ubiquitously available that it should not be overlooked.


Despite the importance of minimizing ongoing lead exposure for patients who have elevated blood lead concentrations but are asymptomatic, evidence that mitigating ongoing exposure will reverse or improve the damage that was done, especially in terms of subtle neurocognitive changes in children, is lacking.[25] Patients with mild to moderate symptoms may experience improvement or resolution of some symptoms, such as abdominal complaints and malaise, while others, such as growth parameters in children, fail to improve.[26][27] The mortality rate associated with acute lead encephalopathy before the advent of chelation therapy was approximately 65%, which dropped to under 5% with the advent of combination therapy with BAL and calcium disodium EDTA.[28][29] However, the advent of chelation therapy also coincided with dramatic improvements in critical care, such that it is not clear that chelation alone accounts for this improvement in survival. Even in the post-chelation era, many patients who are treated for acute lead encephalopathy and survive will have permanent neurologic sequelae such as intellectual disability, hemiparesis, and seizure disorders.[29]


The most widespread complication related to elevated blood lead concentrations aside from the collective loss of IQ points is the burden of cardiovascular morbidity and mortality linked to hypertension associated with lead exposure.[30] Patients with mild symptoms may experience subtle complications that can go unnoticed, such as secondary nutritional deficiencies attributable to poor intake because of chronic or recurrent abdominal pain. As patients become more symptomatic, there is an increasing number and severity of potential complications. Patients requiring ICU-level care because of acute lead encephalopathy and possibly increased ICP are at risk of developing the same complications that plague critically ill patients in general, such as line-associated infections and ICU delirium. Complications related to chelation therapy itself include the possibility of inducing a trace mineral deficiency by chelating metals other than lead and the possibility of mobilizing lead from the relatively stable bone compartment to the relatively labile soft tissue compartment as described above. Chelator-specific adverse effects and complications include GI upset (succimer and BAL), nephrotoxicity (potentially secondary to calcium disodium EDTA), and fever, hypertension, and tachycardia (BAL), among others.[24]

Enhancing Healthcare Team Outcomes

Caring for patients with an elevated blood lead concentration requires the cooperation of a large number of interprofessional individuals. Even in the simplest case of an asymptomatic patient with an elevated blood lead level, identifying and mitigating the source of lead may require the participation of the patient, family, primary care physician, nurse practitioner, teachers or daycare providers (in the case of a child), the employer in the case of an adult, state or local health department officials, industrial hygienists, and abatement professionals.

It is extremely important for children with evidence of possible neurocognitive or behavioral changes to undergo formal assessments to see if they qualify for services such as speech therapy, occupational therapy or behavioral therapy and additionally, in the case of a school-age child, if they qualify for an individualized education plan (IEP) or a 504 plan.

In these cases, other ancillary professionals such as nurses and therapists might come into the patient’s care. Many patients would also benefit from formal nutritional assessments and counseling by a nutritionist or dietician. If patients are overtly symptomatic or may require chelation therapy, consultation with a medical or clinical toxicologist a strong recommendation, and patients with severe toxicity will likely require ICU level care under the direction of a pediatric or adult intensivist.

The social worker and the public health nurse should be involved when a child is diagnosed with lead toxicity. It is vital to assess the home environment and determine how the lead toxicity occurred. The biggest morbidity of lead toxicity is moderate to severe deficits in learning, cognition, and behavior, which are not reversible. Thus, open communication between the interprofessional team members is vital to ensure that patients with lead toxicity not only receive optimal care but that they are no longer at risk for additional lead exposure.



Laurie Halmo


Thomas M. Nappe


7/4/2023 12:17:45 AM



Needleman HL. The persistent threat of lead: medical and sociological issues. Current problems in pediatrics. 1988 Dec:18(12):697-744     [PubMed PMID: 3063440]


Eisinger J. Lead and wine. Eberhard Gockel and the colica Pictonum. Medical history. 1982 Jul:26(3):279-302     [PubMed PMID: 6750289]


Mitra P, Sharma S, Purohit P, Sharma P. Clinical and molecular aspects of lead toxicity: An update. Critical reviews in clinical laboratory sciences. 2017 Nov-Dec:54(7-8):506-528. doi: 10.1080/10408363.2017.1408562. Epub 2017 Dec 7     [PubMed PMID: 29214886]


COUNCIL ON ENVIRONMENTAL HEALTH. Prevention of Childhood Lead Toxicity. Pediatrics. 2016 Jul:138(1):. pii: e20161493. doi: 10.1542/peds.2016-1493. Epub 2016 Jun 20     [PubMed PMID: 27325637]


Whitehead LS, Buchanan SD. Childhood Lead Poisoning: A Perpetual Environmental Justice Issue? Journal of public health management and practice : JPHMP. 2019 Jan/Feb:25 Suppl 1, Lead Poisoning Prevention():S115-S120. doi: 10.1097/PHH.0000000000000891. Epub     [PubMed PMID: 30507780]


Egan KB, Tsai RJ, Chuke SO. Integrating Childhood and Adult Blood Lead Surveillance to Improve Identification and Intervention Efforts. Journal of public health management and practice : JPHMP. 2019 Jan/Feb:25 Suppl 1, Lead Poisoning Prevention(Suppl 1 LEAD POISONING PREVENTION):S98-S104. doi: 10.1097/PHH.0000000000000872. Epub     [PubMed PMID: 30507777]


Quail MT. Retained bullet or bullet fragments: A potential source of elevated blood lead levels. Nursing. 2018 Oct:48(10):15. doi: 10.1097/01.NURSE.0000545014.98790.6e. Epub     [PubMed PMID: 30256286]


Raymond J, Brown MJ. Childhood Blood Lead Levels in Children Aged {5 Years - United States, 2009-2014. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002). 2017 Jan 20:66(3):1-10. doi: 10.15585/mmwr.ss6603a1. Epub 2017 Jan 20     [PubMed PMID: 28103215]


Alarcon WA, State Adult Blood Lead Epidemiology and Surveillance (ABLES) Program Investigators. Elevated Blood Lead Levels Among Employed Adults - United States, 1994-2013. MMWR. Morbidity and mortality weekly report. 2016 Oct 14:63(55):59-65. doi: 10.15585/mmwr.mm6355a5. Epub 2016 Oct 14     [PubMed PMID: 27736830]


Lidsky TI, Schneider JS. Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain : a journal of neurology. 2003 Jan:126(Pt 1):5-19     [PubMed PMID: 12477693]


de Souza A, Narvencar KP, Desai PK, D'Costa Z, Nilajkar G. Adult lead encephalopathy. Neurological research. 2013 Jan:35(1):54-8. doi: 10.1179/1743132812Y.0000000115. Epub     [PubMed PMID: 23317799]


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. The Journal of clinical investigation. 1976 Oct:58(4):926-32     [PubMed PMID: 965496]


Nolan CV, Shaikh ZA. Lead nephrotoxicity and associated disorders: biochemical mechanisms. Toxicology. 1992:73(2):127-46     [PubMed PMID: 1319092]


Mahaffey KR. Quantities of lead producing health effects in humans: sources and bioavailability. Environmental health perspectives. 1977 Aug:19():285-95     [PubMed PMID: 908307]

Level 3 (low-level) evidence


Wang H, Shi H, Chang L, Zhang X, Li J, Yang Y, Jiang Y. Association of blood lead with calcium, iron, zinc and hemoglobin in children aged 0-7 years: a large population-based study. Biological trace element research. 2012 Nov:149(2):143-7. doi: 10.1007/s12011-012-9413-x. Epub 2012 Apr 18     [PubMed PMID: 22528781]


Reddy YS, Y A, Ramalaksmi BA, Kumar BD. Lead and trace element levels in placenta, maternal and cord blood: a cross-sectional pilot study. The journal of obstetrics and gynaecology research. 2014 Dec:40(12):2184-90. doi: 10.1111/jog.12469. Epub 2014 Aug 11     [PubMed PMID: 25132559]

Level 2 (mid-level) evidence


Hoppin JA, Aro A, Hu H, Ryan PB. In vivo bone lead measurement in suburban teenagers. Pediatrics. 1997 Sep:100(3 Pt 1):365-70     [PubMed PMID: 9282707]


Ziegler EE, Edwards BB, Jensen RL, Mahaffey KR, Fomon SJ. Absorption and retention of lead by infants. Pediatric research. 1978 Jan:12(1):29-34     [PubMed PMID: 643372]


Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, Canfield RL, Dietrich KN, Bornschein R, Greene T, Rothenberg SJ, Needleman HL, Schnaas L, Wasserman G, Graziano J, Roberts R. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environmental health perspectives. 2005 Jul:113(7):894-9     [PubMed PMID: 16002379]

Level 3 (low-level) evidence


Zhang N, Baker HW, Tufts M, Raymond RE, Salihu H, Elliott MR. Early childhood lead exposure and academic achievement: evidence from Detroit public schools, 2008-2010. American journal of public health. 2013 Mar:103(3):e72-7. doi: 10.2105/AJPH.2012.301164. Epub 2013 Jan 17     [PubMed PMID: 23327265]


Needleman H. Lead poisoning. Annual review of medicine. 2004:55():209-22     [PubMed PMID: 14746518]


Wengrovitz AM, Brown MJ, Advisory Committee on Childhood Lead Poisoning, Division of Environmental and Emergency Health Services, National Center for Environmental Health, Centers for Disease Control and Prevention. Recommendations for blood lead screening of Medicaid-eligible children aged 1-5 years: an updated approach to targeting a group at high risk. MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports. 2009 Aug 7:58(RR-9):1-11     [PubMed PMID: 19661858]


Kosnett MJ, Wedeen RP, Rothenberg SJ, Hipkins KL, Materna BL, Schwartz BS, Hu H, Woolf A. Recommendations for medical management of adult lead exposure. Environmental health perspectives. 2007 Mar:115(3):463-71     [PubMed PMID: 17431500]

Level 3 (low-level) evidence


Kim HC, Jang TW, Chae HJ, Choi WJ, Ha MN, Ye BJ, Kim BG, Jeon MJ, Kim SY, Hong YS. Evaluation and management of lead exposure. Annals of occupational and environmental medicine. 2015:27():30. doi: 10.1186/s40557-015-0085-9. Epub 2015 Dec 15     [PubMed PMID: 26677413]


Dietrich KN, Ware JH, Salganik M, Radcliffe J, Rogan WJ, Rhoads GG, Fay ME, Davoli CT, Denckla MB, Bornschein RL, Schwarz D, Dockery DW, Adubato S, Jones RL, Treatment of Lead-Exposed Children Clinical Trial Group. Effect of chelation therapy on the neuropsychological and behavioral development of lead-exposed children after school entry. Pediatrics. 2004 Jul:114(1):19-26     [PubMed PMID: 15231903]


Rae CE, Bell CN Jr, Elliott CE, Shannon M. Ten cases of acute lead intoxication among bridge workers in Louisiana. DICP : the annals of pharmacotherapy. 1991 Sep:25(9):932-7     [PubMed PMID: 1949969]

Level 3 (low-level) evidence


Peterson KE, Salganik M, Campbell C, Rhoads GG, Rubin J, Berger O, Ware JH, Rogan W. Effect of succimer on growth of preschool children with moderate blood lead levels. Environmental health perspectives. 2004 Feb:112(2):233-7     [PubMed PMID: 14754579]

Level 3 (low-level) evidence


ENNIS JM, HARRISON HE. Treatment of lead encephalopathy with PAL (2.3-dimercaptopropanol). Pediatrics. 1950 May:5(5):853-68     [PubMed PMID: 15417286]


Coffin R,Phillips JL,Staples WI,Spector S, Treatment of lead encephalopathy in children. The Journal of pediatrics. 1966 Aug;     [PubMed PMID: 4957770]


Navas-Acien A, Guallar E, Silbergeld EK, Rothenberg SJ. Lead exposure and cardiovascular disease--a systematic review. Environmental health perspectives. 2007 Mar:115(3):472-82     [PubMed PMID: 17431501]

Level 3 (low-level) evidence