eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Toxicology

Toxicity, Lead

Author: Mohamed K Badawy, MB, BCh, MD, Assistant Professor, Departments of Emergency Medicine and Pediatrics, University of Rochester and Golisano Children's Hospital at Strong Memorial Hospital
Coauthor(s): Gregory P Conners, MD, MPH, MBA, Interim Chair of Emergency Medicine, Professor of Emergency Medicine and Pediatrics, Departments of Emergency Medicine and Pediatrics, University of Rochester School of Medicine and Dentistry
Contributor Information and Disclosures

Updated: Nov 12, 2008

Introduction

Background

Childhood lead poisoning is a worldwide problem. Although recent data continue to demonstrate a decline in the prevalence of elevated blood lead levels (BLL) in children in the industrialized world, lead remains a common, preventable, environmental health threat.

Lead is a ubiquitous and versatile metal. It has been extensively used since ancient times, and the history of public exposure to lead in food and drink is extensive. Lead poisoning was common in Roman times because of the use of lead in water pipes and in wine containers. Lead poisoning became common among industrial workers in the 19th and 20th centuries, when workers were exposed to lead in smelting, painting, plumbing, printing, and many other industrial activities. Following the advent of motor vehicles at the beginning of the 20th century and the introduction of leaded gasoline, environmental lead contamination substantially increased.

In 1904, Gibson concluded that lead paint in the home was responsible for poisoning children. Despite this, lead was not banned from American household paints until 1978. Other common sources of lead exposure include batteries, putty, cement, imported canned food, cosmetics, jewelry, leaded glass artwork, farm equipment, and illicit intravenous drugs.

Children are more susceptible than adults to the adverse effects of lead exposure.1 Toddlers often place objects in their mouths, resulting in ingestion of dust and soil and, possibly, an increased intake of lead. The physiological uptake rates of lead in children are higher than those in adults. In addition, children are rapidly growing, and their systems are not fully developed, which renders them more susceptible to the effects of lead.

Lead poisoning in children has been the focus of many researchers. The American Academy of Pediatrics (APP) currently defines lead poisoning as a venous BLL equal to or higher than 10 μ g/dL (0.50 µmol/L).2,3 This level, which was originally intended to trigger community-wide prevention strategies, has often been misinterpreted as a definitive toxicologic threshold. Studies have indicated intellectual impairment in children with BLLs of less than 10 µg/dL.4 However, the lack of a specific BLL cutoff for adverse effects, the rather small sample size of these studies, and the absence of effective clinical or public health interventions that reliably and consistently lower BLLs that are already less than 10 µg/dL have made the Centers for Disease Control's (CDC's) Advisory Committee on Childhood Lead Poisoning Prevention keep the current level of concern at BLLs equal to or higher than10µg/dl.5,6

Pathophysiology

Lead toxicity may be caused by inorganic or organic lead. Most cases of lead poisoning are caused by inorganic lead. Lead may enter the body through ingestion, inhalation, or transdermal absorption. Ingestion is the most common source of lead poisoning in children because of their normal hand-to-mouth activities. Inorganic lead absorption occurs via the mechanisms involved in absorption of essential elements, such as calcium and iron, and depends on the following factors:

  • Solubility: Lead salts are more soluble in acidic media.
  • Particle size: Large particles (eg, paint chips) are poorly absorbed, whereas fine dust particles licked from the fingers or other objects may contribute to an increased lead load.
  • Nutritional deficiencies: Iron, calcium, zinc, copper, and protein deficiencies result in greater lead absorption.
  • Dietary fats and oils: Excess intake results in increased lead absorption.
  • Other dietary components (eg, phytates found in leafy green vegetables) bind lead particles and increase their elimination.

Transcutaneous absorption of inorganic lead is minimal. However, organic lead, such as tetraethyl lead found in leaded gasoline, may enter through the skin. Tetraethyl lead, the main organic compound in leaded gasoline, is converted in the body to triethyl lead and inorganic lead.

Inhalation adds little lead burden to the body in children. Lead particles are frequently large and coughed up. However, because children do not expectorate well, these particles are likely to travel up the mucociliary system and be swallowed, allowing for some absorption. Lead toxicity may also develop in adolescents who sniff leaded gasoline recreationally.

Absorbed lead is attracted to sulfur, nitrogen, and oxides. Its toxicity is elicited by inhibiting sulfhydryl-dependent enzymes. Most of the lead is sequestered in the bone, and the rest is distributed in the blood and soft tissues. Lead interferes with hematopoiesis at several steps. This results in less heme synthesis and the accumulation of toxic products (eg, aminolevulinic acid, protoporphyrin). The half-life of lead in the soft tissues and blood is approximately 30-70 days. Conversely, lead deposits in the bones for several years. Lead is primarily excreted by glomerular filtration.

Frequency

United States

According to the National Health and Nutrition Examination Survey (NHANES), from 1999-2002, the overall prevalence of elevated BLLs for the US population aged 1 year or older was 0.7%, a decrease of 68% from 2.2% in the 1991-1994 survey. In addition, the prevalence of elevated BLLs in children aged 1-5 years of age, who had the highest prevalence, was 1.6%, a decrease of 64% from 4.4% in the 1991-1994 survey. Children in minority populations, from low-income families, and who live in older homes are particularly at risk.

International

Lead continues to be a significant public health problem in developing countries. In general, children with heavy exposure to automobile exhaust, lead-based paint, or home-industry manufacture of batteries, ceramics, or painted artifacts have high lead burdens. Children living in rural areas who are not engaged in manufacturing pursuits do not usually have high lead burdens.

Mortality/Morbidity

Presently, death from lead encephalopathy is rarely encountered because of the aggressive approach to using chelating agents. However, complications may arise from the chelated lead complex. Therefore, careful monitoring of mental status, cardiovascular function, and renal and hepatic functions are essential parts of the ongoing evaluation.

Race

Overall, from 1999-2002, non-Hispanic blacks and Mexican Americans had higher percentages of elevated BLLs (1.4% and 1.5%, respectively) than non-Hispanic whites (0.5%).

Age

Lead poisoning chiefly affects children younger than 6 years and adults in lead-risk occupations.

Clinical

History

The clinical picture associated with lead poisoning is vague. Symptoms are not specific enough to alarm the physician about lead toxicity. Most cases are currently identified through effective screening of the population at risk. However, patients with lead poisoning frequently have constipation, abdominal pain, and/or anorexia.

  • GI symptoms
    • Anorexia
    • Vomiting
    • Constipation
    • Abdominal pain
  • Neurobehavioral changes
    • Inattentiveness
    • Distractibility
    • Impulsiveness
    • Learning problems
  • Peripheral nervous system effects (rare in children)
    • Weakness
    • Peripheral palsies

Physical

No specific physical signs for lead poisoning are recognized.

  • Pallor (due to associated anemia)
  • Hyperactivity
  • Signs of increased intracranial pressure
    • Impaired consciousness
    • Bradycardia
    • Hypertension
    • Respiratory depression
    • Papilledema
    • Coma

Causes

Children are more susceptible than adults to the adverse effects of lead exposure. Toddlers often place objects in their mouths, resulting in dust and soil being ingested and, possibly, an increased intake of lead. Physiological uptake rates of lead in children are higher than those in adults. In addition, children are rapidly growing, and their systems are not fully developed, rendering them more susceptible to the effects of lead.

  • Several environmental factors expose children to lead hazards, among which are dust, soil, paint chips, folk remedies, and the use of old ceramic cookware.
  • Several parental occupations place children at risk, including lead mining, glass making, printing, and welding. Workers should be instructed to change their working clothes at work.
  • Inadequate nutrition, such as a diet deficient in iron, may promote lead absorption.

More on Toxicity, Lead

Overview: Toxicity, Lead
Differential Diagnoses & Workup: Toxicity, Lead
Treatment & Medication: Toxicity, Lead
Follow-up: Toxicity, Lead
References

References

  1. 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. Nov 6 2008;[Medline].

  2. American Academy of Pediatrics Committee on Environmental Health. Lead exposure in children: prevention, detection, and management. Pediatrics. Oct 2005;116(4):1036-46. [Medline][Full Text].

  3. 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.

  4. 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. Apr 17 2003;348(16):1517-26. [Medline].

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

  6. 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].

  7. Rogan WJ, Dietrich KN, Ware JH, et al. The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead. N Engl J Med. May 10 2001;344(19):1421-6. [Medline].

  8. Lanphear BP, Winter NL, Apetz L, Eberly S, Weitzman M. A randomized trial of the effect of dust control on children's blood lead levels. Pediatrics. Jul 1996;98(1):35-40. [Medline].

  9. Florin TA, Brent RL, Weitzman M. The need for vigilance: the persistence of lead poisoning in children. Pediatrics. Jun 2005;115(6):1767-8. [Medline].

  10. Graeme KA, Pollack CV. Heavy metal toxicity, part II: lead and metal fume fever. J Emerg Med. Mar-Apr 1998;16, No.2:171-177. [Medline].

  11. Koller K, Brown T, Spurgeon A, Levy L. Recent developments in low-level lead exposure and intellectual impairment in children. Environ Health Perspect. Jun 2004;112(9):987-94. [Medline].

  12. Lanphear BP, Hornung R, Ho M. Screening housing to prevent lead toxicity in children. Public Health Rep. May-Jun 2005;120(3):305-10. [Medline].

  13. Markowitz M. Lead poisoning. Pediatr Rev. Oct 2000;21(10):327-35. [Medline].

  14. Moss ME, Lanphear BP, Auinger P. Association of dental caries and blood lead levels. JAMA. Jun 23-30 1999;281(24):2294-8. [Medline].

  15. Schaffer SJ, Campbell JR. The new CDC and AAP lead poisoning prevention recommendations: consensus versus controversy. Pediatr Ann. Nov 1994;23(11):592-9. [Medline].

  16. Tong S, von Schirnding YE, Prapamontol T. Environmental lead exposure: a public health problem of global dimensions. Bull World Health Organ. 2000;78(9):1068-77. [Medline].

Further Reading

Keywords

lead toxicity, plumbism, blood lead level, BLL, lead poisoning, lead-based paint, paint chips, lead encephalopathy, anorexia, vomiting, constipation, abdominal pain, hyperactivity, respiratory depression, hypertension

Contributor Information and Disclosures

Author

Mohamed K Badawy, MB, BCh, MD, Assistant Professor, Departments of Emergency Medicine and Pediatrics, University of Rochester and Golisano Children's Hospital at Strong Memorial Hospital
Mohamed K Badawy, MB, BCh, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Gregory P Conners, MD, MPH, MBA, Interim Chair of Emergency Medicine, Professor of Emergency Medicine and Pediatrics, Departments of Emergency Medicine and Pediatrics, University of Rochester School of Medicine and Dentistry
Gregory P Conners, MD, MPH, MBA is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

William T Zempsky, MD, Associate Director, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
William T Zempsky, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
Jeffrey R Tucker, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, and Massachusetts Medical Society
Disclosure: Merck Salary Employment

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
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