Temple University School of Pharmacy is approved by the American Council on Pharmaceutical Education (ACPE) as a provider of continuing pharmaceutical education. Its CE programs are developed in accordance with the “Criteria for Quality and Interpretive Guidelines” of ACPE.
This program is acceptable for 2.0 hours of Continuing Education Credits (0.2 CEU) through May 31, 2003.
ACPE Program
I.D. Number:
057-999-99-028-H01

The Prevention and Treatment of Childhood Lead Poisoning

Patrick J. McDonnell, PharmD

Dr. McDonnell is an Assistant Professor of Clinical Pharmacy at the Temple University School of Pharmacy in Philadelphia, Pennsylvania.

Introduction

Childhood lead poisoning is one of the most common pediatric health problems in the United States today, and it is considered to be entirely preventable. Sources of lead and pathways of exposure are well known, and, theoretically, childhood toxicity from lead should be almost non-existent. However, the persistence of lead poisoning in the United States still presents a direct challenge to public health authorities, clinicians, and society.

In the first half of this century, the adverse effects of lead exposure were unknown. In fact, lead was considered to be useful as a medical treatment—it was incorporated into vaginal ointments as a treatment for syphilis, as well as in ointments for nursing mothers to treat nipple irritation. In the latter half of this century, lead has been proven to cause anemia, nephropathy, visceral organ damage, neuropathy, developmental toxicity, encephalopathy, and death.

Here are some facts about lead and lead poisoning in children. Lead is ubiquitous in the environment as a result of industrialization. Lead has no known physiologic value. It is estimated that 9% of pre-school children in America have abnormally high blood lead levels (BLLs).¹ In some metropolitan areas, especially in the large cities of the Northeast, the percentage of children with abnormally high BLLs are alarmingly high. In Philadelphia, approximately 40% of children were reported to have elevated BLLs.² It is important to note, however, that lead poisoning is not solely a problem of inner-city children. Lead poisoning is widespread, and no socioeconomic group, racial or ethnic population, or geographic area is spared. Most cases of lead poisoning, also known as “plumbism,” are asymptomatic or mimic other diseases and therefore go untreated. Based on these facts, lead poisoning still remains one of the most common and preventable pediatric health problems today.

Over the years, the recommended BLL that should result in medical intervention has steadily decreased (Table 1). This is based on new data that indicate significant adverse effects of lead exposure in children previously believed to be safe. Studies have shown that when BLLs are >10 mcg/dL there is a correlation with decreased IQ scores.³ It has also been shown that when BLLs are >10 mcg/dL, there is decreased synthesis of vitamin D, leading to bone malformation in children. BLLs > 10 mcg/dL in pregnant women have been correlated with premature and low-birth-weight infants. The goal of all lead poisoning prevention and treatment activities is to reduce children’s BLL to <10 mcg/dL.³

Table 1. Lead Levels of Concern

Sources of Lead in the Child’s Environment³

Paint

As stated earlier, lead is ubiquitous in the environment. The main source of lead in the environment of children is paint, and it still remains their most common source for lead poisoining. Greater than 75% of dwellings built in the United States before 1978 contain lead paint. Homes built before 1960 may contain lead paint with concentrations of up to 50% lead by weight. In 1978, the Consumer Product Safety Commission banned the manufacture of paint containing more than 0.06% lead by weight on interior and exterior residential surfaces, furniture, and toys. Lead-based paint is still available for industrial, military, and marine usage, and, unfortunately, occasionally ends up being used in homes. Lead is absorbed by the ingestion of paint chips, also known as pica, or more commonly by children getting lead-containing paint dust on their hands and toys and placing them in their mouths. Inhalation of lead-tainted dust via renovation or removal of paint from older homes or demolition sites can also poison a child. In the city of Philadelphia, which has one of the highest rates of lead poisoning in the nation, approximately 600,000 persons occupy housing units in the city. Ninety-five percent of these units were built prior to 1978 and over half of these units were built before 1940.²

Soil and Dust

Soil and dust can be pathways for lead when children are exposed to contaminated paint and other industrial sources of lead. Lead does not dissipate, biodegrade, or decay; therefore, the lead deposited into dust and soil becomes a long-term source of lead exposure to children.

Water

The Environmental Protection Agency estimates that drinking water is the source of about 20% of Americans’ exposure to lead. The main source of lead in drinking water is from plumbing that contains lead pipes and solder. Homes built before 1920 that retain the original plumbing contain pipes and solder that are made entirely of lead. In 1986, the Safe Drinking Water Act Amendments banned the use of lead in public drinking water distribution systems and limited the lead content of brass used for plumbing to 8%. Water storage containers known as cisterns are still common in some states, especially Florida and Pennsylvania. These cisterns collect rainwater for drinking and are lined with lead. Lead from pipes, solder, and cisterns leaches into the water, especially if the water is acidic (rainwater and “soft water”). Lead also is more likely to leach into hot water than cold water. Common water filters containing sand and carbon will not remove lead. Lead-contaminated water used in the preparation of formulas can cause lead poisoning in infants. Older preschoolers drinking lead-contaminated water in, for example, home- made juices can also be at risk.

Food

Food can also be a source of lead if it is grown in lead-contaminated soil and is not properly washed. Also food served in containers that contain lead, such as glazed pottery, crystal, ceramics, and porcelain, can lead to an untoward exposure as the lead is leached from containers into the food. Lead soldering in food and soft drink cans used to be a source of lead in the United States; however, since November 1991, lead-soldered food or soft drink cans are no longer manufactured in the United States. However, lead soldering is still used in many other countries, and imported canned food and drinks can be a source of lead, especially if the food is stored for prolonged periods of time after opening.

Folk Remedies

Certain folk and herbal remedies mainly used in Arab, Chinese, Indo-Pakistani, and Latino cultures may be contaminated with or actually contain lead. The folk remedies azarcon and greta used to treat diarrhea and gastrointestinal (GI) upset contain substantial quantities of lead. Other folk remedies that contain lead include alarcon, alkohl, bali goli, coral, ghasard, liga, pay-loo-ah, and rueda.

Occupations and Hobbies

Certain occupations and hobbies can be sources of lead contamination to children. Children can come in contact with lead-tainted clothes or with actual materials used in hobbies that contain lead (Table 2).

Table 2. Hobbies and Occupations
as Sources of Lead Exposure

Pharmacokinetics of Lead

Lead has no known physiologic function. The major routes of absorption of lead are the GI and respiratory tracts. GI absorption of lead varies with age; adults absorb approximately 10% of ingested lead. Children, on the other hand, can absorb up to 40% of ingested lead. The difference between the two age groups may be because of the way lead is absorbed across the GI mucosa. It is speculated that lead and calcium may compete for a common transport mechanism. There is a reciprocal relationship between the dietary content of calcium (Ca2+) and lead (Pb2+) absorption. Growing children rapidly utilize calcium in bone formation and growth, and dietary demands for calcium are high. Children who do not get adequate amounts of dietary calcium will absorb more exposed lead based on this reciprocal relationship. Iron deficiency, another common pediatric problem, has also been shown to enhance the intestinal absorption of lead. Children who do not eat regular meals also have enhanced lead absorption, because more lead is absorbed on an empty stomach.⁴ Lead is also absorbed through the respiratory tract—approximately 90% of inhaled lead particles are absorbed. The elimination of lead-containing gasoline in the United States has shown to be significant in the reduction of BLL in Americans.¹

After absorption, lead is distributed initially to the soft tissues, especially the kidneys and liver. Lead is then redistributed to teeth, hair, and bone. The disposition of lead in bone closely resembles that of calcium. Disposition of lead in growing bones and teeth may lead to a series of transverse lines along the growing plates, forming so-called lead lines. Factors that affect the distribution of calcium also affect that of lead. Thus, a high intake of phosphate will favor the skeletal storage of lead and a lower storage concentration in soft tissue. Conversely, a low phosphate intake mobilizes lead in bone and shifts it to the soft tissue. Nearly all circulating lead is contained in red blood cells. Only a small amount of inorganic lead accumulates in the brain, with most of that in the basal ganglia and gray matter. Preschool children and younger (<4 years old) are at greater risk for central nervous system (CNS) accumulation of lead, as the blood-brain barrier is not completely formed. The half-life of lead in the blood can be 1 to 2 months. A consistent exposure to lead, which can lead to a positive lead balance (absorption >> excretion), can lead to a half-life in the bones of up to 20 years.⁴

The majority of lead in humans is excreted renally, with a smaller portion being excreted into the bile and feces. The concentration of lead in urine is directly proportional to that in plasma.

The Effects of Lead Toxicity

Hematological

One of the first manifestations of lead toxicity is anemia. Anemia results from an inhibition of heme synthesis. Heme is the iron-containing component of hemoglobin. Lead inhibits several steps in the heme synthesis pathway (Figure 1).⁵ The inhibition of the enzyme delta aminolevulonic acid dehydratase (d-ALA dehydratase) leads to increased levels of delta aminolevulonic acid (d-ALA), which can be measured in the urine. Lead also inhibits the final enzyme in the synthesis of heme, which is ferrochelatase. Inhibition of this enzyme leads to an increase in the heme precursor called protoporphyrin IX, which can be measured in the blood. Both these precursors become elevated in lead poisoning before frank anemia results. Manifestations of anemia usually are seen when BLLs become >40 mcg/dL.⁶ When BLLs are >60 mcg/dL, red blood cell inclusions known as basophilic stippling is common, although not pathognomonic of lead poisoning.

Lead-induced anemia manifests as a microcytic (small red blood cells), hypochromic (lacking color from hemoglobin) anemia. Iron deficiency, which also manifests as a microcytic, hypochromic anemia, cannot only mask lead toxicity symptoms, but can worsen it. Lead absorption is increased when iron stores are low. It can be recommended that if a preschooler presents with such an anemia and has a history of lead exposure, a blood lead level should be tested along with an iron-deficiency panel of blood tests.

Figure 1. Lead Inhibition of Heme Synthesis

Gastrointestinal Effects

Lead toxicity can manifest itself with GI effects. Increased levels of lead affect the smooth muscle of the GI tract, producing a vague abdominal syndrome. This syndrome is manifested by anorexia, nausea, cramping, and a metallic taste in the mouth. The abdominal side affects caused by lead are usually the earliest manifestations of toxicity. Higher levels of lead (>50 mcg/ dL) can lead to what is referred to as lead colic—severe abdominal cramps caused by intestinal spasm and abdominal wall rigidity, with or without constipation.⁶

Neuromuscular Effects

Effects of the neuromuscular system due to lead toxicity result from a degeneration of motor neurons and axons. These effects can start as a peripheral neuritis that is usually painless and limited to the extensor muscles. A condition known as lead palsy can also result from lead poisoning. This palsy is manifested by a “wrist and/or foot drop” and, when this occurs with a history of lead exposure, is pathognomonic for lead toxicity.⁶

Central Nervous System Effects

CNS effects from lead can result from BLLs as low as 10 mcg/dL. Lead levels of 10 to 15 mcg/dL have been linked to lower IQ scores in children.³ Early exposure to lead (from 12 to 18 months of age) have be shown to lead to a steady loss of motor skills and delayed speech development. Learning impairment and aggressive behavior have also been linked to elevated BLLs in this age group.

Lead encephalopathy is the most serious manifestation of lead toxicity, and is a medical emergency. It can be seen in children with BLLs as low as 50 mcg/dL, and is usually present in all children with BLLs >100 mcg/dL.^3,4 Early signs of lead encephalopathy include clumsiness, vertigo, headache, insomnia, and irritability. Progressive manifestations of lead encephalopathy include excited and confused behavior, projectile emesis, tonic-clonic convulsions, coma, and death.

Other Manifestations of Lead Poisoning⁴

Lead is a nephrotoxin. It can lead to reversible or irreversible tubular necrosis. As a result of the anemia, the skin takes on a pale or ashen color, especially in the face and lips. A blue-black line along the gingival margin, a “lead line,” may be seen. A premature-aging syndrome has also been described in children with lead poisoning, manifested by a stooped posture, poor muscle tone, and a wasting or emaciation syndrome.

Diagnosing Lead Poisoning

d-ALA, which can be detected in the urine, and protoporphyrin IX or erythrocyte protoporphyrin (EP), which can be detected in the blood, are both elevated in lead poisoning. However, these two heme precursors are not recommended for use in screening tests for diagnosing lead poisoning in children. These precursors are not sensitive enough to detect BLL concentrations <25 mcg/dL.

Screening should be done by using a BLL test. Venous blood samples are preferred over capillary samples (blood collected by fingersticks or heelsticks). If blood is to be collected by a finger- or heelstick, the skin must be adequately cleaned to wipe away any trace amounts of lead that may be on the skin, so as not to taint the sample.

Abdominal X rays may be of some use, because they may reveal the presence of ingested lead particles or if pica is suspected. Radiographs of the bones may also be of use because they may reveal a “lead line.”

Agents Used in the Treatment of Lead Poisoning3,4

The mainstay of treatment for lead poisoning is chelation therapy. In chelation therapy, molecules of a heavy metal, such as lead, form a stable complex with the chelating agent. This complex is then available for excretion.

Dimercaprol or British Anti-Lewisite

Dimercaprol or British Anti-Lewisite (BAL)is a chelating agent that is used for heavy metal toxicity. It is used to remove lead, mercury, and arsenic. Two molecules of dimercaprol combine with one atom of heavy metal forming a stable complex. This complex is then excreted in the urine, bile, and feces.

Dimercaprol is water-insoluble. It is suspended in peanut oil; therefore, it is only available for intramuscular (IM) administration. Dimercaprol is rarely used alone as a chelating agent for lead poisoning.

The dose of dimercaprol when used for childhood lead poisoning is 4 mg/kg per dose or 75 mg/m2 per dose given every 4 hours for 5 to 7 days.³

Precautions with the use of dimercaprol include:

	Do not use in children with a peanut allergy.
	Dimercaprol contains an oxidative sulfhydryl group and is generally contraindicated in children with G-6PD deficiency because of the risk of hemolytic anemia.
	Adverse reactions related to dimercaprol include febrile reactions, transient liver enzyme/ transaminase elevation, nausea, vomiting, headache, lacrimation or excessive tearing, and rhinorrhea. These side effects are generally mild and transient, and may be seen in up to one third of patients receiving this agent.
	Dimercaprol is a potential nephrotoxin. To reduce the risk of nephrotoxicity, the urine should be kept alkaline (sodium bicarbonate at 1 to 10 mEq/kg per day orally in divided doses, titrating to desired urinary pH) during therapy to prevent dissociation of the dimercaprol-lead complex and to ensure complete excretion.

Calcium Disodium Edetate

(CaNa2EDTA—Versenate)

CaNa2EDTA is also a very effective chelating agent used in lead poisoning. It binds to extracellular lead, forming stable complexes that are excreted in the urine. CaNa2EDTA increases the urinary excretion of lead by 20- to 50-fold. CaNa2EDTA can be given intravenously, intramuscularly, or by subcutaneous injection. IM administration is actually the preferred route for CaNa2EDTA since it may reduce the incidence of some adverse effects; procaine may be added to the injection to reduce pain from this route of administration.

There are several dosing guidelines for CaNa2EDTA depending on the BLL and manifestations of lead poisoning.³

Asymptomatic lead poisoning with a BLL of >50 mcg/dL, or symptomatic lead poisoning without encephalopathy and a BLL of <100 mcg/dL: Dose of CaNa2EDTA: 1.5 g/m2 per day intramuscularly or intravenously in divided doses q12h for 5 days.

CaNa2EDTA is usually used in combination with dimercaprol; however, this dose of CaNa2EDTA may be used alone if the BLL is
< 70 mcg/dL.

Symptomatic lead poisoning with encephalopathy, or BLL > 100 mcg/dL: Dose of CaNa2EDTA: 250 mg/m2/dose q4h for 5 days. Based on symptoms, a repeat course may be given at 5-day intervals (to be given 4 hours after first dose of BAL; use different IM injection sites for each agent when given in combination). It is important to keep in mind that lead encephalopathy is a medical emergency, and combination chelation therapy with both CaNa2EDTA and dimercaprol is recommended.

Only CaNa2EDTA can be used for EDTA chelation therapy.Disodium edetate (Na2EDTA) must never be used as a chelating agent for lead poisoning. Disodium edetate will not only chelate and remove lead, but will chelate calcium, which can induce tetany and possible fatal hypocalcemia. CaNa2 EDTA should not be administered for more than 5 days because of serious mineral depletion, particularly that of zinc, iron, and copper.

Adverse reactions and precautions to monitor with CaNa2EDTA therapy include potential nephrotoxicity. Patient should be kept adequately hydrated. Daily monitoring of renal function tests (blood urea nitrogen, creatinine, and urinalysis) is recommended for children receiving CaNa2EDTA.

Hepatocellular damage may occur at the end of chelation therapy, however, this is usually reversible about 1 week after discontinuation of CaNa2EDTA.

Succimer (Chemet)

Succimer was introduced in 1991 as the only oral agent approved by the FDA for the treatment of lead toxicity. It is usually used when BLLs are >45 mcg/dL; however, some pediatricians may decide to use succimer for chelation therapy when BLLs are lower (between 25 and 44 mcg/dL). Succimer works similarly to dimercaprol, but it is water-soluble, has a high therapeutic index, and is adequately absorbed through the GI tract. Succimer is highly selective for chelating lead, because it has a low selectivity for other trace elements.

The dose of succimer used for lead poisoning is 10 mg/kg po q8h for 5 days followed by 10 mg/kg po BID for 2 weeks, for a total of 19 days of therapy. Repeat courses of succimer may be given at 2-week intervals for chronically elevated BLLs.

Succimer is available in 100-mg capsules. If children cannot swallow the capsules, the beads can be sprinkled in soft food or a spoonful of fruit drink. Succimer contains a sulfhydryl group and is quite foul smelling. This “rotten egg” odor may prevent easy administration of succimer to children. Sprinkling the beads into soft food for 5 to 10 minutes before administration for some of the odor to dissipate may reduce the odor of succimer. Chocolate pudding or applesauce may help mask the smell.

Again, succimer has a higher therapeutic index when compared to its water-insoluble counterpart, dimercaprol; therefore, side effects tend to be milder. Adverse effects seen with succimer therapy include a transient and reversible increase in liver function tests, nausea, vomiting, diarrhea, and rash. There is limited data demonstrating that succimer can be used as a sole agent with lead levels >70 mcg/dL; therefore, combination therapy with dimercaprol and CaNa2EDTA is still preferred with these higher BLLs because of the higher risk of lead encephalopathy.

It is important to note that the absorption of lead is enhanced if the child is not in a lead-free environment while receiving outpatient chelation therapy with succimer. If the home is not lead-free, succimer cannot be given as outpatient therapy.

Penicillamine
(Cuprime, Depen)

Penicillamine is used as chelation therapy for other heavy metal poisonings. It is sometimes used as a lead chelator; however, it is not FDA-approved for the treatment of lead poisoning. If used for lead poisoning, the dose is 25 to 35 mg/kg per day orally in divided doses. Therapy can be several weeks in duration.

Penicillamine is noted for having a higher incidence of adverse effects when compared to other chelation therapy. Adverse effects seen with penicillamine include hypersensitivity reactions, blood dyscrasias such as neutropenia, hemolytic anemia, thrombocytopenia, increased liver enzymes, anorexia, nausea, and vomiting. Penicillamine should not be used in patients with a penicillin allergy.

Based on these adverse effects, the recommended monitoring for penicillamine therapy included a complete blood count with differential, urinalysis, and LFTs on days 1, 14, and 28 of therapy, and monthly thereafter. Therapy with penicillamine is to be discontinued if a patient’s absolute neutrophil count (ANC) declines to <1,200 cells/mm³.

Follow-up to chelation therapy includes rechecking a BLL at 7 to 21 days post-chelation therapy. At the end of each treatment, BLLs usually decline to <25 mcg/dL. If levels are >25 mcg/dL, retreatment may be necessary. If a patient was treated with dimercaprol or CaNa2EDTA, oral succimer may be continued as an outpatient if BLLs are still >25 mcg/dL (providing that the child returns to a lead-free environment). It is important to note that if BLLs are rechecked too early after chelation therapy (<5 to 7 days), the BLL can be a result of “lead rebound.” Lead rebound is the phenomenon that occurs when lead in the body has re-equilibrated after chelation therapy as lead leaves the soft tissues and enters the blood, therefore, falsely elevating the BLL.

The child should not be returned to a lead-tainted environment. This may be more of a social problem than financial. The child may be made to remain in the hospital or placed in some other setting until their home is made lead-free. Once a child is in a safe environment, pediatric follow-up visits for children treated with chelation therapy should be biweekly for the first 6 to 8 weeks, then monthly for the next 10 to 12 months.

Educating Parents About the Prevention of Childhood Lead Poisoning

Pharmacists and other health care providers can help in educating parents and provide interventions that will reduce their children’s exposure to lead. By some simple interventional techniques, lead poisoning in children can be prevented.

Housekeeping Interventions

Many of the most common sources of lead poisoning are in the household. Some of the most important interventions around the household are very simple, yet can provide the most benefit in reducing a child’s exposure to lead.³

	Make sure that the child does not have access to peeling paint. If peeling paint is not removed, make the area inaccessible to a child (eg, placing furniture in front of the site of the peeling paint).
	For homes built before 1960, since they are likely to have paint with a high lead content, hardwood floor and painted surfaces should be wet-mopped with a high phosphate solution (5% to 8%), such as trisodium phosphate, which usually can be found in hardware or home improvement stores. Some dishwasher machine soap powders also have a high trisodium content.
	Do not vacuum hard surfaces, because this activity will scatter lead-tainted dust.
	Children’s increased hand-to- mouth activity is the leading portal of entry of lead to the GI tract. Washing your child’s face and hands frequently is key to preventing the ingestion of lead. It is important to wash your child’s hands prior to bedtime, especially for children who suck their thumbs as they sleep. Frequent washing of your child’s toys and pacifiers is also important.
	If an inspection reveals that the house has lead-based paint, the family should not attempt to remove the paint themselves. Improperly removed paint will only make the lead airborne, directly contaminating the family and more household surfaces. Professionals should perform removal of paint. The family should not be in the home during paint removal or renovations.

Nutritional Interventions

	Be sure that your child eats regular nutritious meals, because more lead is absorbed on an empty stomach.
	Your child’s diet should contain adequate amounts of calcium and iron. The body will “recognize” lead as being calcium or iron in diets deficient in these minerals, and absorb lead more readily.
	Do not store food in containers that may contain lead—these include open cans, especially imported food stored in cans, decorative pottery or porcelain, or leaded crystal.

Other Interventions

	Keep your child away from material that may contain lead, or from lead-contaminated clothes that are used in work or hobbies.
	If the lead content of your water is higher than the drinking water standard (to get information on how to get your water tested call the EPA’s Safe Drinking Water Hotline at 800-426-4791), let the water run for several minutes before using it. Use only cold tap water for drinking, cooking, and preparing infant formula.

Screening for Lead Poisoning
in Children

Since nearly all U.S. children are at risk for lead poisoning, some may advocate universal screening for BLL. Unless it can be shown that the community in which a child lives does not have a high rate of lead poisoning, the following screening schedule is recommended.³

After questioning the parent or caregiver about sources of lead in the child’s environment, low-risk children should be screened for BLL at 12 months then again at 24 months, if resources allow. If a child is at higher risk for lead poisoning, the screening process should begin at 6 months of age. Children at higher risk include those who live in housing built before 1960, those who live in communities with a higher incidence of lead poisoning, children with parents whose work or hobbies involve lead, or children who live near lead smelters or other industries where lead is processed. Children who engage in pica or have noticeably increased hand-to-mouth activity may also be considered at higher risk.

Children who have unexplained seizures or other symptoms of lead poisoning, such as neurologic symptoms, abdominal pain, or anemia, should also have their blood level measured.

Conclusion

Pharmacists can play an instrumental role in the treatment and prevention of childhood lead poisoning. Providing drug information to physicians and other health care providers regarding chelation therapy for lead poisoning is one avenue in which pharmacists can play a role. An even more important role in which pharmacists can participate is increasing lead poisoning awareness in the community. Providing pamphlets and other literature and offering counseling sessions to parents, especially in higher-risk areas, on ways to reduce a child’s exposure to lead is simple, yet invaluable advice. It is this anticipatory guidance on preventing lead poisoning that should become a routine role for the pharmacist in any type of pediatric setting.

(For more information on lead poisoning in children, call the National Lead Information Center at 800-LEAD-FYI.)

References

1. Pirkel JL, Brody DJ, Gunter EW, et al. The decline in blood lead levels in the United States: the National Heath and Nutrition Examination Surveys (NHANES). JAMA 1994: 272: 284-291.
2. Philadelphia Department of Public Health Childhood Lead Poisoning Prevention Program. Recommendations for the Screening and Management of Young Children Potentially Exposed to Lead. November 1997.
3. Centers for Disease Control, U.S. Dept. of HHS. Preventing Lead Poisoning in Young Children. October 1991.
4. Klaasen, CD. "Heavy Metals and Heavy Metal Antagonists" in Goodman and Gilman’s The Pharmacological Basic of Therapeutics. Eighth Edition; ed. Goodman Gilman, A, Rall TW, et al. Elmsford, NY: 1990, 1592-1598.
5. Junghans, RP, Sacher, RA. "Iron Metabolism and Hypochromic Anemias" in Clinical Hematology and Fundamentals of Hemostasis; ed. Pittiglio, DH, Sacher RA. Philadelphia: 1987, 41-47.
6. Chao, J, Kikano, G. Lead poisoning in children. American Family Physician. 1993:47: 113-120.

[Introduction] [References]

Behavioral Objectives

After completing this continuing education article, the pharmacist should be able to:

1. Identify sources of lead in a child’s environment.

2. Describe the mechanism and manifestations of lead poisoning in children.

3. Be familiar with diagnostic tests used for detecting lead toxicity.

4. Outline a therapeutic plan for chelation treatment of childhood lead poisoning.

5. Counsel a parent or care-giver regarding methods in which they may reduce their child’s exposure to lead.