Introduction
Background
Lead is a ubiquitous metal that has been used by humans for more than 3 millennia. Its toxic effects on humans are well documented in history. Early reports of toxicity in adult metal workers suggest that they suffered from 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 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 when treating their pediatric patients.
Recent 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.1
Occupational exposure to lead is a continuing problem. 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
Pathophysiology
Lead perturbs multiple enzyme systems. As in most heavy metals, any ligand with sulfhydryl groups is vulnerable. Perhaps the best-known effect is that on the production of heme. Lead interferes with the critical phases of the dehydration of aminolevulinic acid and the incorporation of iron into the protoporphyrin molecule; the result is a decrease in heme production. Because heme is essential for cellular oxidation, deficiencies have far-reaching effects.
The effects of lead poisoning on the brain are manifold and include delayed or reversed development, permanent learning disabilities, seizures, coma, and even death.
Lead is primarily excreted in urine and bile, but the elimination rate varies, depending on the tissue that absorbed the lead.
Frequency
United States
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.
Lead poisoning occurs in every group, 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 a 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 over the time frame 1988-1991 to 1999-2004. According to the NHANES data, the prevalence of children with lead levels over 10 mcg/dL decreased from 8.4% during the period 1988-1991 to 1.4% in 1999-2004, representing an 84% decline.3 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.
International
Lead poisoning has been reported in almost every country on earth. 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.
Mortality/Morbidity
Mortality is rare today. However, death during the 1960s from lead encephalopathy was not rare in urban centers.
- Morbidity is common. Because lead is an enzymatic poison, it perturbs multiple essential bodily functions, producing a wide array of symptoms and signs.
- Mounting evidence suggests that lead poisoning in childhood produces a long-term problem with learning, intelligence, and earning power.
- Adults with lead poisoning have increased incidences of depression, aggressive behavior, and antisocial behavior. Men with lead poisoning tend to have lower sperm counts; women have an increase in miscarriages and smaller babies.
Race
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.
- A recent 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.3
Age
- Children are at risk for lead toxicity if they live in homes with lead-based paint; 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.
- Physicians and other health care professionals must be aware that lead poisoning can occur in children of any age.
- Recently, the level at which adults are thought to be affected has been lowered. This has sparked renewed interest in the occupational exposure to lead and its consequences. Careful attention needs to be paid to the occupation of adults who present with uncommon peculiar symptoms and signs.
Clinical
History
No pathognomonic symptoms exist. Consider lead poisoning whenever a small child presents with peculiar symptoms that do not match any one particular disease entity. Many states now have mandatory lead screening programs for children to aid in fulfilling the public health goal of finding all lead-affected children.
- Irritability
- Sleeplessness or excess lethargy
- Poor appetite
- Headaches
- Abdominal pain with or without vomiting (but usually without diarrhea)
- Constipation
- Vague changes in a child's activity level may be observed.
- The presence of fever does not mitigate the diagnosis and consideration still must be made.
- Use of herbal folk remedies: Hispanic and Asian families occasionally use herbal folk remedies that may contain lead.
- Exposure to food and additives produced outside of the USA: Some spices or food coloring may also contain lead pigments. Some candies have been reported to be contaminated with lead.
- Evidence suggests that delayed weaning is associated with excessive pica and lead poisoning. It is commonly found that lead-poisoned children are bottle fed for protracted periods.
- Determine the approximate age of the home. Houses built after 1978 are unlikely to contain lead-pigmented paints.
- Lead contamination still may be present in plumbing fixtures, but the lead dose in plumbing fixtures is an order of magnitude less than that of paint.
- Homes built from 1920-1950 are more likely to contain lead pigment-based paint than newer homes.
- In cases of lead poisoning, query families about the condition of the home, the presence of peeling or cracking paint and plaster, the occupations or hobbies of the family members, and the presence of industry in the immediate vicinity.
- Adults present with minor nonspecific findings. Always ask patients not just the name of their job but also the duties the job entails. This may uncover an obvious cause of exposure.
- Adults with lead poisoning frequently have sleep disorders. They may be hypersomnolent or have difficulty falling asleep at the appropriate time.
- In adults, obtaining a careful occupational and hobby history is important. The history of ingestion of illicit liquor may be an important clue to the etiology of lead poisoning. According to a study performed in a large urban ED, of the patients reporting ingestion of "moonshine" sometime during the previous 5 years, 51% had elevated blood lead levels and 31% had levels in the very elevated range of 50 mcg/dL or higher.4
- More than 900 occupations have been associated with cases of lead poisoning.
- Additionally, numerous reports document lead poisoning resulting from retained bullet or shrapnel fragments; thus, history of military or other penetrating trauma may be important.
Physical
No distinctive physical findings of lead poisoning exist.
- A child with lead toxicity is frequently iron deficient and pale because of anemia.
- The child may be either hyperactive or lethargic.
- Lead lines appearing on gingival tissue are very unusual in children.
- The dentition of children does not promote poor enough hygiene to produce pyorrhea and the subsequent precipitation of lead sulfide.
- Adults with poor dental hygiene may demonstrate this characteristic finding in any heavy metal poisoning.
Lead line on the gingival border of an adult with lead poisoning.
- A report indicates that relative hypertension is related to elevated lead levels, but this finding has never been duplicated.
- Lead exposure can precipitate gout attack. Observe for the joint changes suggestive of acute arthritis.
- Assess for the evidence of peripheral neuropathy (footdrop, wristdrop), where motor nerves are predominantly affected (classic, but not very common presentation of occupational lead toxicity).
Wrist-drop in adult with lead poisoning and renal failure.
- Identify gun shot wounds (GSW) in patients with history of penetrating or military trauma
- Severe CNS toxicity: Evaluate for papilledema, cranial nerve abnormalities, and signs of increased intracranial pressure.
Causes
- The department of labor lists more than 900 occupations that are associated with lead use. These occupations include lead workers, welders, glassmakers, and scrap metal workers. Parents employed in any of these occupations may bring lead dust on their persons or clothing into the home.
- 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.
- Some cosmetics and folk remedies contain lead pigments or salts.
- Frequently, one or two 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 biological evidence of lead's effects, while this is less likely in fraternal twins.
- Several reports exist of lead poisoning that develops as the result of absorption of lead from retained bullet or shrapnel fragments. Incidental finding of such fragments on an x-ray should prompt consideration of possible elevated lead levels, though most of these cases occur only with intraarticular fragments.
- Several reports have documented cases of childhood lead poisoning resulting from the ingestion of lead-based foreign bodies. Lead dissolves reasonably quickly in acid solutions such as in the stomach; thus, significant amounts of lead may be absorbed. The full extent of the problem is unclear; however, exercise caution when treating a child who has ingested an object that contains a significant concentration of lead.
- Diet is a strong contributing factor in the pathogenesis of lead poisoning. Strong animal evidence suggests that malnutrition is highly significantly associated with increased levels of blood lead.5
More on Toxicity, Lead |
 Overview: Toxicity, Lead |
| Differential Diagnoses & Workup: Toxicity, Lead |
| Treatment & Medication: Toxicity, Lead |
| Follow-up: Toxicity, Lead |
| Multimedia: Toxicity, Lead |
| References |
| Next Page » |
References
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. Jul 2005;113(7):894-9. [Medline].
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].
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. Mar 2009;123(3):e376-85. [Medline].
Morgan BW, Todd KH, Moore B. Elevated blood lead levels in urban moonshine drinkers. Ann Emerg Med. Jan 2001;37(1):51-4. [Medline].
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.
[Guideline] Lead exposure in children: prevention, detection, and management. Pediatrics. Oct 2005;116(4):1036-46. [Medline]. [Full Text].
[Guideline] Interpreting and managing blood lead levels < 10 microg/dL in children and reducing childhood exposures to lead: recommendations of CDC's Advisory Committee on Childhood Lead Poisoning Prevention. MMWR Recomm Rep. Nov 2 2007;56:1-16. [Medline]. [Full Text].
[Guideline] Centers for Disease Control and Prevention (CDC). Preventing lead poisoning in young children. Aug 2005;[Full Text].
[Guideline] U.S. Preventive Services Task Force (USPSTF). Rockville (MD): Agency for Healthcare Research and Quality (AHRQ). Screening for elevated blood lead levels in children and pregnant women: recommendation statement. Dec 12 2006;[Full Text].
Chisolm JJ Jr. Evaluation of the potential role of chelation therapy in treatment of low to moderate lead exposures. Environ Health Perspect. Nov 1990;89:67-74. [Medline].
Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP, 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].
Cory-Slechta DA, Weiss B, Cox C. Mobilization and redistribution of lead over the course of calcium disodium ethylenediamine tetraacetate chelation therapy. J Pharmacol Exp ther. 1987;243:804-13. [Medline].
Seaton CL, Lasman J, Smith DR. The effects of CaNa(2)EDTA on brain lead mobilization in rodents determined using a stable lead isotope tracer. Toxicol Appl Pharmacol. Sep 15 1999;159(3):153-60. [Medline].
Sanchez-Fructuoso AI, Cano M, Arroyo M, Fernandez C, Prats D, Barrientos A. Lead mobilization during calcium disodium ethylenediaminetetraacetate chelation therapy in treatment of chronic lead poisoning. Am J Kidney Dis. Jul 2002;40(1):51-8. [Medline].
Chisolm JJ Jr. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatr. Jul 1968;73(1):1-38. [Medline].
Smith DR, Markowitz ME, Crick J, Rosen JF, Flegal AR. The effects of succimer on the absorption of lead in adults determined by using the stable isotope 204Pb. Environ Res. Oct 1994;67(1):39-53. [Medline].
Cremin JD Jr, Luck ML, Laughlin NK, Smith DR. Oral succimer decreases the gastrointestinal absorption of lead in juvenile monkeys. Environ Health Perspect. Jun 2001;109(6):613-9. [Medline].
Varnai VM, Piasek M, Blanusa M, Saric MM, Kostial K. Succimer treatment during ongoing lead exposure reduces tissue lead in suckling rats. J Appl Toxicol. Sep-Oct 2001;21(5):415-6. [Medline].
Flora SJ, Pande M, Mehta A. Beneficial effect of combined administration of some naturally occurring antioxidants (vitamins) and thiol chelators in the treatment of chronic lead intoxication. Chem Biol Interact. Jun 15 2003;145(3):267-80. [Medline].
Varnai VM, Piasek M, Blanusa M, Juresa D, Saric M, Kostial K. Ascorbic acid supplementation does not improve efficacy of meso-dimercaptosuccinic acid treatment in lead-exposed suckling rats. Pharmacol Toxicol. Oct 2003;93(4):180-5. [Medline].
Thomas DJ, Chisolm J Jr. Lead, zinc and copper decorporation during calcium disodium ethylenediamine tetraacetate treatment of lead-poisoned children. J Pharmacol Exp Ther. Dec 1986;239(3):829-35. [Medline].
Besunder JB, Super DM, Anderson RL. Comparison of dimercaptosuccinic acid and calcium disodium ethylenediaminetetraacetic acid versus dimercaptopropanol and ethylenediaminetetraacetic acid in children with lead poisoning. J Pediatr. Jun 1997;130(6):966-71. [Medline].
Blank E, Howieson J. Lead poisoning from a curtain weight. JAMA. Apr 22-29 1983;249(16):2176-7. [Medline].
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. Apr 17 2003;348(16):1517-26. [Medline].
Ciriza C, Garcia L, Suarez P, Jimenez C, Romero MJ, Urquiza O. What predictive parameters best indicate the need for emergent gastrointestinal endoscopy after foreign body ingestion?. J Clin Gastroenterol. Jul 2000;31(1):23-8. [Medline].
Cocco P, Hua F, Boffetta P, Carta P, Flore C, Flore V. Mortality of Italian lead smelter workers. Scand J Work Environ Health. Feb 1997;23(1):15-23. [Medline].
Farrell SE, Vandevander P, Schoffstall JM, Lee DC. Blood lead levels in emergency department patients with retained lead bullets and shrapnel. Acad Emerg Med. Mar 1999;6(3):208-12. [Medline].
Fergusson JA, Malecky G, Simpson E. Lead foreign body ingestion in children. J Paediatr Child Health. Dec 1997;33(6):542-4. [Medline].
Glotzer DE, Weitzman M. Commonly asked questions about childhood lead poisoning. Pediatr Ann. Dec 1995;24(12):630-2, 637-9. [Medline].
Hotz M, Kniepmann K, Kohn L. Occupational therapy in pediatric lead exposure prevention. Am J Occup Ther. Jan 1998;52(1):53-9. [Medline].
Kostial K, Blanusa M, Piasek M, Restek-Samarzija N, Jones MM, Singh PK. Combined chelation therapy in reducing tissue lead concentrations in suckling rats. J Appl Toxicol. May-Jun 1999;19(3):143-7. [Medline].
Lioy PJ, Yiin LM, Adgate J, Weisel C, Rhoads GG. The effectiveness of a home cleaning intervention strategy in reducing potential dust and lead exposures. J Expo Anal Environ Epidemiol. Jan-Mar 1998;8(1):17-35. [Medline].
Macgregor D, Ferguson J. Foreign body ingestion in children: an audit of transit time. J Accid Emerg Med. Nov 1998;15(6):371-3. [Medline].
McKinney PE. Acute elevation of blood lead levels within hours of ingestion of large quantities of lead shot. J Toxicol Clin Toxicol. 2000;38(4):435-40. [Medline].
Mowad E, Haddad I, Gemmel DJ. Management of lead poisoning from ingested fishing sinkers. Arch Pediatr Adolesc Med. May 1998;152(5):485-8. [Medline].
Osorio AM, Melius J. Lead poisoning in construction. Occup Med. Apr-Jun 1995;10(2):353-61. [Medline].
Perazella MA. Lead and the kidney: nephropathy, hypertension, and gout. Conn Med. Sep 1996;60(9):521-6. [Medline].
Rosen JF. Adverse health effects of lead at low exposure levels: trends in the management of childhood lead poisoning. Toxicology. 1995;97:11-7. [Medline].
Ruprecht J. Scientific Monograph Dimaval (DMPS). In: Investigators Brochure. Houston, Tex: Heyltex Corporation: 1997.
Sun JB, Wang JP. Recommended diagnostic criteria for occupational chronic lead poisoning. Biomed Environ Sci. Dec 1995;8(4):318-29. [Medline].
Trachtenbarg DE. Getting the lead out: when is treatment necessary?. Postgrad Med. Mar 1996;99(3):201-2, 207-18. [Medline].
Winneke G, Lilienthal H, Kramer U. The neurobehavioural toxicology and teratology of lead. Arch Toxicol Suppl. 1996;18:57-70. [Medline].
Further Reading
Keywords
lead toxicity, lead poisoning, lead consumption, lead poisoning causes, lead poisoning treatment, adult lead poisoning, pediatric lead poisoning, effects of lead poisoning, lead contamination, lead paint, lead exposure, childhood lead exposure, childhood lead poisoning, lead-related occupations, lead-pigmented paint, iron deficiency
