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Lead Toxicity

  • Author: Pranay Kathuria, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
Updated: Feb 08, 2016


For centuries, lead toxicity has been one of the most significant preventable causes of neurologic morbidity from an environmental toxin. A heavy metal, lead is ubiquitous in our environment but has no physiologic role in biological systems. Lead toxicity is a particularly insidious hazard with the potential of causing irreversible health effects. It interferes with a number of body functions primarily affecting the central nervous, hematopoietic, hepatic and renal system producing serious disorders.  Acute toxicity is related to occupational exposure and is quite uncommon. Chronic toxicity on the other hand is much more common. Research on the effects of lead on adults has prompted the suggestion that acceptable levels of lead in adults be dropped almost to those of children.[2]

The ongoing emphasis on abatement of lead environments places added emphasis on occupational exposure to lead (eg, among workers at smelters or battery recycling plants).[3] Such exposure is a continuing problem. Whereas occupational exposure remains an occasional concern, the greatest public health issue related to lead at present is exposure of young children to decaying fragments of leaded paint.

Pediatric lead poisoning

Compared with adult lead poisoning, pediatric lead poisoning is a somewhat newer problem. First reported in the late 1800s in Australia, interest in childhood lead poisoning and its manifold clinical presentations has burgeoned.

Lead poisoning is probably the most important chronic environmental illness affecting modern children. Despite efforts to control it and despite apparent success in decreasing incidence, serious cases of lead poisoning still appear in hospital emergency departments (EDs), clinics, and private physicians’ offices.

In children, virtually no organ system is immune to the effects of lead poisoning. Perhaps the organ of most concern is the developing brain. Any disorganizing influence that affects an individual at a critical time in development is likely to have long-lasting effects. Such is the effect of lead on the developing brain. Effects on the brain appear to continue into the teenaged years and beyond. A high index of suspicion is necessary for physicians treating pediatric patients.

The literature suggests that significant insult to the brain of children occurs at very low levels and that medical intervention with chelation fails to reverse such effects.[4, 5, 6, 7, 8]



The major mechanism of lead toxicity is due to increased generation of reactive oxygen species (ROS) and interference with generation of antioxidants. Lead causes the generation of ROS like hydroperoxide, hydrogen peroxide, and singlet oxygen. ROS are stabilized by glutathione in the body.  Ninety percent of glutathione in the cell exists in reduced form and 10% in oxidative form, and it typically acts as an antioxidant defense mechanism. Glutathione stabilizes ROS, and after being converted (oxidizing) to glutathione disulfide, it is reduced back to GSH by glutathione reductase. Lead inactivates glutathione by binding to GSH’s sulfhydryl group, which causes GSH replenishment to become inefficient, thereby increasing oxidative stress. Lead also interferes with the activity of other antioxidant enzymes including superoxide dismutase and catalase. The increase in oxidative stress leads to cell membrane damage due to lipid peroxidation. Lead blocks the activity of 5-aminolevulinic acid dehydratase and leads to hemoglobin oxidation, which along with the lipid peroxidation can result in red cell hemolysis.[42]

Lead entering the intravascular space binds quickly to red blood cells. Lead has a half-life of approximately 30 days in the blood, from where it diffuses into the soft tissues, including the kidneys, brain, liver, and bone marrow.

Lead then diffuses into bone and is stored there for a period that corresponds to a half-life of several decades. Increased bone turnover with pregnancy, menopause, lactation, or immobilization can increase blood lead levels. Estimations of blood lead levels are more useful for diagnosing acute lead poisoning, whereas the extent of past lead exposure can be estimated by determining the body burden of lead on the basis of results from the edetate (EDTA) calcium disodium (CaNa2 EDTA) lead mobilization test.

Lead is primarily excreted in urine and bile, but the elimination rate varies, depending on the tissue that absorbed the lead. The kidney excretes lead by means of glomerular filtration and tubular secretion. Lead has bidirectional transport across the tubular epithelium. The clearance of lead ranges from 1 to 3 mL/min and is relatively independent of kidney function.

The effects of lead poisoning on the brain are manifold and include delayed or reversed development, permanent learning disabilities, seizures, coma, and even death. The long-term effect of lead exposure is maximal during the first 2 or 3 years of life, when the developing brain is in a critical formative stage.




The most significant lead exposure in adults usually occurs at the workplace, whereas for children, other forms of environmental exposure are more important. Although lead toxicity can occur after a single event, it is usually a result of chronic exposure.

Workplace exposure

Sites and occupations associated with lead exposure include pipe cutting, lead mining and ore crushing, lead and copper smelting, welding operations, construction, the rubber industry, the plastic industry, radiator repair, battery manufacturing, soldering of lead products, the printing industry, glass manufacture, organic lead production, solid waste combustion, frit manufacture, and paint and pigment manufacture. Persons employed in these occupations may also expose family members to lead by transporting lead dust from the workplace to their homes.

Other environmental exposure

Exposure from lead-based paint was significant among children in the past. Although lead was banned from use in residential paint, it continues to be used in nonresidential settings, and as a result of its past use, lead paint can still be found in many older homes.

Leaded gasoline contaminates the atmosphere. Although lead has been removed from gasoline in Western countries, leaded gasoline continues to be used in the developing world. Huffing of leaded gasoline (ie, deeply inhaling fumes to achieve a “high”) could also cause poisoning.

Food has been an important source of lead exposure. Surface contamination of homegrown vegetables, storage cans with lead solder seams (banned in 1991), and kitchenware are sources of lead contamination in food. Strong animal evidence suggests that malnutrition is highly significantly associated with increased levels of blood lead.[9]

Water remains an important source of lead poisoning because lead from the atmosphere contaminates bodies of water.[10] The nature of plumbing also may be important in this regard. Although use of lead pipes (largely replaced by copper or polyvinyl pipes) has declined considerably since the 1950s, old public water systems continue to have networks that include lead piping. Because the use of lead-based soldering of copper pipes was permitted until 1986, homes with copper plumbing may have substantial lead in the water. In May 2015, at least 28 children under the age of five have been killed by drinking stream water contaminated with lead in Nigeria's Niger state.[11]

Some hobbies are associated with exposures to lead. These hobbies may include making bullets, making fishing-weights, soldering, indoor firearm shooting, and remodeling older homes.

Soil contaminated with lead, such as may be found surrounding lead smelters and in homes from deterioration of exterior surfaces, can be an important source of lead exposure.

Moonshine ethanol (ie, illegally distilled corn whiskey) made in lead-containing vessels, such as discarded automobile radiators, has been associated with lead poisoning and even local epidemics.[12]

Topical agents that contain lead, such as kohl and surma, may be ingested accidentally.

Several reports exist of lead poisoning that develops as the result of absorption of lead from retained bullet or shrapnel fragments. Bullets located in areas bathed by fluids are more likely to dissolve, while those embedded in soft tissues are likely to be walled off by inflammation.

An incidental finding of bullet or shrapnel fragments on an x-ray should prompt consideration of possible elevated lead levels, though most of these cases occur only with intra-articular fragments. Of particular concern is a retained bullet in the spine, an area where removal is often considered too dangerous to attempt.[13]

Familial factors

Frequently, 1 or 2 children in a family develop more lead poisoning than other siblings. This observation may be related to age, activity, or genetics. Identical twins seem to have concordant lead levels and biologic evidence of lead’s effects, but this is less likely to be the case with fraternal twins.

For further information on etiology, see Pathophysiology and Etiology of Lead Toxicity.



United States statistics

Lead poisoning is said to be the most common environmental illness of children in the United States. The incidence varies with age, socioeconomic status, the population of a given community, race, and the age of the home.

Although no blood level of lead is considered safe, the Centers for Disease Control and Prevention (CDC) has established 10 µg/dL as the level of concern. Approximately 9% of children aged 1-5 years have blood levels higher than 10 µg/dL. Because low socioeconomic status is also a risk factor for lead exposure, children in inner cities are at highest risk. In some rural areas of the United States, 20% of children have been reported to have levels higher than 10 µg/dL.[14]

Lead poisoning occurs in every group, and only the frequency varies; it is not just a disease of black inner-city children. According to the 1997 National Health and Nutrition Examination Survey (NHANES), 16.4% of children living in cities with more than 1 million people and in homes built before 1946 have elevated lead levels.

Of interest is the remarkable decrease in the prevalence of elevated lead levels in children in the 1999-2004 time frame as compared with the 1988-1991 time frame. According to the NHANES data, the prevalence of children with lead levels over 10 µg/dL was 8.4% in 1988-1991 but only 1.4% in 1999-2004, representing an 84% decline.[15] levels continue to be highest among non-Hispanic black children, Mexican American, and non-Hispanic white children, with the greatest risk being in the non-Hispanic black population.

Generally, adults develop lead poisoning as the result of an occupational exposure or from exposure through a hobby. Several states cooperate in the SENSOR program, which monitors lead exposure in adults from occupational sources.

According to a report from the CDC’s Adult Blood Lead Epidemiology and Surveillance (ABLES) program, the incidence of BLLs of 25 µg/dL or higher in adults (persons aged 16 years or older) declined nationally from 14.0/100,000 in 1994 to 6.4/100,000 in 2011.[16] (Although BLLs lower than 40 µg/dL have been considered acceptable in adults, research data have raised concerns about the effects of low-level lead exposure.)

The highest numbers of workers exposed to lead with BLLs of 25 µg/dL or greater included employees in the storage battery manufacturing and lead and zinc ore mining industries, according to the ABLES report.[17]

International statistics

Lead poisoning has been reported in almost every country on earth. Blood lead levels are higher in developing countries because of continued use or later phaseout of leaded gasoline and paint. Occupational exposure in these countries is higher as well. In particular, the old “iron-curtain” countries had less strict guidelines for occupational and environmental exposures than other places in the world; thus, exposures there were common.

A Swedish study by Evans et al, which reported on 926 patients with incident severe CKD and 998 controls with a 7- to 9-year follow-up, suggested that low-level exposure to lead may not cause an increased risk of severe chronic kidney disease (CKD).[18] However, the authors cautioned that because only native Swedes were used in their study, the generalizability of the data may be limited; they also noted that whereas an expert rating method was used to assess lead exposure, BLLs were not measured to confirm the rating method’s validity.[18]

Age-related demographics

Young children who are independently mobile are at greatest neurologic risk from chronic exposure to low or moderate levels of lead. From the time children are able to crawl until they enter school, they are at risk of ingesting lead-containing dust. Although this sometimes is associated with pica and intentional ingestion of paint chips, lead poisoning often occurs without such behavior. Children may also be at risk for lead toxicity if folk remedies are used or if their parents, siblings, or caregivers are involved in lead-related occupations.

Children younger than 3 years are at the greatest risk for lead poisoning. This is because these children are most likely to put things containing lead into their mouths and because their brains are rapidly developing and are most vulnerable to any disorganizing influence. However, physicians and other health care professionals must be aware that lead poisoning can occur in children of any age.

Adults are now believed to be affected at a lower level of exposure than was once assumed. This has sparked renewed interest in occupational exposure to lead and its consequences. Careful attention must be paid to the occupations of adults who present with uncommon peculiar symptoms and signs.

Sex-related demographics

Because of occupational exposures, men have higher lead levels than women. No sex difference in incidence is reported in children.

Racial differences in incidence

Although no compelling evidence exists that any particular race is biologically predisposed to lead toxicity, covariant conditions such as poor nutrition and lower socioeconomic status clearly are associated with chronic lead poisoning.

Certain populations, such as African American children and new immigrants living in homes with decaying lead-based paint in low-income urban centers, are at increased risk of lead poisoning. The NHANES III data have shown higher lead levels among non-Hispanic blacks and Mexican Americans. Whether this translates into a higher incidence of lead nephropathy among these persons is not known.

Overall, black non-Hispanic children appear to have the greatest risk of developing lead poisoning. The NHANES figures for 1997 reveal a prevalence rate of 21.9% among black non-Hispanic children living in homes built before 1946, a rate of 13.7% in those living in homes built in 1946-1973, and a rate of 3.4% in those living in homes built subsequent to 1973.

This compares to a prevalence of 13%, 2.3%, and 1.6% among Mexican-American children and 5.6%, 1.4%, and 1.5% among white non-Hispanic children living in homes built before 1946, living in homes built in 1946-1973, and living in homes built subsequent to 1973, respectively.

An analysis of trends in blood lead levels over the past 20 years shows that, although the overall geometric mean blood lead level in children has dropped dramatically, disparities still exist, causing increased risk to certain populations. The factors of living in older housing, poverty, age, and being non-Hispanic black places a child at risk for elevated blood lead levels.[15]



Essentially, 2 syndromes of lead poisoning exist, depending on exposure: one syndrome is associated with acute or subacute high-level lead exposure, and the other is associated with chronic low-level lead exposure.

With exposure to high levels of lead, patients develop lethargy, progressing to coma and seizures. Death is uncommon with appropriate medical management. Long-term sequelae depend on the duration, as well as the amount, of exposure. Acute lead nephropathy is usually completely reversible with chelation therapy. Deaths may result from the elevated intracranial pressure (ICP) associated with lead encephalopathy.

With chronic exposure to low or moderate levels of lead, subacute symptoms develop. Patients with chronic lead nephropathy may have a progressive decline in kidney function and eventually require renal replacement therapy.

Mortality related to lead toxicity is rare today. However, morbidity remains common. Because lead is an enzymatic poison, it perturbs multiple essential bodily functions, producing a wide array of symptoms and signs.

Adults generally do not develop central effects but may develop distal motor neuropathies. Some reports document an increase in depressive disorders, aggressive behavior, and other maladaptive affective disorders in adult patients with lead poisoning. Men with lead poisoning tend to have lower sperm counts and may experience frank impotence; women have an increase in miscarriages and smaller babies.

In the pediatric population, fatalities associated with lead encephalopathy were reported in the 1960s. Today, with aggressive management of ICP, these deaths are preventable. Occasional cases of acute lead encephalopathy still occur, and these often result in severe neurologic damage. Mounting evidence suggests that lead poisoning in childhood produces a long-term problem with learning, intelligence, and earning power. Asymptomatic lead poisoning has a far better prognosis.


Patient Education

In cooperation with local health departments, the physician should educate families about the following:

  • Causes and effects of lead poisoning
  • Relationship between blood lead level and anticipated medical or neuropsychological problems
  • Importance of follow-up or serial blood lead level determinations to monitor effects of treatment and environmental lead abatement
  • Identifying and eliminating possible sources of lead exposure
  • Increased lead absorption in patients with iron-deficiency anemia
  • Local resources about lead exposure and treatment

All patients must be educated in lead avoidance. The termination of exposure to lead is imperative. In particular, workers should be educated regarding the health risks of lead and sources that may cause poisoning.

A good, substantial diet is important; lead absorption is increased when a diet rich in fats is consumed. Also, diets low in iron, calcium, and vitamin C increase the likelihood of lead absorption and resultant lead poisoning. Dietary fiber helps promote good peristalsis and decreases the opportunity for lead absorption; thus, at least 15 g of dietary fiber is suggested for children each day.

Contributor Information and Disclosures

Pranay Kathuria, MD FACP, FASN, FNKF, Professor of Medicine, Director, Division of Nephrology and Hypertension, University of Oklahoma School of Community Medicine

Pranay Kathuria, MD 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

Disclosure: Nothing to disclose.


Adam 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

Adam 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

Disclosure: Nothing to disclose.

Rika Nagakuni O'Malley, MD Instructor, Department of Emergency Medicine, Thomas Jefferson University Hospital

Disclosure: Nothing to disclose.

Chief Editor

Tarakad 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

Tarakad 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

Disclosure: Nothing to disclose.


David A Griesemer, MD, Professor, Departments of Neuroscience and Pediatrics, Medical University of South Carolina

David 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

Disclosure: Nothing to disclose.

Christopher 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

Christopher 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

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J 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

Disclosure: Nothing to disclose.

Jonathan S Rutchik, MD, MPH Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco

Jonathan 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

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

  1. Fadrowski 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].

  2. Murata 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].

  3. Berg R. Lead in adults: the lesser concern rears its head. J Environ Health. 2009 Dec. 72(5):8-13. [Medline].

  4. Canfield 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].

  5. Bellinger 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].

  6. Chen 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].

  7. Hornung 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].

  8. Lanphear 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].

  9. Herman 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.

  10. Elevated Lead in D.C. Drinking Water - A Study of Potential Causative Events, Final Summary Report. EPA; August 2007:[Full Text].

  11. Onuah, F and Abrak, I. At Least 28 Children Killed by Lead Poisoning in Nigeria. Medscape Medical News. Available at May 18, 2015; Accessed: September 22, 2015.

  12. Holstege CP, Ferguson JD, Wolf CE, Baer AB, Poklis A. Analysis of moonshine for contaminants. J Toxicol Clin Toxicol. 2004. 42(5):597-601. [Medline].

  13. Cristante 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].

  14. Norman 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].

  15. Jones 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].

  16. CDC. US Department of Health and Human Services, National Institute for Occupational Safety and Health; 2013. Adult Blood Lead Epidemiology and Surveillance (ABLES). [Full Text].

  17. Guérin 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].

  18. Evans 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].

  19. Morgan BW, Todd KH, Moore B. Elevated blood lead levels in urban moonshine drinkers. Ann Emerg Med. 2001 Jan. 37(1):51-4. [Medline].

  20. Dietrich 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].

  21. Fluri 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].

  22. Lead exposure in children: prevention, detection, and management. Pediatrics. 2005 Oct. 116(4):1036-46. [Medline].

  23. American 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.:

  24. CDC. Preventing Lead Poisoning in Young Children. DC, United States Department of Health and Human Services:1991:[Full Text].

  25. CDC. 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].

  26. Treatment guidelines for lead exposure in children. American Academy of Pediatrics Committee on Drugs. Pediatrics. 1995 Jul. 96(1 Pt 1):155-60. [Medline].

  27. Carton 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].

  28. Dietrich 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].

  29. Atre 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].

  30. Rogan 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].

  31. Thurtle 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].

  32. Wedeen RP, Malik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med. 1979 Jan. 139(1):53-7. [Medline].

  33. 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 Jan 5. 130(1):7-13. [Medline].

  34. Lin 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].

  35. Lin 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].

  36. Mushak 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].

  37. Roberts 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].

  38. Rust 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].

  39. Rabinowitz MB. Toxicokinetics of bone lead. Environ Health Perspect. 1991 Feb. 91:33-7. [Medline]. [Full Text].

  40. Rabinowitz 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].

  41. Centers 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].

  42. Flora G, Gupta D, Tiwari A. Toxicity of lead: A review with recent updates. Interdiscip Toxicol. 2012 Jun. 5 (2):47-58. [Medline].

Peripheral smear taken from 8-year-old Pakistani girl who presented with acute hemolytic anemia and lead level of 125 µg/dL.
Growth arrest lines, also known as lead lines, in bones of child who recovered from lead poisoning.
Lead line on gingival border of adult with lead poisoning.
Wrist drop in adult with lead poisoning and renal failure.
Abdominal flat plate showing multiple radiopaque foreign bodies, including paint chips and earring.
Kidney 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.
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