eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Lead

Steven Marcus, MD, Professor, Department of Preventive Medicine and Community Health, Associate Professor, Department of Pediatrics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey; Executive and Medical Director, New Jersey Poison Information and Education System; Consulting Staff, Departments of Pediatrics and Internal Medicine, University Hospital, University of Medicine and Dentistry of New Jersey; Consulting Staff, Department of Pediatrics, Newark Beth Israel Medical Center

Updated: Aug 10, 2009

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

Differential Diagnoses

Other Problems to Be Considered

Neuropathies

Workup

Laboratory Studies

• The criterion standard is a whole blood lead level (BLL). Any BLL above 10 micrograms/dL is considered positive and consequential. Patients with lead levels between 10 and 20 micrograms/dL require removal from the exposure, repeated testing, and follow-up.
  • 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.
  • 
    

    

    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.

    
    
• Lead interferes with the enzyme ferrochelatase, blocking the incorporation of iron into the protoporphyrin molecule; thus, a free erythrocyte protoporphyrin (EP) level may be useful in demonstrating the degree of biological abnormalities that exist. EP can also be used to help distinguish recent acute lead exposure from chronic exposure.
• 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.

Abdominal flat plate showing multiple radio-opaque foreign bodies including paint chips and an earring.

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.

Growth arrest lines, also known as lead lines, in bones of a child who recovered from lead poisoning.

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 spinal tap may be needed in evaluation of patients with altered mental status. However, it is contraindicated in patients with lead encephalopathy due to possible risk of herniation resulting from elevated intracranial pressure.
• A provocative chelation test was used in the past in order to provide additional information (total body burden). Urine was collected after administering a dose of chelator. Calcium disodium edetate was the most commonly used chelator for this test. Recently, the potential dangers of such provocative chelation have decreased the frequency of its use and it is not recommended as the standard of care.

Treatment

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. Several guidelines and recommendations on prevention, treatment, diagnosis, and screening are available from the Centers for Disease Control and Prevention, American Academy of Pediatrics, and United States Preventive Services Task Force.^6,7,8,9

• 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 whole-bowel irrigation (WBI) 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 laboratory work results are pending.
• Individuals can probably be treated on an outpatient basis 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.
• Pregnant and symptomatic patient with elevated BLL should be treated with chelation in consultation and under supervision of medical toxicologist.
• Treatment of asymptomatic pregnant patients with elevated BLL should not be initiated without consultation with medical toxicologist. Very limited data exist in regard to teratogenicity of chelation therapy.

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

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.¹⁰  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.¹¹   

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 CaNa₂ EDTA and the possible increase in brain lead in the first 24 hours of therapy.^12,13,14  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 Na ₂ CaEDTA.¹⁵  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 CaNa ₂ EDTA 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.^{16,17  18} 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.¹⁹

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.^19,20

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.²¹

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.

Dimercaprol (British antilewisite; BAL)

The first chelator used in encephalopathic individuals. Rapidly crosses the blood-brain barrier. Is more effective at preventing lead from forming a ligand binding than reversing it. Usually used in combination with calcium disodium edetate. Adverse effects are fever, pain at the injection site, nausea, vomiting, headache, and sterile abscess formation.
In very severely poisoned patients, the dose is increased to 7 mg/kg with great caution.

Dosing

Adult

3-5 mg/kg IM q4h

Pediatric

Administer as in adults

Interactions

May form toxic complexes with iron, cadmium, and selenium; may interfere with thyroid iodine accumulation

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid concurrent iron therapy

Edetate calcium disodium (Calcium Disodium Versenate)

Nearly the perfect chelator. Is water-soluble and can be used either IV or IM. Allows lead to be renally eliminated, is not metabolized, and has few toxic effects.
When IM, the same daily dose is used, divided into 2-6 doses. Is extremely irritating to muscle and intensely painful. Lidocaine or procaine with the IM preparation lessens the pain.

Dosing

Adult

50-75 mg/kg/d IV continuous infusion over 8-24 h for 5 d or divided; or given IM in 2-6 divided doses; mixing with lidocaine preferably when given with IM dose to lessen discomfort

Pediatric

Administer as in adults

Interactions

IV incompatibility with amphotericin-B, D10W, and hydralazine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause hypertension, headache, eosinophilia, and fever; there is controversy regarding possible mobilization of lead from bony storage sites into the brain in the first 24 h; consider pretreating with BAL; adequately hydrate
Since Pb may cause impairment of fluid balance and SIADH, it might be prudent to avoid hypotonic fluids. Thus, the authors suggest using normal saline to mix the IV CaNa ₂ EDTA solution and carefully monitoring fluid intake and output as well as serum electrolytes
Do not confuse with the similarly named product edetate disodium (Endrate), which is indicated for hypercalcemia and ventricular arrhythmia secondary to digitalis toxicity; each of these 2 products are commonly referred to as EDTA and as a result, the 2 products are easily mistaken for each other when prescribing, dispensing, and administering; deaths occurred in patients when mistakenly given edetate disodium instead of edetate calcium disodium or when edetate disodium was used for chelation therapy; for more information, see the FDA MedWatch Safety Information

D-Penicillamine

Hydrolysis product of penicillin approved for the treatment of Wilson disease and cystinosis. Used as oral chelator of lead for 30 years but has never been licensed for such by the FDA. Effective orally and has few adverse effects.

Dosing

Adult

25-35 mg/kg PO divided

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause GI irritation, Stevens-Johnson syndrome, nephrotic syndrome, and neutropenia

Succimer (DMSA)

In January 1991, became the only drug approved by the FDA specifically for lead chelation in children and the only drug approved to treat a specific laboratory test, a lead level higher than 45 mcg/dL (2.17 mmol/L). Has been shown to be an effective oral chelator that produces plumburesis, approaching that of the combination of CaNa₂ EDTA and BAL. Although never a substitute for careful environmental controls, produces a rapid decline in lead level and reverses many of the biochemical indicators of toxicity. Not currently licensed for use in adults. Although experience suggests that it is safe and effective, its use must be considered carefully. Adults exposed from an occupational source must be carefully excluded from further exposure.

Dosing

Adult

10 mg/kg PO q8h, days 1-5; 10 mg/kg PO q12h days 6-14

Pediatric

Administer as in adults; has very low bioavailability and is very difficult to administer; does not dissolve in water or juice; should be given on empty stomach and can be dumped onto surface of applesauce in teaspoon and immediately administered

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause mild reversible liver enzyme elevations and rash

Dimerval (DMPS)

Has received much attention worldwide but is not yet available in the US except under special FDA IND permits. Has become DOC for most heavy metal intoxications in Europe and Asia. Available in the oral form and in a water-based parenteral form.

Dosing

Adult

No accepted dose established
Parenteral form comes as injectable form; one ampule contains 250 mg of active drug
Limited data suggest use of 250 mg q4h for 7 d, changing to 100 mg oral capsules q6h until levels drop, then shifting to q12h, and then weaning

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Occasional shivering, fever, and skin rash are generally felt to be reversible

Follow-up

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.
  • 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.
• Consideration for discharge must include the following:
  • Source of lead must be determined and possibility of re-exposure eliminated.
  • If outpatient chelation is indicated, the medication must be in the hand of the responsible individual related to administration of the medication.
  • The individual must demonstrate knowledge about and ability to dose the patient.
  • The lead level must have dropped an appreciable amount while on in-patient 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.

Inpatient & Outpatient Medications

• 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 patients with lead poisoning.
• 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

Medicolegal 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.
• Failure to initiate removal of the patient from the area of the exposure (eg, lead-based paint)
• Failure to diagnose and treat other members of the family/friends with similar lead exposure
• Failure to suspect lead toxicity/encephalopathy in patients presenting with afebrile seizures
• Spinal tap performed on the patients with lead encephalopathy and increased intracranial pressure can precipitate cerebral herniation and death.

Multimedia

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.

Media file 2: Growth arrest lines, also known as lead lines, in bones of a child who recovered from lead poisoning.

Media file 3: Lead line on the gingival border of an adult with lead poisoning.

Media file 4: Wrist-drop in adult with lead poisoning and renal failure.

Media file 5: Abdominal flat plate showing multiple radio-opaque foreign bodies including paint chips and an earring.

References

1. 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].

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. 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].

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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

Contributor Information and Disclosures

Author

Steven Marcus, MD, Professor, Department of Preventive Medicine and Community Health, Associate Professor, Department of Pediatrics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey; Executive and Medical Director, New Jersey Poison Information and Education System; Consulting Staff, Departments of Pediatrics and Internal Medicine, University Hospital, University of Medicine and Dentistry of New Jersey; Consulting Staff, Department of Pediatrics, Newark Beth Israel Medical Center
Steven Marcus, MD is a member of the following medical societies: Academy of Medicine of New Jersey, American Academy of Clinical Toxicology, American Academy of Pediatrics, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, and Medical Society of New Jersey
Disclosure: Nothing to disclose.

Medical Editor

Mark S Slabinski, MD, FACEP, FAAEM, Vice President, EMP Medical Group
Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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