AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 occurs at very low levels and that medical intervention with chelation fails to reverse such effects.

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 renally excreted, 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 US. 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. Generally, adults develop lead poisoning as the result of an occupational exposure or from exposure through a hobby.

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.

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.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.
• Hispanic and Asian families occasionally use herbal folk remedies that may contain lead. 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.
  • 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 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.
• A report indicates that relative hypertension is related to elevated lead levels, but this finding has never been duplicated.

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.
• The history of illicit liquor ingestion 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Neuropathies

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• The criterion standard is a whole blood lead level.
• • The blood must be drawn in an anticoagulated and lead-free tube. Only one tube is certified by the manufacturer as being lead free. Trace metal tubes and anticoagulated tubes are available, but aside from the certified tube, they all tend to give high-biased levels.
  • The result may not be immediately available at all institutions because of laboratory limitations.
• A baseline hemogram may be indicated to look for the presence of a microcytic hypochromic anemia.
• • Lead toxicity causes what appears to be a typical pattern of iron-deficiency anemia with hypochromia and microcytosis. Iron deficiency does frequently coexist. Assessing iron storage status (ferritin) in all cases of lead poisoning is important.
• • In pregnant women, some evidence suggests that lead also causes a decrease in erythropoietin production and a depression in red cell production.
• • Lead is a surface-acting poison and may produce increased red cell fragility and acute hemolytic anemias.
• Lead interferes with the enzyme ferrochelatase, blocking the incorporation of iron into the protoporphyrin molecule; thus, a free erythrocyte protoporphyrin level may be useful in demonstrating the degree of biological abnormalities that exist.
• A chemistry profile including renal studies, liver studies, and a uric acid is advisable.
• • Children often have low uric acids and leak uric acid into their urine.
• • Adults, because of the disturbance of enzymatic amino hydrolases, manifest elevated uric acid levels and, possibly, clinical gout.
• Lead may produce subtle nephrogenic effects, which, if unappreciated, may lead to treatment failures or complications.
• • For example, a child may appear to have a mild degree of dehydration based on decreased urine output, increased urine specific gravity, and poor appetite.
• • This may be the predictor of impending inappropriate secretion of antidiuretic hormone and should lead to a careful analysis of fluid intake, plasma volume, and, perhaps, fluid restriction.

Imaging Studies

• Obtain a radiograph of the abdomen in children with suspected elevated lead levels.
• • The presence of radio-opaque foreign bodies throughout the GI tract may highlight the diagnosis and prompt immediate intervention. A radiograph also helps guide therapy as to the prevention of further absorption through GI decontamination.
  • A radiodensity in the distal metaphyseal plate is a frequent occurrence in children with chronic lead poisoning of a moderate degree. These findings are unlikely to be observed in adults.
  • Radiographs of the long bones in growing children may reveal the characteristic lead lines. These lines, actually growth arrest lines, are not pathognomonic but are associated with lead levels in excess of 40 mcg/dL over a protracted period of time.
• If an alteration of mental status is present, consider a CT scan of the head or MRI to rule out cerebral edema or structural lesions.

Other Tests

• A provocative chelation test may provide additional information. Obtain a timed urine collection after administering a dose of chelator. This will enable the physician to estimate the total body burden of lead and the efficacy of treatment. Calcium disodium edetate is the most commonly used chelator for this test. Recently, the potential dangers of such provocative chelation have decreased the frequency of its use.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Prehospital Care

The treatment of lead poisoning is separating the child from the source of lead exposure. Chelation is used only when separation fails to drop the lead fast enough or far enough or when the lead level is in the potentially encephalopathogenic level (>60 mcg/dL).

• Protect the airway if the patient is comatose or seizing.
• Aside from initial workup and treatment, immediate transportation to a hospital with experienced personnel and facilities for treating patients with lead poisoning is imperative.

Emergency Department Care

Base initial therapy on the history, likelihood of actual lead toxicity, symptoms present, and the physical examination. Offer all patients appropriate symptom relief.

• The following are indicated for the severely symptomatic patient with lead poisoning:
• • Begin an intravenous drip of normal saline.
  • Obtain laboratory work and imaging studies without delay.
  • In a child with acute lead ingestion, an orogastric or nasogastric catheter may be needed to enable intestinal irrigation with polyethylene glycol.
  • Do not delay with administration of chelation therapy to clear any pica from the gut. Immediately institute chelation therapy if lead poisoning is seriously considered. Simultaneous therapy to evacuate the lead-laden particles from the GI tract should be begun.
• The patient without severe poisoning or one in whom the diagnosis is unclear can be treated symptomatically while lab work results are pending.
• Individuals can probably be treated as outpatients if they have lead levels below that which is considered potentially encephalopathogenic (ie, <60 mcg/dL) and they successfully can be kept away from further lead exposure.

Consultations

• Consultation with a clinical toxicologist or a physician conversant with treating lead poisoning is beneficial.
• Consultations from a hematologist and a nephrologist may be helpful.
• The local poison control center may provide useful information to facilitate treatment and follow-up.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

The most important treatment of lead poisoning is the separation from the source of lead. 

In commenting on children with moderate levels of lead in the blood without encephalopathy, Chisolm suggested that there is no evidence that chelation with EDTA does anything to lower the brain lead level.¹ While studying the effects of treatment with the chelator succimer in the primate model, Cremin failed to find a significant effect on brain lead levels with chelation with this agent beyond that achieved simply by separation from the source of lead.²  

The DOCs are all chelators. The word chelator is derived from the Greek term for claw; chelators form a chemical claw around the heavy metal and allow them to be excreted. Two parenteral and 2 oral drugs may be used.

Dimercaprol, also known as BAL (for British antilewisite), is the prototype chelator. A bisulfide molecule, this lipid-soluble drug must be administered intramuscularly. It has the typical sulfide odor, and patients often complain of the taste and bad feeling when the drug is administered. Calcium disodium edetate may be used intramuscularly or intravenously (in many centers the intramuscular route has been abandoned in favor of a continuous intravenous drip that appears to improve outcome and decrease adverse effects of the intramuscular route).

Some controversy exists regarding the use of parenteral CaNa₂EDTA and the possible increase in brain lead in the first 24 hours of therapy.^{3, 4, 5} Chisolm, in his classic article describing the improvement in the outcome of children with symptomatic lead poisoning reported that often children deteriorated during the early stages of treatment and postulated that this was due to shifts in lead subsequent to the use of Na₂CaEDTA.⁶ He  suggested the combined use of both BAL and EDTA. No significant studies have been undertaken to allow any evidence-based decision on this. The author of this article is aware of at least 3 patients whose clinical course deteriorated during the first 3 days of therapy with CaNa₂EDTA chelation and in which severe hyponatremia and elevated vasopressin levels were found. Thus, use of combined therapy for the first few days to prevent such deterioration may be prudent.

The 2 currently used oral chelators in the United States are D-penicillamine and succimer. Although the Food and Drug Administration (FDA) approved succimer for use in children with lead levels higher than 45 mcg/dL, D-penicillamine has not yet been approved, despite its widespread use for the past 2 decades.

Some controversy exists regarding the use of chelation while there is continued exposure either to external sources or if there is possibly lead present in the GI tract.^{7, 8 9} Although it has long been the dogma that chelation should not be delayed to empty the intestines, just how to chelate in such a circumstance has not been subjected to scientific investigation. The controversy regarding possible redistribution of lead to brain during EDTA therapy adds to this conundrum.

Another chelator, 2,3 dimercaptopropane-1-sulfonic acid sodium salt (DMPS) is available in Europe both orally and parenterally. It has not been approved or licensed in the United States, but it has been used in various forms in alternative medicine clinics.

The use of multiple chelators at once has often been suggested, but recent data suggest that it may not be more advantageous than using just one.¹⁰

In the era of use of alternative medicines, there are those who suggest the use of various vitamins and other antioxidants. Recent data suggest that this does not alter efficacy of chelation with standard medications.^{10, 11}

Remember that all chelators have nonspecific effects, that is, they will chelate other metals as well as lead. Thus, chelation must be carefully considered, that is "Primum non nocere", first do no harm.¹²

Drug Category: Chelating agents

These agents bind lead in the vascular compartment and prevent it from reaching the end organs of toxicity. Chelators promote the excretion of lead.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Careful attention to renal and hepatic function is important while administering chelation therapy.
• • Monitor fluid and electrolyte levels carefully because fluid shifts may occur during therapy.
  • Reports in the 1960s document cases of children who deteriorated after the onset of chelation therapy.
  • Recently, several children have been reported to develop the syndrome of inappropriate secretion of antidiuretic hormone shortly after beginning chelation therapy.
• All patients must have careful follow-up at weekly intervals to watch for unexpected re-exposure or re-equilibration of lead from bony stores after discontinuation of chelation.

Further Outpatient Care

• All patients treated for lead poisoning require extensive outpatient follow-up. The intent of such follow-up is to avoid further exposure to lead and to maintain lead levels in the acceptable range. It is imperative that children not be exposed to more lead, if they are, their lead levels will rapidly rise again.

In/Out Patient Meds

• Although separation of the patient from continued exposure to lead is of paramount importance, consider the use of chelation therapy to acutely lower blood lead levels.

Transfer

• Transfer patients with symptomatic lead poisoning, particularly those with lead encephalopathy, to an institution adept at treating patients with critical increases in intracranial pressure. Children should be treated in specialized pediatric intensive care units.

Deterrence/Prevention

• Many local health departments have programs for appropriate lead screening of children, in cooperation with local pediatricians. Stressing the need for screening in any patient at risk (because of housing, industrial, ethnic, recreational concerns) is important. Repairs of older homes must be done carefully to avoid lead exposure. Proper lead abatement in older homes prevents future exposure to lead and, thus, prevents further lead poisoning.

Complications

• Lead poisoning, with or without encephalopathy, may result in neurological, renal, hepatic, or cardiac damage. All organ systems may be potentially damaged by lead. A possibility that symptoms may progress with chelation exists, and the treating physician must be prepared to manage them. Such complications may consist of syndrome of inappropriate excretion of antidiuretic hormone (SIADH), increased intracranial pressure (ICP), renal impairment from the chelated lead complex, and hypertension.

Prognosis

• In the pediatric population, fatalities associated with lead encephalopathy were reported in the 1960s. Today, with aggressive management of ICP, these deaths are preventable and no such reports have been made in recent years. Occasional cases of acute lead encephalopathy still occur, and these often result in severe neurological damage. Asymptomatic lead poisoning has a far better prognosis. Long-term effects range from seizure disorders to hyperactivity, depressed school function, learning disability, and dyslexia.
• 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 lead poisoned patients.
• Defects in sexual performance, frank impotence, infertility, and increased fetal wastage have been associated with lead poisoning in adults.

Patient Education

• All patients must be educated in lead avoidance. The termination of exposure to lead is imperative.
• 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 are suggested for children each day.
• For excellent patient education resources, visit eMedicine's Poisoning Center. Also, see eMedicine's patient education article Poisoning.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• The greatest danger is failure to recognize the possibility of lead poisoning.
• • The symptoms and signs of lead toxicity are subtle and easily overlooked.
  • One suit developed after a child was seen in several hospital EDs, presenting with the symptoms of poor appetite, vomiting, and sore throat. A throat culture obtained at one ED revealed beta-hemolytic streptococcus and the child received appropriate penicillin therapy only to return several days later actively convulsing with a lead level higher than 170 mcg/dL.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Peripheral smear taken from an 8-year-old Pakistani girl who presented with an acute hemolytic anemia and a lead level of 125 mcg/dL.
	View Full Size Image
Media type:  Photo

Media file 2:  Growth arrest lines, also known as lead lines, in bones of a child who recovered from lead poisoning.
	View Full Size Image
Media type:  X-RAY

Media file 3:  Lead line on the gingival border of an adult with lead poisoning.
	View Full Size Image
Media type:  Photo

Media file 4:  Wrist-drop in adult with lead poisoning and renal failure.
	View Full Size Image
Media type:  Photo

Media file 5:  Abdominal flat plate showing multiple radio-opaque foreign bodies including paint chips and an earring.
	View Full Size Image
Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. 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].
2. 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].
3. 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].
4. 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].
5. 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].
6. 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].
7. 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].
8. 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].
9. 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].
10. 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].
11. 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].
12. 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].
13. 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].
14. Blank E, Howieson J. Lead poisoning from a curtain weight. JAMA. Apr 22-29 1983;249(16):2176-7. [Medline].
15. 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].
16. 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].
17. 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].
18. 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].
19. Fergusson JA, Malecky G, Simpson E. Lead foreign body ingestion in children. J Paediatr Child Health. Dec 1997;33(6):542-4. [Medline].
20. Glotzer DE, Weitzman M. Commonly asked questions about childhood lead poisoning. Pediatr Ann. Dec 1995;24(12):630-2, 637-9. [Medline].
21. Hotz M, Kniepmann K, Kohn L. Occupational therapy in pediatric lead exposure prevention. Am J Occup Ther. Jan 1998;52(1):53-9. [Medline].
22. 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].
23. 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].
24. 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].
25. 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].
26. 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].
27. Morgan BW, Todd KH, Moore B. Elevated blood lead levels in urban moonshine drinkers. Ann Emerg Med. Jan 2001;37(1):51-4. [Medline].
28. 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].
29. Osorio AM, Melius J. Lead poisoning in construction. Occup Med. Apr-Jun 1995;10(2):353-61. [Medline].
30. Perazella MA. Lead and the kidney: nephropathy, hypertension, and gout. Conn Med. Sep 1996;60(9):521-6. [Medline].
31. 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].
32. Ruprecht J. Scientific Monograph Dimaval (DMPS). In: Investigators Brochure. Houston, Tex: Heyltex Corporation: 1997.
33. Sun JB, Wang JP. Recommended diagnostic criteria for occupational chronic lead poisoning. Biomed Environ Sci. Dec 1995;8(4):318-29. [Medline].
34. Trachtenbarg DE. Getting the lead out: when is treatment necessary?. Postgrad Med. Mar 1996;99(3):201-2, 207-18. [Medline].
35. Winneke G, Lilienthal H, Kramer U. The neurobehavioural toxicology and teratology of lead. Arch Toxicol Suppl. 1996;18:57-70. [Medline].

Article Last Updated: Dec 12, 2007