Lead poisoning

On this page, risk factors, complications.

Lead poisoning occurs when lead builds up in the body, often over months or years. Even small amounts of lead can cause serious health problems. Children younger than 6 years are especially vulnerable to lead poisoning, which can severely affect mental and physical development. At very high levels, lead poisoning can be fatal.

Lead-based paint and lead-contaminated dust in older buildings are common sources of lead poisoning in children. Other sources include contaminated air, water and soil. Adults who work with batteries, do home renovations or work in auto repair shops also might be exposed to lead.

There is treatment for lead poisoning, but taking some simple precautions can help protect you and your family from lead exposure before harm is done.

Initially, lead poisoning can be hard to detect — even people who seem healthy can have high blood levels of lead. Signs and symptoms usually don't appear until dangerous amounts have accumulated.

Lead poisoning symptoms in children

Signs and symptoms of lead poisoning in children include:

  • Developmental delay
  • Learning difficulties
  • Irritability
  • Loss of appetite
  • Weight loss
  • Sluggishness and fatigue
  • Abdominal pain
  • Constipation
  • Hearing loss
  • Eating things, such as paint chips, that aren't food (pica)

Lead poisoning symptoms in newborns

Babies exposed to lead before birth might:

  • Be born prematurely
  • Have lower birth weight
  • Have slowed growth

Lead poisoning symptoms in adults

Although children are primarily at risk, lead poisoning is also dangerous for adults. Signs and symptoms in adults might include:

  • High blood pressure
  • Joint and muscle pain
  • Difficulties with memory or concentration
  • Mood disorders
  • Reduced sperm count and abnormal sperm
  • Miscarriage, stillbirth or premature birth in pregnant women

From Mayo Clinic to your inbox

Lead is a metal that occurs naturally in the earth's crust, but human activity — mining, burning fossil fuels and manufacturing — has caused it to become more widespread. Lead was also once used in paint and gasoline and is still used in batteries, solder, pipes, pottery, roofing materials and some cosmetics.

Lead in paint

Lead-based paints for homes, children's toys and household furniture have been banned in the United States since 1978. But lead-based paint is still on walls and woodwork in many older homes and apartments. Most lead poisoning in children results from eating chips of deteriorating lead-based paint.

Water pipes and imported canned goods

Lead pipes, brass plumbing fixtures and copper pipes soldered with lead can release lead particles into tap water. Lead solder in food cans, banned in the United States, is still used in some countries.

Other sources of lead exposure

Lead sometimes can also be found in:

  • Soil. Lead particles from leaded gasoline or paint settle on soil and can last years. Lead-contaminated soil is still a major problem around highways and in some urban settings. Some soil close to walls of older houses contains lead.
  • Household dust. Household dust can contain lead from lead paint chips or from contaminated soil brought in from outside.
  • Pottery. Glazes found on some ceramics, china and porcelain can contain lead that can leach into food served or stored in the pottery.
  • Toys. Lead is sometimes found in toys and other products produced abroad.
  • Cosmetics. Tiro, an eye cosmetic from Nigeria, has been linked to lead poisoning. Kohl is another eye makeup that may contain lead.
  • Herbal or folk remedies. Lead poisoning has been linked to greta and azarcon, traditional Hispanic medicines, as well as some from India, China and other countries.
  • Mexican candy. Tamarind, an ingredient used in some candies made in Mexico, might contain lead.
  • Lead bullets. Time spent at firing ranges can lead to exposure.
  • Occupations. People are exposed to lead and can bring it home on their clothes when they work in auto repair, mining, pipe fitting, battery manufacturing, painting, construction and certain other fields.

Factors that may increase your risk of lead poisoning include:

  • Age. Infants and young children are more likely to be exposed to lead than are older children. They might chew paint that flakes off walls and woodwork, and their hands can be contaminated with lead dust. Young children also absorb lead more easily, and it's more harmful for them than it is for adults and older children.
  • Living in an older home. Although the use of lead-based paints has been banned since the 1970s, older homes and buildings often retain remnants of this paint. People renovating an older home are at even higher risk.
  • Certain hobbies. Making stained glass and some jewelry requires the use of lead solder. Refinishing old furniture might put you in contact with layers of lead paint.
  • Living in developing countries. Developing countries often have less strict rules regarding exposure to lead than do developed countries. American families who adopt a child from another country might want to have the child's blood tested for lead poisoning. Immigrant and refugee children also should be tested.

Lead can harm an unborn child. If you're pregnant or planning a pregnancy, be especially careful to avoid exposure to lead.

Exposure to even low levels of lead can cause damage over time, especially in children. The greatest risk is to brain development, where irreversible damage can occur. Higher levels can damage the kidneys and nervous system in both children and adults. Very high lead levels may cause seizures, unconsciousness and death.

Simple measures can help protect you and your family from lead poisoning:

  • Wash hands and toys. To help reduce hand-to-mouth transfer of contaminated dust or soil, wash your children's hands after outdoor play, before eating and at bedtime. Wash their toys regularly.
  • Clean dusty surfaces. Clean your floors with a wet mop and wipe furniture, windowsills and other dusty surfaces with a damp cloth.
  • Remove shoes before entering the house. This will help keep lead-based soil outside.
  • Run cold water. If you have older plumbing containing lead pipes or fittings, run your cold water for at least a minute before using. Don't use hot tap water to make baby formula or for cooking.
  • Prevent children from playing on soil. Provide them with a sandbox that's covered when not in use. Plant grass or cover bare soil with mulch.
  • Eat a healthy diet. Regular meals and good nutrition might help lower lead absorption. Children especially need enough calcium, vitamin C and iron in their diets to help keep lead from being absorbed.
  • Keep your home well maintained. If your home has lead-based paint, check regularly for peeling paint and fix problems promptly. Try not to sand, which generates dust particles that contain lead.

Jan 21, 2022

  • Sample JA. Childhood lead poisoning: Clinical manifestations and diagnosis. https://www.uptodate.com/contents/search. Accessed Nov. 10, 2021.
  • Lead FAQs. Centers for Disease Control and Prevention. https://www.cdc.gov/nceh/lead/faqs/lead-faqs.htm. Accessed Nov. 11, 2021.
  • Sample JA. Childhood lead poisoning: Management. https://www.uptodate.com/contents/search. Accessed Nov. 10, 2021.
  • Markowitz M. Lead poisoning: An update. Pediatrics in Review. 2021; doi:10.1542/pir.2020-0026.
  • Lead poisoning. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/lead-poisoning-and-health. Accessed Nov. 11, 2021.
  • Goldman RH, et al. Lead exposure and poisoning in adults. https://www.uptodate.com/contents/search. Accessed Nov. 10, 2021.
  • Protect your family from sources of lead. U.S. Environmental Protection Agency. https://www.epa.gov/lead/protect-your-family-sources-lead. Accessed Nov. 11, 2021.
  • Sample JA. Childhood lead poisoning: Exposure and prevention. https://www.uptodate.com/contents/search. Accessed Nov. 10, 2021.
  • What are possible health effects from lead exposure? Agency for Toxic Substances and Disease Registry. https://www.atsdr.cdc.gov/csem/leadtoxicity/physiological_effects.html. Accessed Nov. 11, 2021.
  • Ferri FF. Lead poisoning. In: Ferri's Clinical Advisor 2022. Elsevier; 2022. https://www.clinicalkey.com. Accessed Nov. 22, 2021.
  • Diseases & Conditions
  • Lead poisoning symptoms & causes


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National Academies Press: OpenBook

Environmental Medicine: Integrating a Missing Element into Medical Education (1995)

Chapter: case study 19: lead toxicity.

essay on lead poisoning

1 Lead Toxicity

This monograph is one in a series of self-instructional publications designed to increase the primary care provider’s knowledge of hazardous substances in the environment and to aid in the evaluation of potentially exposed patients. See page 27 for more information about continuing medical education credits and continuing education units.

essay on lead poisoning


Public Health Service

Agency for Toxic Substances and Disease Registry

A hyperactive 5-year-old with disturbed hearing and hypochromic anemia

A 5-year-old boy is brought to your office by his mother, who is concerned that her child is hyperactive. At a parent-teacher conference last week, the kindergarten teacher said that the boy seems impulsive and has trouble concentrating, and recommended evaluation by a physician as well as by the school psychologist. The mother states that he has always seemed restless and easily distracted, but that these first 6 months in kindergarten have been especially trying.

Family history reveals that the boy lives with his sister, mother, and maternal grandparents in an older suburb of your community. The child’s monthly weekend visits to his father’s house are working out fine. However, he seems to be fighting more with his sister, who has an attention-deficit disorder and is repeating first grade. Since the mother moved in with her parents after her divorce 4 years ago, she has worked with the grandfather in an automobile radiator repair shop, where her children often come to play after school. She was just laid off, however, and expressed worry about increasing financial dependence on her parents. She also worries that the grandfather, who has gout and complains increasingly of abdominal pain, may become even more irritable when he learns that she is pregnant. Her third child is due in 4 months.

On chart review, you see that the boy was last seen in your clinic for his preschool physical 1 year ago, results of which were normal. A note describes a very active 4-year-old who could dress himself without help but could not correctly name the primary colors. His vision was normal, but hearing acuity was below normal, and speech and language were slightly delayed. Immunizations are up to date.

Further history on that visit indicated adequate diet, with no previous pica. Spun hematocrit was diminished at 30%. Peripheral blood smear showed hypochromia and microcytosis. There was no evidence of blood loss, and stool examination was negative for occult blood. The diagnosis was “mild iron deficiency anemia,” and iron therapy was prescribed. The family failed to keep several follow-up appointments, but the child did apparently complete the prescribed 3-month course of iron supplements. He receives no medications at this time and has no known allergies.

On physical examination today, you note that the boy is in the tenth percentile for height and weight. His attention span is very short, making him appear restless, and he has difficulty following simple instructions. Except for language and social skills, he has reached most important developmental milestones.

essay on lead poisoning

(a) What should be included in this boy’s problem list?


(b) List several possible causes for the anemia.

(c) What tests would you order to confirm or rule out your diagnosis?

Answers are incorporated in Challenge answers (11) through (14) on page 25.

Who’s at Risk

❑ Young children have a great potential for lead exposure and are especially susceptible to its toxic effects.

❑ Since blood lead readily crosses the placenta, lead poses a substantial threat to the developing fetus.

❑ Workers may bring lead dust home on skin and clothes and unknowingly expose family members.

By and large, children show a greater sensitivity to lead’s effects than adults do. The incomplete development of the blood-brain barrier in very young children (up to 36 months of age) increases the risk of lead’s entry into the developing nervous system, which can result in prolonged neurobehavioral disorders. Children absorb and retain more lead in proportion to their weight than do adults. Young children also show a greater prevalence of iron deficiency, a condition that can increase gastrointestinal absorption of lead.

No economic or racial subgroup of children is free from the risk of having blood lead levels high enough to cause adverse health effects. In 1984, approximately 17% of children in the United States were estimated to be at risk of lead poisoning. Sizable numbers of children from families with incomes well above the poverty line have been reported to have elevated blood lead levels. The prevalence of elevated levels, nevertheless, remains highest among inner-city, underprivileged children who live in deteriorating pre-1970s housing containing leaded-paint surfaces. Lead in paint and lead in soil and dust are the principal sources of exposure.

The percentage of African-American children affected by lead is disproportionate to their number in the U.S. population. In 1984 African-American children constituted 46% of the children at risk. The family income categories of these children show that the higher percentage is related to economic factors. African-American children are over represented in the poor and low-income groups as well as in inner-city areas. Other minorities are similarly affected; 15% of Mexican-Americans and 20% of Puerto Rican-Americans exceed a blood lead cutoff of 15 µg/dL As blood lead levels in the general population are declining because of restrictions on leaded gasoline use, race and income will become better indicators of the likelihood of exposure to leaded paint and, consequently, elevated blood lead levels.

Since lead readily crosses the placenta, the fetus is at risk. Fetal exposure can cause potentially adverse neurologic effects in utero and during postnatal development. According to the Public Health Service, in 1984, more than 400,000 fetuses were exposed to lead through maternal blood lead concentrations associated with early developmental effects.

More than 1 million workers in over 100 different occupations may be exposed to lead. In lead-related industries, workers not only may inhale lead dust and lead oxide fumes, but may eat, drink, and smoke in or near contaminated areas, increasing the probability of lead ingestion. If showers and changes of clothing are not provided, workers can bring lead dust home on their skin, shoes, and clothing, thus inadvertently exposing family members.

Exposure Pathways

❑ The primary sources of environmental exposure to lead are leaded paint, auto emissions, and drinking water.

Lead is a naturally occurring element that has been used almost since the beginning of civilization. Because of the many industrial activities that have brought about its wide distribution, lead is ubiquitous in the environment today. All humans have lead in their bodies, primarily as a result of exposure to manmade sources.

Today, the major environmental sources of metallic lead and its salts are paint, auto exhaust, food, and water. For children, the most important pathways are ingestion of chips from lead-painted surfaces, inhalation of lead from automobile emissions, food from lead-soldered cans, drinking water from lead-soldered plumbing, and medications in the form of folk remedies.

❑ A wide variety of workers, hobbyists, and substance abusers may encounter potentially high levels of lead. Certain folk remedies may also cause lead poisoning.

Automobile emissions have been an important source of lead exposure for urban residents, particularly in areas with congested traffic. Although inhalation of lead from gasoline is no longer considered a public health problem, the lead from dust in automobile emissions has been deposited in the soil. Children playing near roads and freeways may come in contact with contaminated soil.

The lead content of paint was not regulated until 1977. Many older structures, residential and commercial, have leaded paint that is peeling, flaking, and chipping. Children can ingest loose paint as a result of pica (compulsive eating of nonfood items) and through mouthing of items contaminated with lead from paint, dust, and soil. High levels of lead in soil and house dust have been associated with increased blood lead levels in children.

❑ Lead enters the body primarily through ingestion and inhalation.

Food may contain lead from the environment or from containers. Agricultural vehicles are not required to use unleaded gasoline; consequently, lead can be deposited on and retained by crops, particularly leafy vegetables. Acidic foods have been found to leach lead from lead solder in cans and lead glazes used in making pottery and ceramicware. Water from leaded pipes, soldered plumbing, or water coolers is another potential source of lead exposure. Stationary or point sources of lead include mines and smelters.

Several folk remedies used in this country have been shown to contain large amounts of lead. Two Mexican folk remedies are azarcon and greta, which are used to treat “empacho,” a colic-like illness. Azarcon and greta are also known as liga, Maria Luisa, alarcon, coral, and rueda . Lead-containing remedies and cosmetics used by some Asian communities are chuifong tokuwan, pay-looah, ghasard, bali goli, and kandu . Middle Eastern remedies and cosmetics include alkohl, kohl, surma, saoott, and cebagin .

In addition to these environmental sources, many occupations, hobbies, and other activities result in potential exposures to high levels of lead and can put the entire family at risk of lead poisoning. Sources of lead exposure are listed below. Lead-glazed pottery, particularly if it is imported, is a potential source of exposure that is often overlooked. Even “safe” ceramicware can become harmful; dishwashing may chip or wear off the protective glaze and expose lead-containing pigments.

Inorganic lead enters the body primarily through inhalation and ingestion and does not undergo biologic transformation. In contrast, organic lead, found primarily in gasoline as tetraethyl lead, enters the body through inhalation and skin contact and is metabolized in the liver. In 1976 and in 1984, federal regulation drastically reduced the amount of lead in gasoline, and today organic lead in gasoline is not as great an environmental concern in the United States as it is in other countries, where it remains a serious hazard.

Sources of lead exposure


Plumbers, pipe fitters

Lead miners

Auto repairers

Glass manufacturers


Plastic manufacturers

Lead smelters and refiners

Police officers

Steel welders or cutters

Construction workers

Rubber product manufacturers

Gas station attendants

Battery manufacturers

Bridge reconstruction workers

Firing range instructors


Lead-containing paint

Soil/dust near lead industries, roadways, lead-painted homes

Plumbing leachate


Leaded gasoline

Hobbies and Related Activities

Glazed pottery making

Target shooting at firing ranges

Lead soldering (e.g., electronics)

Preparing lead shot, fishing sinkers

Stained-glass making

Car or boat repair

Home remodeling

Substance Use

Folk remedies

“Health foods”

Moonshine whiskey

Gasoline “huffing”

Biologic Fate

❑ Once in the bloodstream, lead is primarily distributed among three compartments—blood, soft tissue, and mineralizing tissue. The bones and teeth of adults contain more than 95% of total lead in the body.

❑ In times of stress, the body can mobilize lead stores, thereby increasing the level of lead in the blood.

❑ The body accumulates lead over a lifetime and normally releases it very slowly.

In the human body, inorganic lead is not metabolized but is directly absorbed, distributed, and excreted. The rate at which lead is absorbed depends on its chemical and physical form and on the physiologic characteristics of the exposed person (e.g., nutritional status and age). Inhaled lead deposited in the lower respiratory tract is completely absorbed. The amount of lead absorbed from the GI tract of adults is typically 10% to 15% of the ingested quantity; for pregnant women and children, the amount absorbed can increase to as much as 50%. The quantity absorbed increases significantly under fasting conditions and with iron or calcium deficiency.

Once in the blood, lead is distributed primarily among three compartments—blood, soft tissue (kidney, bone marrow, liver, and brain), and mineralizing tissue (bones and teeth). Mineralizing tissue contains about 95% of the total body burden of lead in adults.

The lead in mineralizing tissues accumulates in subcompartments that differ in the rate at which lead is resorbed. In bone, there is both a labile component, which readily exchanges lead with the blood, and an inert pool. The lead in the inert pool poses a special risk because it is a potential endogenous source of lead. When the body is under physiologic stress such as pregnancy, lactation, or chronic disease, this normally inert lead can be mobilized, increasing the lead level in blood. Because of these mobile lead stores, significant drops in a person’s blood lead level can take several months or sometimes years, even after complete removal from the source of lead exposure.

Of the lead in the blood, 99% is associated with erythrocytes; the remaining 1% is in the plasma, where it is available for transport to the tissues. The blood lead not retained is either excreted by the kidneys or through biliary clearance into the gastrointestinal tract. In single-exposure studies with adults, lead has a half-life, in blood, of approximately 25 days; in soft tissue, about 40 days; and in the non-labile portion of bone, more than 25 years. Consequently, after a single exposure a person’s blood lead level may begin to return to normal; the total body burden, however, may still be elevated.

For lead poisoning to develop, major acute exposures to lead need not occur. The body accumulates this metal over a lifetime and releases it slowly, so even small doses, over time, can cause lead poisoning. It is the total body burden of lead that is related to the risk of adverse effects.

Physiologic Effects

❑ Lead affects primarily the peripheral and central nervous systems, the blood cells, and metabolism of vitamin D and calcium. Lead also causes reproductive toxicity.

Whether lead enters the body through inhalation or ingestion, the biologic effects are the same; there is interference with normal cell function and with a number of physiologic processes. The lowest observable blood lead levels associated with specific health effects in chronically exposed children and adults are shown in Figure 1 .

Neurologic Effects

❑ Neurologic deficits, as well as other effects caused by lead poisoning, may be irreversible.

The most sensitive target of lead poisoning is the nervous system. In children, neurologic deficits have been documented at exposure levels once thought to cause no harmful effects. In addition to the lack of a precise threshold, childhood lead toxicity may have permanent effects. One study showed that damage to the central nervous system (CNS) that occurred as a result of lead exposure at age 2 resulted in continued deficits in neurologic development, such as

❑ Effects in children generally occur at lower blood lead levels than in adults.

❑ The developing nervous system in children can be affected adversely at blood lead levels of less than 10 µg/dL.

Figure 1 . Effects of inorganic lead on children and adults— lowest observable adverse effect levels

essay on lead poisoning

Adapted from ATSDR, Toxicological Profile for Lead (1989)

lower IQ scores and cognitive deficits, at age 5. In another study that measured total body burden, primary school children with high tooth lead levels but with no known history of lead poisoning had larger deficits in psychometric intelligence scores, speech and language processing, attention, and classroom performance than children

with lower levels of lead. A 1990 follow-up report of children with elevated lead levels in their teeth noted a sevenfold increase in the odds of failure to graduate from high school, lower class standing, greater absenteeism, more reading disabilities, and deficits in vocabulary, fine motor skills, reaction time, and hand-eye coordination 11 years later. The reported effects are more likely caused by the enduring toxicity of lead than by recent excessive exposures because the blood lead levels found in the young adults were low (less than 10 micrograms per deciliter [µg/dL]).

Hearing acuity, particularly at higher frequencies, has been found to decrease with increasing blood lead levels. Hearing loss may contribute to the apparent learning disabilities or poor classroom behavior exhibited by children with lead intoxication.

Adults also experience CNS effects at relatively low blood lead levels, manifested by subtle behavioral changes, fatigue, and impaired concentration. Peripheral nervous system damage, primarily motor, is seen mainly in adults. Peripheral neuropathy with mild slowing of nerve conduction velocity has been reported in asymptomatic lead workers. Lead neuropathy is believed to be a motor neuron, anterior horn cell disease with peripheral dying-back of the axons. Frank wrist drop occurs only as a late sign of lead intoxication.

Hematologic Effects

❑ Lead inhibits several enzymes that are critical to the synthesis of heme.

❑ Lead poisoning in children only rarely results in anemia.

Lead inhibits the body’s ability to make hemoglobin by interfering with several enzymatic steps in the heme pathway. Ferrochelatase, which catalyzes the insertion of iron into protoporphyrin IX, is quite sensitive to lead. A decrease in the activity of this enzyme results in an increase of the substrate, erythrocyte protoporphyrin (EP), in the red blood cells. Recent data indicate that the EP level, which has been used to screen for lead toxicity in the past, is not sufficiently sensitive at lower levels of blood lead and is therefore not as use ful a screening test for lead poisoning as previously thought. (See Laboratory Evaluation for further discussion of EP testing.)

Lead can induce two types of anemia. Acute high-level lead poisoning has been associated with hemolytic anemia. In chronic lead poisoning, lead induces anemia by both interfering with erythropoiesis and by diminishing red blood cell survival. It should be emphasized, however, that anemia is not an early manifestation of lead poisoning and is evident only when the blood lead level is significantly elevated for prolonged periods.

Endocrine Effects

❑ Lead interferes with a hormonal form of vitamin D, which affects multiple processes in the body, including cell maturation and skeletal growth.

A strong inverse correlation exists between blood lead levels and levels of vitamin D. Because the vitamin D-endocrine system is responsible in large part for the maintenance of extra- and intracellular calcium homeostasis, it is likely that lead impairs cell growth and maturation and tooth and bone development.

Renal Effects

❑ Lead-induced chronic renal insufficiency may result in gout.

A direct effect on the kidney of long-term lead exposure is nephropathy. Impairment of proximal tubular function manifests in aminoaciduria, glycosuria, and hyperphosphaturia (a Fanconi-like syndrome). There is also evidence of an association between lead exposure and hypertension, an effect that maybe mediated through renal mechanisms. Gout may develop as a result of lead-induced hyperuricemia, with selective decreases in the fractional excretion of uric acid before a decline in creatinine clearance. Renal failure accounts for 10% of deaths in patients with gout.

Reproductive and Developmental Effects

❑ Maternal lead stores readily cross the placenta, placing the fetus at risk.

An increased frequency of miscarriages and stillbirths among women working in the lead trades was reported as early as the turn of the century. Although the data concerning exposure levels are incomplete, these effects were probably a result of far greater exposures than are currently found in lead industries. Reliable dose-effect data for reproductive effects in women are still lacking today.

Increasing evidence indicates that lead not only affects the viability of the fetus, but development as well. Developmental consequences of prenatal exposure to low levels of lead include reduced birth weight and premature birth. Lead is an animal teratogen; however, most studies in humans have failed to show a relationship between lead levels and congenital malformations.

The effects of lead on the male reproductive system in humans have not been well characterized. The available data support a tentative conclusion that testicular effects, including reduced sperm counts and motility, may result from chronic exposure to lead.

Carcinogenic Effects

❑ EPA’s Science Advisory Board has recommended that lead be considered a probable human carcinogen.

Case reports have implicated lead as a potential renal carcinogen in humans, but the association remains uncertain. Soluble salts, such as lead acetate and lead phosphate, have been reported to cause kidney tumors in rats.

Clinical Evaluation

History and physical examination.

❑ The first signs of lead poisoning in children are often subtle neurobehavioral problems that adversely affect classroom behavior and social interaction.

❑ Speech or hearing impairments, or both, are not uncommon in lead-exposed children.

Medical evaluation of a patient with suspected lead exposure includes a full workup and medical history. Clues to potential exposure are often obtained by discussing the following with the family:

occupational history of all home occupants

family history, including use of unusual medicines

location, age, and physical condition of residence, school, day-care center, etc.

home remodeling activities

condition of household pets

hobbies of all family members

use of imported or glazed ceramics

drinking water source and type of pipe

nutritional status

proximity to industrial facilities and hazardous waste sites

The physical examination should include special attention to the hematologic, cardiovascular, gastrointestinal, and renal systems. The nervous system, including behavioral changes, should be carefully evaluated. A purplish line on the gums (lead line) is rarely seen today, but if present, usually indicates severe and prolonged lead poisoning.

For children, hearing, speech, and other developmental milestones should be carefully evaluated and documented. In certain geographic areas, iron deficiency is common in children 9 to 24 months of age. Since iron and calcium deficiencies are known to enhance the absorption of lead and to aggravate pica, it is especially important to assess the nutritional status of young children.

Signs and Symptoms

❑ Most persons with lead toxicity are not overtly symptomatic.

Because of differences in individual susceptibility, symptoms of lead intoxication and their onset may vary. With increasing exposure, the severity of symptoms can be expected to increase. Those symptoms most often associated with varying degrees of lead toxicity are listed below. In symptomatic lead intoxication, blood lead levels generally range from 35 to 50 µg/dL in children and 40 to 60 µg/dL in adults. Severe toxicity is frequently found in association with blood lead levels of 70 µg/dL or more in children and 100 µg/dL or more in adults.

Continuum of signs and symptoms associated with lead toxicity

Mild Toxicity

Myalgia or paresthesia

Mild fatigue


Occasional abdominal discomfort

Moderate Toxicity

General fatigue

Difficulty concentrating

Muscular exhaustibility

Diffuse abdominal pain

Weight loss


Severe Toxicity

Paresis or paralysis

Encephalopathy-may abruptly lead to seizures, changes in consciousness, coma, and death

Lead line (blue-black) on gingival tissue

Colic (intermittent, severe abdominal cramps)

Some of the hematologic signs of lead poisoning mimic other diseases or conditions. In the differential diagnosis of microcytic anemia, lead poisoning can usually be ruled out by obtaining a venous blood lead concentration; if the blood lead level is less than 25 µg/dL, the anemia usually reflects iron deficiency or hemoglobinopathy. Two rare diseases, acute intermittent porphyria and coproporphyria, also result in heme abnormalities similar to those of lead poisoning.

Other effects of lead poisoning can be misleading. Patients exhibiting neurologic signs due to lead poisoning have been treated only for peripheral neuropathy or carpal tunnel syndrome, delaying treatment for lead intoxication. Failure to correctly diagnose lead-induced gastrointestinal distress has led to inappropriate abdominal surgery.

Laboratory Evaluation

If pica or accidental ingestion of lead-containing objects (such as curtain weights or fishing sinkers) is suspected, an abdominal radiograph should be taken. Hair analysis is not usually an appropriate assay for lead toxicity because no correlation has been found between the amount of lead in the hair and the exposure level. The probability of environmental lead contamination of a laboratory specimen and inconsistent sample preparation make the results of hair analysis difficult to interpret. Suggested laboratory tests to evaluate lead intoxication include the following:

CBC with peripheral smear

Blood lead level

Erythrocyte protoporphyrin level

BUN and creatinine level

❑ Basophilic stippling is not always seen in lead-poisoned patients.

CBC with Peripheral Smear . In a lead-poisoned patient, the hematocrit and hemoglobin values may be slightly to moderately low. The differential and total white count may appear normal. The peripheral smear may be either normochromic and normocytic or hypochromic and microcytic. Basophilic stippling is usually seen only in patients who have been significantly poisoned for a prolonged period. Eosinophilia may appear in patients with lead toxicity but does not show a clear dose-response effect.

❑ The best screening and diagnostic test for lead poisoning is a blood lead level.

Blood Lead Level. A blood lead level is the most useful screening and diagnostic test for lead exposure. A blood lead level reflects lead’s dynamic equilibrium between absorption, excretion, and deposition in soft- and hard-tissue compartments. For chronic exposures, blood lead levels often underrepresent the total body burden; nevertheless, it is the most widely accepted and commonly used measure of lead exposure. Blood lead levels respond relatively rapidly to abrupt or intermittent changes in lead intake (for example, ingestion of lead paint chips by children) and, within a limited range, bear a linear relationship to those intake levels.

Lead is most harmful to children under 6 years of age. Every child who has a developmental delay, behavioral disorder, or speech impairment, or who may have been lead-exposed, should be considered for a blood lead test. Equally important, siblings, housemates, and playmates of children with suspected lead toxicity probably have similar exposures to lead and should be promptly screened. For occupationally exposed adults, consult the federal lead standard for the mandated type and frequency of lead screening (p. 20, Workplace, Air).

Today, the average blood lead level in the U.S. population is below 10 µg/dL, down from an average of 16 µg/dL (in the 1970s), the level before the legislated removal of lead from gasoline. A blood lead level of 10 µg/dL is about 3 times higher than the average level found in some remote populations.

The levels defining lead poisoning have been progressively declining. (See Biologic Guidelines in Standards and Regulations.) Currently, the consensus level of concern for children is 10 to 14 µg/dL (see Table 1 ). Effects on stature have been reported to begin at levels as low as 4 µg/dL, the present limit for accurate blood lead measurement. Taken together, effects occur over a wide range of blood lead concentrations, with no indication of a threshold. No safe level has yet been found for children. Even in adults, effects are being discovered at lower and lower levels as more sensitive analyses and measures are developed.

❑ Using an EP or ZPP assay to screen children for lead poisoning is not as useful as once thought.

EP and ZPP Levels . Until recently, the test of choice for screening asymptomatic children and other populations at risk was erythrocyte protoporphyrin (EP), commonly assayed as zinc protoporphyrin (ZPP). An elevated level of protoporphyrin in the blood is a result of accumulation secondary to enzyme dysfunction in the erythrocytes. It reaches a steady state in the blood only after the entire population of circulating erythrocytes has turned over, about 120 days. Consequently, it lags behind blood lead levels and is an indirect measure of long-term lead exposure.

Table 1 . Interpretation of blood lead test results and follow-up activities: class of child based on blood lead concentration

The major disadvantage of using EP (ZPP) testing as a method for lead screening is that it is not sensitive at the lower levels of lead poisoning. Data from the second National Health and Nutrition Examination Survey (NHANES II) indicate that 58% of 118 children with blood lead levels above 30 µg/dL had EP levels within normal limits. This finding shows that a significant number of children with lead toxicity would be missed by reliance on EP (ZPP) testing alone as the screening tool. An EP (ZPP) level is still useful in screening patients for iron deficiency anemia.

Normal values of ZPP are usually below 35 µg/dL. Hyperbilirubinernia (jaundice) will cause falsely elevated readings when the hematofluorometer is used. EP is elevated in iron deficiency anemia and in sickle cell and other hemolytic anemias. In erythropoietic protoporphyria, an extremely rare disease, EP is markedly elevated (usually above 300 µg/dL).

❑ Renal function may be impaired in lead-exposed persons.

BUN, Creatinine, and Urinalysis . These parameters may reveal only late, significant effects of lead on renal function. Renal function in adults can also be assessed by measuring the fractional excretion of uric acid (normal range 5% to 10%; less than 5% in saturnine gout; greater than 10% in Fanconi syndrome).

Treatment and Management

❑ All therapeutic chelating agents have potentially adverse side effects and should be used cautiously.

❑ The type of therapy required will normally depend on the patient’s blood lead level. Asymptomatic patients with blood lead levels below 25 µg/dL usually require only separation from the source of exposure.

It is not sufficient to provide treatment only; the patient and lead source must be permanently separated. After diagnosing lead poisoning, the physician should call upon the resources of the local health authority to determine the lead source (e.g., home, workplace). If the lead poisoning is caused by leaded paint in the home, the patient and all other family members should be rehoused until the home has undergone safe and satisfactory lead abatement. Family members and other persons likely to have been exposed should be tested for lead poisoning. Steps should be taken to identify and correct dietary deficiencies, particularly of calcium and iron, and to educate family members on the preventable hazards of lead.

The most reliable index of exposure is a measurement of blood lead concentration. In those asymptomatic children having blood lead levels below 25 µg/dL, treatment is probably not indicated, and removal from the source is the most important action. Patient followup to confirm a decreasing blood lead level is needed, however.

❑ Children with blood lead levels of 45 µg/dL or greater should be referred for appropriate chelation therapy immediately.

The Centers for Disease Control (CDC) recommends that children with blood lead levels of 45 µg/dL or greater should be referred for appropriate chelation therapy immediately. Some practitioners routinely treat children with blood lead levels between 25 and 44 µg/dL with chelation therapy and some do not use chelating agents for children with blood lead levels in this range. Other practitioners base this decision on the results of a provocative EDTA test. Only very minimal data exist about chelation therapy for children with blood lead levels below 25 µg/dL, and such children should not be chelated except in the context of approved clinical trials.

❑ The EDTA challenge test will indicate the extent of lead stores in the body. Some practitioners use this test when deciding whether to institute chelation therapy for a patient with a blood lead level between 25 and 44 µg/dL.

Several drugs (see Table 2 ) are used in the treatment of lead poisoning. These drugs, capable of binding or chelating lead, deplete the soft and hard (skeletal) tissues of lead and thus reduce its acute toxicity. All drugs have potential side effects and must be used with caution. In rare cases, the chelating agent, calcium disodium ethylenediaminetetraaceate acid (CaNa 2 EDTA) has caused proteinuria, microscopic hematuria, proximal tubule damage, hypercalcemia, and fever. Before instituting this therapy or using the chelation challenge test, the patient should be hospitalized and a physician experienced in chelation should be consulted. Such physicians can be identified by contacting an accredited regional poison control center, university medical center, or state or local health department.

Table 2 . Chelating agents used in treating children who have lead poisoning

Standards and Regulations

The number of federal standards and regulations reflect the extent to which lead is considered a public health problem. In some cases, the lead levels are mandated; in others, they are only recommended standards ( Table 3 ).

Table 3 . Summary of standards and regulations for lead

Biologic Guidelines

❑ CDC lowered the recommended action level for lead poisoning in children in 1991.

Lead levels that in the past were considered safe are now considered hazardous. As new information has emerged about the neurologic, reproductive, and possible hypertensive toxicity of lead, and as more sensitive parameters are developed, the levels defining lead poisoning have been progressively lowered. Between 1986 and 1988, several studies demonstrated neurobehavioral impairment in lead-exposed children with blood lead levels as low as 10 to 14 µg/dL. As more data become available, the definition of lead toxicity level will likely continue to be lowered ( Figure 2 ).

Figure 2 . CDC’s action level for blood lead in children has steadily declined.

essay on lead poisoning

*Emphasis is on primary prevention efforts (i.e., elimination of lead hazards before children are poisoned).

❑ Several states require primary care physicians to report cases of lead poisoning.

Physician Reporting Requirements. Several states require primary care physicians and persons in charge of screening programs to report both presumptive and confirmed cases of lead toxicity to the appropriate health agency so that abatement of the lead source, education of the patient, and remediation steps can be undertaken. In many states, laboratories performing blood lead or EP (ZPP) tests are also required to report abnormal results to the appropriate health agency.

❑ OSHA has set required standards for the amount of lead allowed in workroom air at 50 µg/m 3 averaged over an 8-hour workday.

The federal lead standard specifies the permissible exposure limit (PEL) of lead in the workplace, the frequency and extent of medical monitoring, and other responsibilities of the employer. The Occupational Safety and Health Administration (OSHA) has set a PEL of lead in workroom air at 50 µg/m 3 averaged over an 8-hour workday for workers in general industry. For those exposed to air concentrations at or above the action level of 30 µg/m 3 for more than 30 days per year, OSHA mandates periodic determination of blood lead levels. If a blood lead level is found to be greater than 40 µg/dL, the worker must be notified in writing and provided with medical examination. If a worker’s blood lead level reaches 60 µg/dL (or averages 50 µg/dL or more), the employer is obligated to remove the employee from excessive exposure, with maintenance of seniority and pay, until the employee’s blood lead level falls below 40 µg/dL (29 CFR §1910.1025). A copy of the lead standard can be obtained by calling your regional office of OSHA.


❑ EPA will probably lower its present ambient air standard for lead.

Occupational exposure limits are generally set to accommodate 8-hour workdays and healthy persons; they bear little relation to environmental limits, which are set to protect the most susceptible persons in the general population. EPA requires that the concentration of lead in air the general public may breathe shall not exceed 1.5 µg/m 3 averaged over a calendar quarter. This standard will probably be lowered. To reduce the amount of lead released into the environment, EPA regulations now limit the level of lead in unleaded gasoline to 0.05 grams per gallon.

Drinking Water

❑ EPA’s proposed goal for lead in drinking water after treatment is zero.

EPA estimates that about 20% of the U.S. population (including 3.8 million children) consumes drinking water with lead levels above 20 µg/dL. EPA is required to set drinking water standards with two levels of protection. The primary standards define contaminant levels in drinking water as levels above which the water source requires treatment. These maximum contaminant levels (MCLs) are limits enforceable by law and are set as close as possible to the maximum contaminant level goals (MCLGs), the levels determined to be safe by toxicologic and biomedical considerations, independent of feasibility. EPA has promulgated a final rule for lead in drinking water: this rule does not establish an MCL; the MCLG is zero and the action level is set at 15 µg/L. If more than 10% of targeted tap water samples exceed the action level, certain actions are required of water system administrators. For further information, call the U.S. EPA Safe Drinking Water Hotline toll-free at 1–800–426–4791.

The use of lead solder and other lead-containing materials in connecting household plumbing to public water supplies was banned by EPA as of June 1988. Many older structures, however, still have lead pipe or lead-soldered plumbing internally, which may substantially increase the lead content of water at the tap. Regulations controlling the lead content of drinking-water coolers in schools went into effect in 1989.

❑ Most lead in food comes from solder in cans or glazes on ceramicware.

Regulating lead contamination in foods is the responsibility of the Food and Drug Administration (FDA). FDA has set a goal of less than 100 µg/day as the total lead intake by children 1 to 5 years of age. Lead in food and beverages is encountered by virtually this entire age group in the United States.

According to a 1988 ATSDR report, FDA has estimated that about 20% of all dietary lead comes from canned food; about two-thirds of that amount results from lead solder in cans. The number of food cans that are lead-soldered continues to decline. In 1979, over 90% of all food cans were lead soldered; in 1986, this figure was 20%, or less than about 2 million cans. It is important to note that imported canned foods are not included in these figures and may still contain lead. Imported glazed ceramics and lead-containing pottery are also potential sources of dangerously high levels of lead.

❑ Today, paint intended for residential use is limited to 0.06% lead content.

Since 1977, the Consumer Product Safety Commission has limited the lead in most paints to 0.06% (600 ppm by dry weight). Paint for bridges and marine use may contain greater amounts of lead.

Suggested Reading List

Cullen MR, Robins JM, Eskenazi B. Adult inorganic lead intoxication: presentation of 31 new cases and a review of recent advances in the literature. Medicine (Baltimore) 1983;62:221–47.

Gerber GB, Leonard IA, Jacquet P. Toxicity, mutagenicity and teratogenicity of lead. Mutat Res 1980;76:115–41.

Kehoe RA. Occupational lead poisoning: clinical types. J Occup Med 1972;14:298–300.

Piomelli S, Needleman HL, Rosen JF. Lead poisoning. American Academy of Pediatrics Update (audiotape available) 1988;9(4):1–9.

Putnam RD. Review of toxicology of inorganic lead. Am Ind Hyg Assoc J 1986;47:700–3.

Chelation Therapy

Chisolm JJ Jr, Kaplan E. Lead poisoning in childhood—comprehensive management and prevention. J Pediatr 1968;73(6):942–50.

Chisolm JJ Jr. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J Pediatr 1968;73(1):1–38.

Markowitz ME, Rosen JF. Assessment of lead stores in children: validation of an 8-hour CaNa 2 EDTA provocative test. J Pediatr 1984;104(3):337–41.

Markowitz ME, Rosen JF. Need for the lead mobilization test in children with lead poisoning. J Pediatr 1991;119(2):305–10.

Piomelli S, Rosen JF, Chisolm JJ Jr, Graef JW. Management of childhood lead poisoning. J Pediatr 1984;105(4):523– 32.

Rosen JF, Markowitz ME, Bijur PE, et al. Sequential measurements of bone lead content by L X-ray fluorescence in CaNa 2 EDTA-treated lead-toxic children. Environ Health Perspect 1991;93:271–7.

Rosen JF, Markowitz ME, Bijur PE, et al. Sequential measurements of bone lead content by L X-ray fluorescence in CaNa 2 EDTA-treated lead-toxic children [published erratum appears in Environ Health Perspect 1991;92:181]. Environ Health Perspect 1991;91:57–62.

Neurobehavioral Development

Bellinger D, Leviton A, Waternaux C, Needleman H, Rabinowitz M. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. N Eng J Med 1987;316:1037–43.

Needleman HL, Gunnor C, Leviton A, et al. Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Engl J Med 1979;300:689–95.

Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN. The long-term effects of exposure to lead in childhood. An 11-year follow-up report. N Engl J Med 1990;322:83–8.

Schwartz J, Otto D. Blood lead, hearing thresholds, and neurobehavioral development in children and youth. Arch Environ Health 1987;42:153–9.

Moore MR, Goldberg A, Yeung-Laiwah AC. Lead effects on the heme biosynthetic pathway. Ann NY Acad Sci 1985;191–202.


Lurakis MF, Pitone JM. Occupational lead exposure, acute intoxication, and chronic nephropathy: report of a case and review of the literature. J Am Osteopath Assoc 1984;83:361–6.

Reproductive Effects

Mitchell JW, ed. Occupational medicine forum: lead toxicity and reproduction. J Occup Med 1987;29:397–9.

Uzych L. Teratogenesis and mutagenesis associated with the exposure of human males to lead: a review. Yale J Biol Med 1985;58:9–17.

Kunkel DB. The toxic emergency. Emergency Medicine 1986;18(Mar):207–17.

Marcus WL. Lead health effects in drinking water. Toxicol Ind Health 1986;2:363–400.

Related Government Documents

Agency for Toxic Substances and Disease Registry. The nature and extent of lead poisoning in children in the United States: A report to Congress. Atlanta: US Department of Health and Human Services, Public Health Service, 1988. DHHS report no. 99–2966.

Agency for Toxic Substances and Disease Registry. Toxicological profile for lead—draft. Atlanta: US Department of Health and Human Services, Public Health Service, 1992.

Centers for Disease Control. Preventing lead poisoning in young children: a statement by the Centers for Disease Control, January 1985. Atlanta: US Department of Health and Human Services, Public Health Service, 1985. DHHS report no. 99–2230. Revised October 1991.

Centers for Disease Control. Criteria for a recommended standard: occupational exposure to inorganic lead revised criteria. Atlanta: US Department of Health, Education, and Welfare, Public Health Service, 1978. Report no. (NIOSH) 78–158.

Centers for Disease Control. Lead poisoning following ingestion of homemade beverage stored in a ceramic jug-New York. Atlanta: US Department of Health and Human Services. MMWR 1989;38(21):379–80.

Centers for Disease Control. Occupational and environmental lead poisoning associated with battery repair shops-Jamaica. Atlanta: US Department of Health and Human Services. MMWR 1989;38(27):474–81.

Centers for Disease Control. Cadmium and lead exposure associated with pharmaceuticals imported from Asia-Texas. Atlanta: US Department of Health and Human Services. MMWR 1989;38(35):612–4.

Centers for Disease Control. Surveillance for occupational lead exposure-United States, 1987. Atlanta: US Department of Health and Human Services. MMWR 1989;38(37):642–6.

Centers for Disease Control. Lead poisoning in bridge demolition workers-Massachusetts. Atlanta: US Department of Health and Human Services. MMWR 1989;38(40):687–94.

Environmental Protection Agency. Air quality criteria for lead, Vol 2. Research Triangle Park, North Carolina: US Environmental Protection Agency, Office of Health and Environmental Assessment. Report no. EPA-600/ 8–83/028bF.

Environmental Protection Agency. Maximum Contaminant Level Goals and National Primary Drinking Water Regulations for Lead and Copper. Federal Register 1991;56:26460, 26477.

Office of the Federal Register. Code of federal regulations; occupational safety and health standards. Appendix C-Medical surveillance guidelines. Washington, DC: Office of the Federal Register, National Archives and Records Administration, 1988. (29 CFR §1910.1025).

Answers to Pretest and Challenge Questions

Pretest questions are found on page 1. Challenge questions begin on page 3.

All members of the family are at risk; they should be promptly evaluated and, if necessary, treated. The mother’s unborn child is also at risk. Workers in the radiator repair shop and their families, and any of the children’s playmates who have accompanied them to the repair shop after school, should also be screened.

The boy’s mother is 5 months pregnant. Since the placenta presents no barrier to lead, the fetus’ blood lead level is likely to be similar to that of the mother. It is during the initial weeks of pregnancy that the neurologic system of the conceptus is formed; therefore, damage to the fetus may have already occurred. The mother is no longer working at the repair shop, but you should alert her and the family to the possibility of continued lead exposure via the grandfather, who may be bringing lead dust home on his skin, shoes, or clothes.

Two of the obvious sources of lead suggested in the case study are leaded paint at home (paint flakes, household dust, and soil) and fumes and dust from solder at the radiator repair shop. You should determine if the boy ever had pica (a compulsive eating of nonfood items, to be distinguished from normal hand-to-mouth behavior of children). Pica is more common in children aged 2 to 5, so it is unlikely that this is a present behavior. Exposure to high levels of lead at the radiator repair shop is very possible, and you need to ascertain the type and length of the boy’s play at the shop.

To evaluate less obvious, but possible, sources of lead exposure, you might inquire about the proximity of the child’s home and play areas to freeways, hazardous waste sites, and industry. The occupations of all adults in the household are important; children of lead-exposed workers have been shown to have higher lead levels than control groups. Do any of the boy’s associates or does the father have hobbies involving lead, such as those mentioned on page 4? You might also inquire whether the home is undergoing remodeling, whether any home or folk remedies are used, if glazed ceramicware is used for food, or if there are lead or lead-soldered pipes in the house that could contaminate the drinking water.

If a child does not have pica and there is nothing to suggest that a lead-containing object has recently been ingested, an abdominal X ray will likely be negative. On long-bone radiograms, opacities in the metaphysial plates may be seen after 4–8 weeks or more of lead exposure. These “lead lines” (which are due to dense zones of calcium and not deposited lead) are more likely to be found in larger bones (e.g., radius and tibia) than in smaller bones (e.g., ulna and fibula). Lead lines seen in the smaller bones may be indicative of a longer exposure, usually several months. Radiographs are helpful only in the rare circumstances that they are positive. Negative X rays do not rule out lead poisoning.

Even with complete removal from the source of exposure, the blood lead level will drop only gradually because, without chelation, lead is only slowly excreted. In addition, even as it is excreted, it may be replaced by lead currently stored in bones and teeth.

This rebound phenomenon is due to the mobilization of lead from the body’s stores in bones and teeth.

The major effects of lead on the human body are damage to the neurologic, hematologic, renal, and reproductive systems.

Because of an incompletely developed blood-brain barrier, children under 36 months of age are particularly susceptible to neurologic damage at very low blood lead levels. Since children (to age 7) are more sensitive to lead’s effects, most adverse effects of lead are often manifested at lower blood lead levels in children than in adults.

History suggests delayed language ability, slightly impaired hearing, short stature, possible attention deficit disorder, and anemia. The child is also experiencing passive exposure to his mother’s cigarette smoke and family disruption related to his parents’ divorce.

Three of the most common causes of microcytic anemia are iron deficiency, hemoglobinopathy, and lead poisoning. In lead-poisoned patients, anemia is usually evident only when the blood lead level is significantly elevated for prolonged periods. It manifests in only a relatively small number of children with chronic lead poisoning. It is possible for a patient to be both lead-poisoned and to have anemia due to some other cause. The relative rarity of nutritional iron deficiency in this boy’s age group and the absence of evidence for blood loss suggest consideration of other etiologies to explain the anemia.

An elevated ZPP level is most often due to iron deficiency anemia, hemolytic anemias, or lead poisoning. A rare disease that may cause the ZPP level to be markedly elevated is erythropoietic protoporphyria.

To confirm lead poisoning, the best test is a venous blood lead level. If the blood lead level is below 25 µg/dl, then a serum ferritin level and other iron studies can be used to determine if iron deficiency anemia exists.

With an elevated blood lead level of 50 µg/dL, the conclusion is that the boy is lead-poisoned. In this case, the child should be referred for appropriate chelation therapy immediately. It is important to immediately identify and eliminate all sources of lead exposure for both the boy and his family. Environmental evaluation, intervention, and remediation should begin immediately. All household members should be screened for lead exposure (See Table 1 , page 15). Adequate diet for the family should be stressed.

You should consult with a physician experienced in treating lead-poisoned patients. To identify such physicians, contact your state or local health department, a university medical center, or a certified regional poison control center.

Knowing the subgroups at greatest risk of lead exposure, you should take every opportunity to educate these subpopulations, your colleagues, and the community about the hazards of lead poisoning and the steps to prevent its occurrence. Those children and members of the community whom you suspect may be in danger of lead poisoning should be promptly screened.

In certain states, public health authorities must be notified if a patient’s blood lead level and ZPP level exceed certain limits. In any case, you should contact your state or local health department so all sources of lead in the home can be identified and abated. You should also notify OSHA so the radiator repair shop can be brought, if required, into compliance with the federal lead standard. A NIOSH health hazard evaluation could also be requested. The reason for notifying these agencies is to prevent lead exposure in others.

The federal lead standard mandates that a worker with a blood lead level of 60 µg/dl or higher (or an average of 50 µg/dL)undergo medical removal from the lead hazard and be reassigned with retention of job seniority and pay. In addition to referring her for obstetrical evaluation, you should recommend that the mother talk to her employer, employee representative, and OSHA to clarify her work status under the lead standard and possible reinstatement procedures.

Sources of Information

More information on the adverse effects of lead and the treatment and management of lead-exposed persons can be obtained from ATSDR, your state and local health departments, and university medical centers. Case Studies in Environmental Medicine: Lead Toxicity is one of a series. For other publications in this series, please use the order form on the back cover. For clinical inquiries, contact ATSDR, Division of Health Education, Office of the Director, at (404) 639–6204.

People are increasingly concerned about potential environmental health hazards and often ask their physicians questions such as: "Is the tap water safe to drink?" "Is it safe to live near power lines?" Unfortunately, physicians often lack the information and training related to environmental health risks needed to answer such questions. This book discusses six competency based learning objectives for all medical school students, discusses the relevance of environmental health to specific courses and clerkships, and demonstrates how to integrate environmental health into the curriculum through published case studies, some of which are included in one of the book's three appendices. Also included is a guide on where to obtain additional information for treatment, referral, and follow-up for diseases with possible environmental and/or occupational origins.

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Investigative Post

Attorney General investigating Buffalo landlords

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A state Attorney General’s probe into lead poisoning is focused on a group believed to own or manage more than 200 Buffalo properties – at least 25 of which were cited for lead-related violations, and at least 11 of which were homes to children who have tested positive for high lead levels, according to court papers.

The nearly year-long investigation was disclosed in court papers filed Friday by Attorney General Letitia James’ office. The filings describe the landlord/management group as “a tangled web of limited liability companies, corporations, and individuals,” who appear to operate out of a boarded-up building on the city’s East Side.

While no action has been taken against the group, state lawyers are demanding an attorney representing some of its members turn over records related to eight individuals and 47 companies that state investigators suspect are affiliated with each other.

The requested records include the business relationships among group members, as well as the properties they own, and information on lead hazards in the buildings.

The investigation, which began last May, follows an Attorney General’s investigation of Buffalo landlord Angel Elliot Dalfin, who owned more than 150 properties, predominantly in low-income communities of color. That investigation tied more than two dozen cases of child lead poisoning to Dalfin’s properties. James in November 2022 won a $5.1 million lawsuit against Dalfin. 

In November, Dalfin pleaded guilty in federal court to lying about lead hazards in those properties. He was sentenced to five years probation and six months home confinement.

In the current case, a number of companies named in the court papers trace back to 1397 Kensington Ave., a commercial building on the city’s East Side.

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Investigative Post reporters visited the address earlier this week and found the majority of windows on the first floor of the building’s exterior covered in plywood. The property appeared to be largely vacant but under renovation. City records list the building owner as Batim Associates. Twenty other companies listed by the Attorney General’s office report ties to that building, including R&E Batim, Diamond Batim and M&M Batim, according to city and state property and corporation records.

A maintenance man at the Kensington Avenue property told Investigative Post he was hired by Moshe Pinchasi, one of the individuals named in the Attorney General’s legal filings. The worker used his cell phone to call Pinchasi, who asked reporters to leave the property and to speak with his lawyer. Pinchasi hung up when asked for the lawyer’s name and contact information.

Court papers list Anthony J. Barone Jr., as a real estate lawyer who has worked for members of the landlord group. Barone is not a subject of the Attorney General’s investigation, according to court papers.

Assistant Attorney General Patrick Omilian stated in the documents that he contacted Barone last May with a subpoena for a range of business-related documents connected to the landlord group. Barone initially indicated he would provide them, the court documents state.

But a month later, Barone told Omilian that his clients advised him — through another of their attorneys, Richard Steiner — not to respond to the subpoena, according to court papers. Barone also cited attorney-client privilege, though Omilian said the subpoena did “not seek privileged attorney-client communications or otherwise protected attorney work product.”

Omilian requested last week that a state Supreme Court judge issue an order compelling Barone to comply with the investigatory subpoena.

Investigative Post reached out to Barone, who did not respond to a request for comment. A receptionist for Steiner’s law firm said the attorney would not speak to the media during an open case.

The state Attorney General’s office said it has nothing further to add beyond what is in the court documents.

None of the lead-contaminated properties mentioned in court papers have yet been identified. 

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Investigative Post filed Freedom of Information Law requests with the Erie County Department of Health and the City of Buffalo Department of Permits and Inspections for properties owned by members of the landlord group that were cited for lead hazards and contamination.

Investigative Post also identified 40 properties — owned either formerly or currently by some of the LLCs and individuals listed in court papers — that have been in Housing Court. The properties were purchased by the landlords between 2007 and 2015, with some sold between members of the group for as little as $1. Sales were as recent as last year. The majority of those properties are on the East Side. None of those houses have been confirmed to have been lead contaminated.

Of the 47 real estate companies listed in court documents, 36 were registered in Western New York — either in Buffalo or Williamsville — and six traced back to Brooklyn. Others were established in Albany and in the State of Florida, according to state records.

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I'Jaz Ja'ciel

Related stories.

  • Community groups question Buffalo’s lead program
  • I’Jaz Ja’ciel’s reporting on Buffalo housing
  • IDAs look to dish out housing tax breaks
  • Working to boost homeownership on the East Side

Commentary | Hunting deer with lead ammunition has the side…

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Commentary | Hunting deer with lead ammunition has the side effect of killing America’s eagles | GUEST COMMENTARY

A pair of Bald eagles spar over a fish as one tries to steal the other’s catch below Conowingo Dam. (Jerry Jackson/Staff photo)

I started hunting as a young boy, and was taught the importance of gun safety, and the ethic of respect for the animals being pursued as a keystone element of “sportsmanship.” I was taught not to pull a trigger if I wasn’t confident of a clean kill, and to pass even the opportunity for a clean kill if another animal was in a line of fire. The use of lead bullets in hunting is essentially putting dozens of other animals in the line of fire after the fact.

The science on the use of lead ammunition is overwhelming and unequivocal. Condors, eagles, hawks, owls, vultures, ravens, magpies, blue jays and dozens upon dozens of other scavenging animals are at risk from dispersed lead ammunition. Upon impact, lead bullets fragment into hundreds of tiny pieces that scatter into the muscle and entrails of hunted animals, like white-tailed deer.

And that’s exactly what is happening across the country, including here in Maryland, where 76,687 deer were harvested in the 2022-2023 hunting season. The vast majority were killed using lead ammunition.

Therefore, the “gut piles” left behind when a deer is field-dressed become a toxic buffet for scavenging animals, and it takes only a piece of lead the size of a grain of rice to incapacitate and perhaps kill an adult bald eagle. That means the lead in a single 150-grain lead bullet has the potential to poison 10 eagles. And even smaller amounts can be disabling, including brain swelling, respiratory distress, weakness, and loss of vision. Acutely poisoned eagles are often described as behaving as if “drunk.” A study published in the journal Science two years ago found that the use of lead bullets in hunting is poisoning one-half of America’s bald and golden eagles.

In 1991, the U.S. Fish and Wildlife Service banned the use of lead “shot” in all waterfowl hunting because spent lead pellets were being ingested by, and poisoning, millions of birds annually. So, since then, Maryland waterfowlers, like me, have been required to use non-lead, non-toxic ammunition. It’s been good for both ducks and duck hunters.

It’s also good for our friends and family who share meals of wild game. Unnecessarily, lead is often the hidden ingredient.

As we learned from scientists like Maryland’s Rachel Carson, what’s good for wildlife is also good for people. The lead fragments in game meat are a health risk to humans. A study examining 324 random venison packages from meat processors found that 34% contained as much as 150 separate lead fragments. Scientific evidence like that is why the Maryland Department of Natural Resources 2023-24 Guide to Hunting and Trapping contains this warning : “Meat from game animals taken with lead fragmenting bullets and shot is a lead poisoning risk.”

But despite overwhelming science, most wildlife management agencies continue to allow the use of toxic bullets. It’s unscientific, inhumane and, frankly, irresponsible.

And it’s perplexing because it’s so easy to eliminate these risks to wildlife and human health. Non-toxic alternatives, such as solid-copper bullets are just as good or better at killing deer. Yes, currently they are slightly more expensive, but for a box of 20 rounds, it’s a difference of between $5 to 20 a box.

Seriously? Compared to the price of gas, food, lodging, meat processing, camo clothing, trail cameras, licenses, land leases and other costs in hunting animals like deer, this is a drop in the proverbial bucket.

As a life-long hunter, wildlife conservationist and the former leader of the U.S. Fish and Wildlife Service, I say with confidence that it is time to end use of poisonous lead bullets in hunting. And with the legislation introduced by Sen. Karen Lewis Young ( SB 983) and Del. Vaughn Stewart ( HB 1473 ), both Democrats, our state can do just that.

Since July 2019, California has required the use of non-toxic ammunition for hunting any wildlife. There is no indication this has affected hunting participation or game harvest. It’s been good for wildlife, from endangered California condors to common crows, and the people who consume game meat.

We can hunt deer and other game, and stop inflicting pain and suffering on untold thousands, likely millions of other innocent wild animals, just as we did in waterfowl hunting.

We have eliminated lead in gasoline, paint and children’s toys. There is no safe level of lead in any animal. Let’s get the lead out of hunting ammunition. It’s one small, relatively painless step for hunters, and one giant leap for wildlife.

Dan Ashe ( [email protected] ) is president and CEO of the Association of Zoos and Aquariums and former director of the U.S. Fish and Wildlife Service (2011-2017).

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An Update on Childhood Lead Poisoning

Marissa hauptman.

* Pediatric Environmental Health Center, Division of General Pediatrics, Department of Medicine, Boston Children’s Hospital

† Department of Pediatrics, Harvard Medical School

‡ Region 1 New England Pediatric Environmental Health Specialty Unit, Boston, MA

Rebecca Bruccoleri

§ Program in Medical Toxicology, Boston Children’s Hospital

Alan D. Woolf

Childhood lead poisoning is a multi-faceted, complex condition, which affects not only the child’s health and well-being, but also the family’s housing security, economic status, job security, and stress level. This review updates the emergency department clinician on the management of childhood lead poisoning. Infants and children are at higher risk than adults for lead exposure due to their smaller size and proportionately larger dose of ingested toxins, their proximity to ground dirt and indoor dust, their energy and curiosity, their oral exploratory and pica behaviors, their proportionately larger daily water and milk intake, and dietary preferences that differ markedly from those of adults. Pediatric health care providers working in the emergency department can provide medical management, as well as preventive counseling and guidance, to parents of children presenting with evidence of acute or chronic lead poisoning.

Children’s exposure to sources of lead contamination continues to be an important public health concern. Lead has no biological role in the body, and any detectable lead level is abnormal. There is indisputable scientific evidence that blood lead levels (BLL) below 10 µg/dL are associated with adverse effects in infants and children. 1 – 3 In response, in 2012, the Centers for Disease Control and Prevention (CDC) lowered the reference value BLL to 5 µg/dL. 4 An estimated 3.6 million American homes with at least one child have significant lead paint hazards. 5 , 6 As many as 500,000 US children (2.5%) under 6 years have BLLs ≥5 µg/dL. Each lead-exposed child costs an estimated $5600 in medical and special educational services. 7 Lead exposure-related cognitive impairments cost an estimated $50.9 billion annually in lost US economic productivity. 6

Nationally, US poison control centers (PCC) received 2241 single exposure calls about possible lead exposures in 2014. 8 Lead exposure is the most frequent inquiry directed toward the professionals staffing the nation’s Pediatric Environmental Health Specialty Units (PEHSUs). 9 Childhood lead poisoning is also a concern for clinicians working in pediatric emergency departments. Using discharge data for lead poisoning from the Agency for Healthcare Research and Quality, Healthcare Cost and Utilization Project from 2006–2014, we found that an average 1558 US emergency department (ED) visits occurred annually for assessment of possible lead exposure; 10 , 11 55% of these ED visits involved patients less than 18 years of age and approximately 35% were admitted to the hospital. 11 Although much of the management of children at risk of lead poisoning is nonclinical, clinicians working in EDs commonly find themselves directing the immediate care needs of lead-poisoned children. 12


Most children with elevated BLLs today are contaminated through exposure to lead laden dust and paint chips from deteriorating lead paint on interior surfaces. Their developmentally appropriate hand-to-mouth exploratory behaviors make them susceptible in an environment that is contaminated with lead dust, even without frank pica. 13 Contaminated soil from ‘legacy’ sources of lead (eg, leaded-gasoline, deteriorating lead-based exterior paint) can re-contaminate remediated houses. 14 , 15 Residual lead in soil deposited there from airborne emissions during nearby industrial operations, such as around smelters, remains a hazard even decades after closure. 16 Children may also inhale lead fumes or respirable dust particles resulting from unsafe remediation practices such as sanding or heating old paint, burning lead-painted wood indoors, burning automobile batteries for heat, or melting lead for use in a hobby or craft.

Other sources of lead hazards to be considered are included in Table 1 . Imported cookware, cosmetics, ethnic remedies, dietary supplements, contaminated tap water, and imported foodstuffs are among the diverse sources of potential lead exposure in a home environment. Some toy jewelry is made of lead; a child who ingested a lead charm died of lead poisoning in 2006. 17 – 19 Antique toys were sometimes painted with lead-based paint, and some plastic toys and vinyl have lead added as a softener. 19 , 20 Since 2008, the US Consumer Product Safety Commission (CPSC) has set requirements to reduce the number of non-complying products entering the market. 21 Novel sources of exposure include foreign-purchased cosmetics; 22 , 23 Southeast Asian spices 24 , 25 and herbs; 26 dietary supplements; 27 religious powders; 25 ayurvedic 28 or ethnic remedies; 22 , 25 occupational take home exposures; 29 – 31 and vocational exposures such as youth firearms marksmanship. 32 , 33

Sources of lead exposure.

Data from American Academy of Pediatrics Council of Environmental Health, Pediatric Environmental Health, 3rd Edition. 76


Not only are young children more likely than older children, adolescents, and adults to have an elevated BLL secondary to differences in absorption from the gastrointestinal tract and exploration of one’s environment, they are also more susceptible to toxic effects than are adults because of direct entry of lead into a developing nervous system. Studies of children with higher BLLs have consistently demonstrated lower IQ scores, 1 , 34 , 35 more language difficulties, 36 learning disorders, attention problems, 37 and behavioral issues. 38 , 39

While BLLs have decreased in all children over the past 30 years, disparities in who has elevated BLLs persist, disproportionately impacting vulnerable groups, such as immigrant children, low-income families, and young children from ethnic and racial minorities, based on age, socioeconomic, occupational, developmental and cultural risk factors. 40 – 44 Children living at or below the poverty line who live in older housing are at greatest risk of lead poisoning. 7 Additionally, children of low socioeconomic status are at increased risk of nutritional problems such as iron deficiency, which has been associated with a 4- to 5-fold increase in baseline risk of lead poisoning due to increased absorption of lead by the divalent metal transporter in the gastrointestinal tract. 45 , 46

Children with developmental conditions such as autism spectrum disorder and other neurological syndromes, who have persistent pica behaviors and/ or poor cognitive discriminatory recognition, are at increased risk of lead contamination. 47 – 52 Their increased risk may persist into school age and adolescence, beyond when children are routinely screened for elevated BLLs. Another vulnerable group may be children living in foster care, 53 whose lead poisoning risk may be related to other neurodevelopmental comorbidities in this population as well as increased residential mobility (especially in regions with older housing stock).

‘Take-home’ lead from the job is a common problem. The National Institute for Occupational Safety and Health (NIOSH) found common jobs with lead exposure include but are not limited to: painting, building renovation, demolition, shooting range work, metal scrap cutting and recycling, plumbing, and other industrial fields. 54 Pediatric emergency physicians should ask about parents’ occupations and hobbies that might involve lead during evaluation of lead poisoned children. 47 – 49

Clinical Diagnosis

Symptomatic childhood lead toxicity should be treated as an emergency. Children who present to the emergency department with unexplained symptoms and signs, especially those who are sluggish or comatose, who have persistent gastrointestinal symptoms (such as constipation or obstipation, abdominal pain, vomiting, recent anorexia, weight loss), or who have unexplained neurological or behavioral changes (eg, headaches, withdrawn, confusion, fatigue, lethargy, irritability, hyperactivity) or whose skin has a distinct pallor from severe anemia, should be suspected of suffering from acute lead poisoning. The differential diagnosis can include other causes of poisoning such as opioid ingestion or carbon monoxide poisoning, iron deficiency, thalassemia, Wilson’s Disease, acute intermittent porphyria, an acute surgical abdomen, encephalitis, and other causes of encephalopathy. Table 2 gives symptoms and signs of lead poisoning based on blood lead levels.

Summary of children’s health effects by blood lead level.

Data from President’s Task Force on Environmental Health Risks and Safety Risks to Children, Key Federal Programs to Reduce Childhood Lead Exposures and Eliminate Associated Health Impacts Report. 21

Keep in mind that children with significant underlying lead poisoning can be relatively asymptomatic. Table 2 links clinical findings with the BLL. Some children with BLLs >45 µg/dL may complain of headaches, abdominal pain, loss of appetite, or constipation or they may be completely asymptomatic. Children displaying clumsiness, agitation, or decreased activity and somnolence are presenting with premonitory symptoms of central nervous system (CNS) involvement that may rapidly proceed to vomiting, stupor, and convulsions. 55 Clinicians must have a high index of suspicion for a child who presents with a recent history of symptoms and/or signs presented in Table 2 . Significant lead exposure in early childhood has been linked to a numerous adverse health outcomes later in childhood, adolescence and adulthood, which are also listed in Table 2 .


The emergency department evaluation of a lead poisoned child often includes blood testing and radiographic studies ( Table 3 ).

Diagnostic evaluation of elevated blood lead levels. 56

Blood Lead Level (BLL)

Measurement of a venous blood lead level (vBLL) is key to the diagnosis of lead poisoning. For screening, a finger-stick sample (fsBLL) can be used if care is taken to avoid contamination. An elevated fsBLL (≥5 µg/dL) should be confirmed with a timely vBLL. 12 , 56 , 57 Hair or urine lead levels give little useful additional information. 58

Zinc-Chelated Protoporphyrin (ZPP)

Lead interferes with heme synthesis beginning at BLLs of approximately 25 µg/dL and after 50–70 days or more of exposure. 59 Both D-aminolevulinate dehydratase, an early-step enzyme, and ferrochelatase, which closes the heme ring, are inhibited. Ferrochelatase inhibition is the basis of a supplemental test for lead poisoning that measures in blood the quantity of zinc-chelated protoporphyrin (ZPP) and free erythrocyte protoporphyrin (FEP), the immediate heme precursor. These markers are insensitive to lower BLL and are not specific since they are also elevated in the presence of iron deficiency, a common comorbidity in children with elevated BLLs. ZPP or FEP can give insight into the chronicity of ongoing exposure and can be used during management, since an unexpected rise in these markers during patient monitoring over a period of weeks or months may indicate re-exposure and the need to reassess the environment.

Iron Status

Many young children with elevated BLLs will have iron insufficiency or iron deficiency anemia. Since lead and iron both use the same GI tract transporter, located in the small intestine, lead absorption is enhanced in children with iron deficits. Thus iron deficiency is an important comorbidity of lead toxicity; pica behavior has sometimes been associated with iron-deficient status. Therefore, markers of iron deficiency such as low ferritin or serum iron levels, even in the absence of anemia, low mean corpuscular volume (MCV), or elevated red cell distribution width (RDW) or low reticulocyte hemoglobin should be treated with therapeutic doses of iron as indicated.

Complete Blood Count

In addition to screening for comorbid anemia or iron deficiency, a complete blood count (CBC) with differential should be obtained before starting chelation, since chelants can cause depression of any or all three cell lines. Basophilic stippling may be seen at higher BLL. Basophilic stippling refers to small blue granules (ie, ribosomes) located inside of the cytoplasm when the smear is stained with Wright’s stain. 60

Liver and Renal Function Tests

Baseline liver and renal function tests, serum electrolytes, and glucose are also indicated in the child with suspected moderate–severe lead poisoning, since chelants commonly used in the medical management can have liver and/or renal toxicity or cause metabolic derangements. Periodic monitoring of the CBC, electrolytes, and liver and kidney function throughout the course of chelation therapy is recommended.


With lead-containing foreign body ingestions, BLLs rise rapidly (within hours to days) and can continue to rise during bowel transit of the object. Once the object has been excreted, the BLL falls to a new body equilibrium over the next month. In the emergency department, an abdominal radiograph to determine the presence of lead-containing substances may be indicated if a child’s BLL is ≥15 µg/dL or, regardless of the BLL, if a parent has witnessed or suspects that the child has recently ingested paint chips or a foreign body. 12 , 56 If the radiograph is positive for metal-density opacities in the stomach or small intestine, then hospitalization and gut decontamination with a polyethylene glycol solution (‘whole bowel irrigation’) may be beneficial. Radiographs of long bones to assess “lead lines” (ie, densemetaphyseal lines of growth arrest) are no longer necessary or recommended.

Multipronged management should be provided to all children with BLLs above the CDC reference value, as of time of manuscript preparation BLL ≥ 5 µg/dL. 4 , 12 , 61 Tables 3 and ​ and4 4 give details of diagnostic evaluation and management strategies to consider based on a child’s BLL. Management includes finding and eliminating the source of the lead, instruction in proper hygienic measures (personal and household), optimizing the child’s diet and nutritional status, and close follow-up. Many children with higher BLLs live in or visit regularly a home with deteriorating lead paint. Successful therapy depends on eliminating the child’s exposure; case management should address and control environmental sources of lead. Families of children with elevated BLLs should be referred to local public health officials and/or a certified lead inspector for an inspection and assessment of the child’s residence(s) for lead hazards. Clinicians as a first step often will start children identified as having an elevated BLL on supplemental iron therapy (3–6 mg/kg per day of free iron) to repair any iron deficiency.

Management of elevated blood lead levels. 56


Hospitalization may be necessary for symptomatic children and for those with BLL ≥ 45 µg/dL. Hospital admission is also determined by several considerations:

  • Is the child symptomatic?
  • Are there unabsorbed lead-containing foreign bodies in the stomach or small intestine?
  • Are there parental or other external factors making a safe discharge and timely follow-up difficult?
  • Is the home unsafe with respect to sources of lead contamination readily accessible to the child?

Discharge Planning

Although the main concern for the pediatric emergency physician regarding disposition is admission or discharge from the emergency department, the following hospital discharge criteria are important to consider when arranging a discharge plan. After inpatient management (eg. whole bowel irrigation, course of parenteral chelation), hospital discharge planning should determine:

  • Sources of lead exposure hazard have been identified and remediated
  • Parents or guardians understand dosing of oral chelants and there is a strong likelihood of adherence to medical instructions
  • The BLL has dropped adequately during inpatient therapy

Discharge counseling should include referral to public health officials for environmental assessment, temporary abatement recommendations to minimize ongoing exposure (eg, taping up chipping interior paint using contact paper or duct/masking tape), frequent hand washing, frequent dusting/wet mopping of the home (several times per week), leaving shoes at the threshold, and dietary recommendations ( Table 5 ).

Home lead hazard reduction measures.

Chelation and Management of Elevated BLLs

Chelants are chemicals whose structures include side-groups that can bind to lead and facilitate its excretion in urine. They are indicated emergently in cases of moderate–severe and life-threatening childhood lead poisoning. Chelation therapy for children with venous BLLs of 20 to 44 µg/dL can be expected to lower BLLs but has not been shown to reverse or diminish cognitive impairment or other behavioral or neuropsychological effects of lead. 62 If the venous BLL is ≥45 µg/dL and the exposure has been identified and controlled, chelation treatment should always be considered. A pediatrician experienced in managing children with lead poisoning should be consulted—these can be found through the PEHSUs, 56 PCCs or through lead programs at state health departments. (See Appendix A ) There are 4 chelants currently recognized as having efficacy in lead poisoning: dimercaprol (British Anti-Lewisite [BAL]), calcium disodium edetate (ethylenediaminetetraacetate; Versenate), dimercapto succinic acid (DMSA; Succimer; Chemet), and d-penicillamine (Cupramine, Depen). See Table 6 for educational purposes for details surrounding the administration of each. Treatment decisions are the responsibility of the treating clinician and should always be tailored to individual clinical circumstances.

Summary of common chelants used in lead poisoning.

Dimercaprol promotes the renal excretion through the formation of stable, nontoxic, soluble lead chelates. Dissolved in peanut oil for deep intramuscular injection, dimercaprol is associated with a high incidence of adverse effects, including fever, rashes, and pain at the injection site. It is contraindicated in persons with a peanut allergy or underlying hepatic insufficiency and may cause hemolysis in individuals who have glucose-6-phosphatase deficiency. Iron therapy needs to be discontinued because dimercaprol and iron form a complex that causes vomiting. NOTE: adequate patient hydration and good urine flow during chelation therapy with dimercaprol are of paramount importance, given its risk of renal toxicity.

Calcium disodium ethylenediaminetetraacetate ( CaNa 2 EDTA ) increases the urinary excretion of lead 20- to 50-fold through the formation of nonionizing salts. CaNa 2 EDTA removes lead only extracellularly; it does not enter cells and thus does not cross the blood brain barrier. WARNING: Some hospitals still stock the incorrect disodium EDTA salt. It is crucial that the calcium disodium salt be used, because the disodium EDTA salt alone avidly binds calcium and can cause severe, life-threatening hypocalcemia. 63 , 64 CaNa 2 EDTA is given intravenously usually for 5 day cycles. Side effects include local reaction at the injection site, fever, calcium abnormalities, renal dysfunction, and excretion of essential minerals. NOTE: maintaining adequate patient hydration and good urine flow during CaNa 2 EDTA chelation therapy is important.

Meso-2,3-dimercaptosuccinic acid ( DMSA ) is a water-soluble analogue of dimercaprol that was approved for oral administration by the US Food and Drug Administration in 1991 for chelating children who have BLL ≥45 µg/dL. DMSA is given orally, has less toxicity than CaNa2 EDTA, and causes less urinary loss of essential minerals. Side effects include abdominal distress, transient rash, elevated liver transaminase enzymes, and neutropenia. The 100-mg gelatin capsules have a strong sulfur (“rotten egg”) odor.

d -Penicillamine is an oral chelating agent used to treat Wilson’s disease (hepatolenticular degeneration). It has also been used by some clinicians for treating lead poisoning. 75 When used for chelation of lead in young children, low doses are recommended, with close monitoring of the CBC and renal function. Allergic rashes, marrow suppression, nephrotoxicity, and anaphylaxis are possible adverse effects.

Other Management

Treatment strategies in the pediatric emergency department setting include family counseling and education on dietary sources of iron, calcium, vitamins C and D, zinc and magnesium to attenuate increased absorption of lead in the setting of nutritional deficiencies.

Educational Enrichment

Another disposition recommended for young children discovered to have an elevated BLL is consideration of referral for neurodevelopmental evaluation and/or therapeutic services (eg, Early Intervention, Individualized Education Program (IEP) or other appropriate neurodevelopmental clinic or education enrichment program. 65


The CDC and American Academy of Pediatrics (AAP) both emphasize that the best way to end childhood lead poisoning is to prevent, control and eliminate lead exposures. 12 The focus is shifting from the care of symptomatic children toward a primary prevention approach targeting high-risk communities, as the most reliable and cost-effective strategy to protect children from lead toxicity. 12 , 66 Table 5 presents some recommendations for families to insure that their home is hazard-free with respect to lead contamination. It is critical that the individuals conducting residential abatement, or the removal, enclosure, or encapsulation of lead-based paint or lead-contaminated dust or soil receive appropriate training, and pregnant women, infants and children are out of the home environment during remediation and renovations in order to minimize further exposure to lead. 15 , 67 , 68 When done safely, paint stripping, covering over painted areas by sealing, encapsulation, or encasement, using high-efficiency particulate arrestance (HEPA) vacuums, HEPA air filters, and soil and dust removal, can be effective methods for lead abatement.

Exposure of children to harmful lead-containing dust, paint, drinking water, and other sources in their environment continues to pose an enormous public health challenge, not only in the United States but around the world. Vulnerable groups include immigrant children, low-income families, children in transitional foster care, young children from ethnic and racial minorities and those with underlying autism or other developmental delays who have persistent pica behaviors. Clinicians working in the emergency department are advised to keep a high index of suspicion for lead poisoning among the possible diagnoses for children presenting with pallor and anemia, loss of appetite, irritability and behavioral changes, colicky abdominal pain, chronic constipation, or other symptoms and signs typical of lead poisoning. Management of children identified as having elevated blood lead levels is multi-faceted and includes attention to diet, mitigation of environmental lead hazards so as to decrease further exposure, referral to community-based agencies, and developmental specialists, and in severe cases, chelation therapy. Prevention of exposure, including the identification of community-based resources to assist families and landlords in lead-hazard abatement, is the most effective public health strategy, requiring the concerted efforts of health care providers, local, state and Federal public health officials, health policy makers, and relevant community-based services and advocacy groups.



This publication was supported by the cooperative agreement award number 1U61TS000237-03 from the Agency for Toxic Substances and Disease Registry (ATSDR). Its contents are the responsibility of the authors and do not necessarily represent the official views of the Agency for Toxic Substances and Disease Registry (ATSDR).

The U.S. Environmental Protection Agency (EPA) supports the PEHSU by providing funds to ATSDR under Inter-Agency Agreement number DW-75-95877701. Neither EPA nor ATSDR endorse the purchase of any commercial products or services mentioned in PEHSU publications.


  • Alliance for Healthy Homes; www.afhh.org.htm ; 202-543-1147; Provides additional information on residential lead contamination and how to safely remove it.
  • American Association of Poison Control Centers www.aapcc.org ; 1-800-222-1212.
  • Coalition to End Childhood Lead Poisoning; www.leadsafe.org.htm ; 800-370-5323; Provides information for parents regarding childhood lead poisoning and its treatment and prevention.

Provides state and local contacts for CDC funded childhood lead poisoning prevention programs.

  • Department of Housing and Human Development (HUD); www.hud.gov/offices/lead.htm Office of Healthy Homes and Lead Hazard Control provides ability to track HUD’s progress in the abatement of lead hazards in residences.

EPA Lead Awareness Program provides information on residential lead abatement. EPA Safe Drinking Water Hotline; 1-800-426-4791.

National Lead Information Center.

1019 19th St, NW, Suite 401.

Washington, DC 20036.

  • US Department of Housing and Urban Development (HUD): 800-RID-LEAD.
  • National Lead Information Center - www.epa.gov/lead ; (800) 424-5323; 800-LEAD-FYI.
  • Pediatric Environmental Health Subspecialty Units (PEHSU); www.pehsu.net (ATSDR and EPA-sponsored regional centers providing clinical evaluation and consultation regarding pediatric environmental health issues, including lead poisoning).

Lead Poisoning in Northwestern Nigeria (The Village of Gold) Essay


An outbreak has erupted in Zamfara province in the northwestern section of Nigeria. Doctors confirmed that three villages within Zamfara province are at the heart of the crisis (CDC, n.d). The deadly outbreak known as lead poisoning has claimed 118 children below the age of five. The number of sick children has grown to 1,400, with 1,150 victims hospitalized. A first stop outside the villages depicts a horrific scene of 100 small newly dug graveyards (CDC, n.d). The situation is alarming because the outbreak came from the mining activities done within the area. The challenge is that the natives cannot stop this business because it is their only source of income. The most exposed population are children because they play on the ground where the contaminants are more concentrated (Kurup et al., 2019). Their parents also return from work soaked in dust that is confirmed to be toxic which increases poisoning. This paper explores some of the epidemiological processes applied in the identification process of lead poisoning (Kurup et al., 2019).

Solve the Outbreak Challenge

“The Village of Gold” is a Center for Disease Control and Prevention game that requires an individual to answer specific entries to define an outbreak (CDC, n.d). After answering the prompts in the game, I discovered the outbreak affecting the people of Zamfara Province (CDC, n.d). Lead poisoning was an outbreak that emerged from the mining activities performed in the area, and this contributed to the poisoning and death of children in the region. The causes, effects, and impact of mineral extractions are revealed through the use of epidemiological processes.

The Epidemiological Processes Applied

Epidemiology is an unbiased process of collection, evaluation, and interpretation of data within a specific population. The principles of epidemiology seek to define the frequency and the pattern of a health situation in a specified area (CDC, n.d). In this scenario of lead poisoning in the Zamfara province, I applied some of the epidemiological checklists approved by the Field Epidemiology Training Program (FETP), which helps extract data on the overall characteristics of an outbreak report and the steps applied (Kurup et al., 2019). The FETP approach used to identify and assess the outbreak included the following steps.

  • Confirmation of the outbreak.
  • Verification of the diagnosis.
  • Case definition.
  • Case finding.
  • Descriptive epidemiology.
  • Hypothesis.
  • Analytical epidemiology.


The sudden surge in the mortality rate and the number of hospitalized children indicated an epidemic. I used the confirmation technique to analyze data gathered from Zamfara province and concluded that there was a rising curve in the number of affected (CDC, n.d.) Initially, the number of infections was at 150, which increased to a total of 1,400 affected children with more than 1000 hospitalized (CDC, n.d). The rising number of the affected automatically indicated an outbreak.

Verification of Diagnosis

Some of the children admitted to the hospital showed symptoms characterized by abdominal pain, headache, vomiting, and convulsions (CDC, n.d). Doctors had tried administering anti-malaria and antibiotic drugs, and none have worked since the first administration. A laboratory test had to be conducted to confirm the outbreak because it could not be physically examined. Laboratory results reveal that the patients (Majorly children) have a high level of lead in their blood, confirming that they have been exposed to lead poisoning (CDC, n.d).

Case Definition

After the test results, it was evident that the patients were suffering from Lead poisoning, something they acquired from the mining site where they spend most of their time (CDC, n.d). Some reported having extended their mining activities to their homes to make ends meet. The incubation period was unknown, and all the residents were at risk.

Descriptive Epidemiology

This technique helped me to analyze the information about the persons associated with the outbreak (Kurup et al., 2019).

Descriptive Epidemiology

The primary cause of lead poisoning is exposure to lead-contaminated soil and air. During the extraction of minerals, exposure to lead-contaminated dust and soil is inevitable (Kurup et al., 2019). Children play with the soil, and this interaction increases their risk of being poisoned (CDC, n.d). Also, the natives do not use any protective clothing during mining, which means that they breathe in a lot of contaminated dust. If the natives take extra caution during mining by wearing protective gear and residing in far areas away from the site, the poisoning could decline.

Analytical epidemiology

At this stage, I applied the case-control study, which compares the exposure among cases and controls (Kurup et al., 2019). In this analysis, I realized that the poverty rate in Zamfara province was a contributing factor to poisoning. The people had no alternative income-generating activity, and this meant that they had to mine. Also, they could not afford to buy protective clothing that secured them from lead exposure.

The epidemiological processes of disease identification have played an essential role in explaining the outbreak investigation. For the Zamfara case scenario, the epidemiological techniques have enabled me to describe the outbreak report by focusing on specific characteristics such as the population affected, the prevalence of infection, zoned area, and the type of outbreak. The descriptive and analytic epidemiology have supported the explanation of the occurrence of the outbreak by providing a comprehensive framework that helped assess the exposures and risks associated with this lead poisoning.

Center for Disease Control and Prevention. (n.d). Solve the outbreak; the village of gold. Web.

Kurup, K. K., John, D., Ponnaiah, M., & George, T. (2019). Use of systematic epidemiological methods in outbreak investigations from India, 2008–2016: A systematic review . Clinical Epidemiology and Global Health, 7(4) , 648-653. Web.

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Small, nonthreatening balloon intercepted over Utah by NORAD

FILE - In this photo released by the North American Aerospace Defense Command (NORAD), a Russian Tu-142 maritime reconnaissance aircraft, top, is intercepted near the Alaska coastline, Monday, March 9, 2020. A small and nonthreatening balloon spotted flying high over the mountainous Western United States was intercepted by fighter jets over Utah, Friday, Feb. 23, 2024, according to the North American Aerospace Defense Command. (North American Aerospace Defense Command via AP, File)

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A small, nonthreatening balloon spotted flying high over the mountainous Western United States was intercepted by a fighter jet over Utah on Friday, according to the North American Aerospace Defense Command.

NORAD fighter pilots sent in the morning to investigate the balloon determined it was “not maneuverable” and did not present a threat to national security, spokesperson John Cornelio said. The balloon was still in the air, under close observation.

NORAD, a joint military command tasked with defending the airspace over the U.S. and Canada, has not said where the balloon came from or why it was flying over Utah and Colorado.

There has been heightened interest in reports of balloon overflights after the military identified — and eventually shot down — a large, white Chinese spy balloon that crossed much of the country last year. But officials said the balloon intercepted Friday was not sent by a foreign adversary and posed no threat to aviation or U.S. security.

NORAD said it was continuing to coordinate with the Federal Aviation Administration to track and monitor the balloon, which was detected at an altitude varying between 43,000 feet (13,100 meters) and 45,000 feet (13,700 meters), Cornelio said. NORAD declined to specify where in Utah pilots encountered it.

Early reports of the balloon sighting had raised concern among lawmakers including U.S. Sen. Jon Tester and U.S. Rep. Matt Rosendale of Montana, who said their offices were monitoring the situation. The office of Utah Gov. Spencer Cox said it had been in touch with local military officials.

The Chinese balloon that was downed last year off the coast of South Carolina after a weeklong path over multiple military sites was part of a global surveillance program that Beijing has been conducting for “several years,” according to the Pentagon. It was outfitted with advanced technology designed to collect intelligence signals, the Biden administration said.

China denied that it was conducting military surveillance and said it was a civilian balloon that accidentally veered off course while collecting weather data. After it was shot down, Chinese officials said they reserved the right to “take further actions” and criticized the U.S. for “an obvious overreaction and a serious violation of international practice.”

Similar spy balloons linked to the People’s Liberation Army — the military wing of China’s ruling Communist Party — have been detected floating over five continents. Just last month, Taiwan’s Defense Ministry detected four Chinese balloons, including three reportedly flying by a key air force base.

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Navalny’s Widow Pledges to Carry On Opposition Leader’s Work

The sudden death of Aleksei Navalny left a vacuum in Russia’s opposition. His wife, Yulia Navalnaya, signaled that she would try to fill the void.

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By Paul Sonne and Ivan Nechepurenko

The widow of Aleksei A. Navalny said on Monday that she would carry on her husband’s work to challenge President Vladimir V. Putin’s autocratic rule, presenting herself for the first time as a political force and calling on his followers to rally alongside her.

Mr. Navalny’s sudden death in prison, which was announced by the Russian authorities on Friday, left a vacuum in a decimated Russian opposition. His supporters had wondered whether his wife, Yulia Navalnaya — who long shunned the spotlight — might step in , despite immense challenges, to fill the void.

In a video released on Monday , Ms. Navalnaya, 47, signaled that she would. She said she was appearing on her husband’s YouTube channel for the first time to tell his followers that the best way to honor his legacy was “to fight more desperately and furiously than before.”

“I am going to continue the work of Aleksei Navalny and continue to fight for our country,” Ms. Navalnaya said. “I call on you to stand beside me, to share not only in the grief and endless pain that has enveloped us and won’t let go. I ask you to share my rage — to share my rage, anger and hatred of those who have dared to kill our future.”

The nearly nine-minute video, which showed Ms. Navalnaya seated with her hands folded on a marble surface under dramatic lighting, was crafted as an introduction of sorts to a new leader of the fractured pro-democracy movement against Mr. Putin. Long plagued by infighting and competing egos, the movement has withered under a multiyear crackdown in Russia that has left its most prominent leaders exiled, jailed or dead.

Ms. Navalnaya had often pushed back against suggestions that she enter politics, telling Germany’s Der Spiegel magazine last year that “I don’t think this is an idea I want to play with.”

Mr. Navalny and Ms. Navalnaya in a crowd with Russian flags.

On Monday, however, she presented a different face in trying to rally her husband’s followers, suggesting that there was no alternative and saying that the movement should derive strength from his memory.

“I know it feels impossible to do any more, but we have to — to come together in one strong fist and strike with it at this maddened regime, at Putin, at his friends and his bandits in uniform, at these thieves and killers who have crippled our country,” she said.

The dangers and hurdles Ms. Navalnaya faces in trying to assume her husband’s mantle and unite the opposition to Mr. Putin from outside Russia are significant.

The Russian government in 2021 disbanded Mr. Navalny’s Anti-Corruption Foundation inside the country by declaring it an extremist organization , sending the group’s main investigators fleeing into exile, where they continue to work and try to reach Russian audiences.

Cooperating with the organization from inside Russia has been made tantamount to abetting terrorism, limiting its ability to recruit the type of young grass-roots members who had electrified past efforts. Supporters of the Kremlin have tried to use the group’s exile to cast it as irrelevant or a puppet of Western security services.

Ms. Navalnaya cannot return to Russia without the threat of arrest. In June 2023, amid rumors that she might attend one of her husband’s many trials, the state-owned network RT quoted an unidentified law enforcement source as saying that Ms. Navalnaya could be arrested on charges of supporting an extremist organization if she were to return.

And much of Mr. Navalny’s appeal to his followers was personal, thanks to his unyielding humor, muckraking zeal and infectious certainty about the capacity for individual Russians to change the country in the face of cynicism and repression.

Ms. Navalnaya, seething with anger, suggested on Monday that she had no choice but to try. The immediate cause of Mr. Navalny’s death remains a mystery, but his family and team have accused Mr. Putin of killing him through a brutal incarceration.

“In killing Aleksei, Putin killed half of me, half of my heart and half of my soul,” Ms. Navalnaya said on Monday. “But I have another half left and it is telling me I have no right to give up.”

She echoed remarks from President Biden last week blaming Mr. Putin for her husband’s death and suggested Mr. Navalny’s team was investigating the circumstances of the death.

“We will name names and show faces,” she said.

She also directly addressed a question that many of Mr. Navalny’s followers have been asking after his death: Why did he return to Russia after his poisoning in 2020, knowing that he would almost certainly be killed?

In theory, she said, Mr. Navalny could have taken up a new life in exile and stopped speaking out against Russian corruption and fighting.

“But he couldn’t,” she said. “Aleksei more than anything else on earth loved Russia, loved our country and you all. He believed in us, in our power, in our future and that we deserved better. He didn’t believe it just in words but in deeds — so deeply and sincerely that he was ready to give his life for it.”

Ms. Navalnaya said that she wanted their two children to live in a free Russia — the “only way for his unthinkable sacrifice not to be in vain.”

Her rousing message was largely welcomed by Mr. Navalny’s supporters, many of whom have been driven out of the country and feel immobilized by grief.

It came as the Russian authorities continued to refuse to hand over Mr. Navalny’s body to his mother in a remote Arctic town close to the prison where he died.

Mr. Navalny’s spokeswoman, Kira Yarmysh, said on Monday that the authorities had told his mother that the body would be subjected to a “chemical examination” for another 14 days.

“One of the lawyers was literally pushed out” from the morgue in the Arctic where Mr. Navalny’s body is believed to be, Ms. Yarmysh said in a post on the social media platform X. She added in another post , “They lie, buy time for themselves and do not even hide it.”

Russian investigators initiated an inquiry into the causes of Mr. Navalny’s death shortly after it was reported, a procedural move that allows them to hold the body for longer than normal.

Ivan Zhdanov, the head of Mr. Navalny’s Anti-Corruption Foundation, said that the delay meant that Russian officials were “cleaning up traces of their crime.”

“They are waiting for the wave of hatred and rage toward them to calm down,” Mr. Zhdanov said in a post on Telegram, the messaging app.

The Kremlin spokesman, Dmitri S. Peskov, rejected any suggestion of impropriety on Monday, saying that the investigation into Mr. Navalny’s death has been continuing “in accordance with the Russian law.”

More than 63,000 people have signed a petition to Russian investigators demanding the release of Mr. Navalny’s body, a campaign initiated by a Russia-based human rights group, OVD-Info.

Mourners have brought flowers to makeshift memorials across Russia, paying tribute to Mr. Navalny with an act of grief that has also served as a form of protest in a country where even the mildest dissent can risk detention.

The Russian authorities have tried to tamp down the scale of public mourning. Flowers have been quickly removed from memorials and the police have detained hundreds of people.

Russian news outlets have also sought to play down Mr. Navalny’s death, limiting mention of it on television broadcasts. Russian officials have accused the West of jumping to conclusions in blaming Mr. Putin, describing the allegations as yet another example of Western unfairness toward Russia.

Anton Troianovski and Neil MacFarquhar contributed reporting.

Paul Sonne is an international correspondent, focusing on Russia and the varied impacts of President Vladimir V. Putin’s domestic and foreign policies, with a focus on the war against Ukraine. More about Paul Sonne

Ivan Nechepurenko covers Russia, Ukraine, Belarus, the countries of the Caucasus, and Central Asia. He is based in Moscow. More about Ivan Nechepurenko


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