Practice Essentials
Lead toxicity is a worldwide pediatric problem. Although data continue to demonstrate a decline in the prevalence of elevated blood lead levels (BLLs) in children in the industrialized world, lead remains a common, preventable, environmental health threat. Sequelae of lead intoxication include intellectual disability and growth failure. (See Epidemiology and Prognosis.)
The mechanisms of contamination include ingestion, inhalation, prenatal exposure, and dermal exposure, but the most common are ingestion and inhalation. Ingestion is more common in children, while the inhalation is more frequent in occupationally-exposed adults. Deteriorating lead paint in pre-1979 housing remains the most common source of lead exposure in children, accounting for up to 70% of elevated levels. [1] Other common sources of lead exposure include batteries, putty, cement, imported canned food, cosmetics, jewelry, leaded glass artwork, farm equipment, and illicit intravenous drugs.
Toddlers often place objects in their mouth, resulting in ingestion of dust and soil and, possibly, an increased intake of lead. The physiologic uptake rates of lead in children are higher than those in adults. In addition, children are rapidly growing, and their systems are not fully developed, which renders them more susceptible than adults to the effects of lead exposure. [2] (See Etiology.)
Lead poisoning in children has been the focus of many researchers. Studies have indicated intellectual impairment in children with BLLs of less than 10 µg/dL. [3, 4] Behavioral disorders are associated with lead exposure even at detectable blood levels at or below 5 µg/dL The current value of 5 µg/dL is used by clinical and public health care providers to identify children with elevated BLLs. [5]
For patient education information, see Lead Poisoning and Kids and the Lead Poisoning Directory. Because the effects of lead poisoning in children can be irreversible, primary prevention is critical; see the CDC's Prevention Tips.
Pathophysiology
Lead typically enters the body through inhalation or ingestion. Once lead is absorbed into the bloodstream, some of it is cleared from the body by excretion in the urine and bile. The clearance rate is approximately 1-3 mL/min and the half-life of lead in blood is approximately 30 days. [6]
The lead that remains binds to red blood cells and is then distributed to the soft tissues and bone. Lead eventually accumulates in bone, where it has a half-life of 20-30 years. Once lead is deposited in bone, it may be released back into the bloodstream during conditions of rapid bone tissue turnover such as pregnancy, menopause, and lactation. [6]
Lead exerts toxic effects through a variety of mechanisms on many different organ systems. Two systems that are particularly sensitive to lead toxicity are the hematologic system and the developing nervous system. [7, 8] In the hematologic system, lead destabilizes the red cell membrane, causing oxidative stress and early cell death. [8] Lead also inhibits the activities of several enzymes involved in heme biosynthesis and may trigger inappropriate production of erythropoietin. [7] These effects contribute to hemolytic anemia. [8]
In the nervous system, lead crosses the blood-brain barrier by displacing calcium ions. Within the brain, it accumulates in astroglial cells and prevents myelin sheath formation. These effects can lead to demyelination and disturbances in neural excitation and memory-related neurotransmitter activity. [8]
Lead has more pronounced adverse effects on the developing brain because it disrupts processes required to establish necessary connections between brain structures, eventually leading to permanent alterations in brain function. These effects can cause irreversible neurobehavioral developmental abnormalities in affected children, even at very low lead levels [9] . [6]
Etiology
Lead toxicity may be caused by inorganic or organic lead. Most cases of lead poisoning are caused by inorganic lead. Lead may enter the body through ingestion, inhalation, or transdermal absorption. Inorganic lead absorption occurs via the mechanisms involved in absorption of essential elements, such as calcium and iron, and depends on the following factors:
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Solubility - Lead salts are more soluble in acidic media
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Particle size - Large particles (eg, paint chips) are poorly absorbed, whereas fine dust particles licked from the fingers or other objects may contribute to an increased lead load
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Nutritional deficiencies - Iron, calcium, zinc, copper, and protein deficiencies result in greater lead absorption
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Dietary fats and oils - Excess intake results in increased lead absorption
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Other dietary components - Dietary components such as phytates, found in leafy green vegetables, bind lead particles and increase their elimination
Factors that increase the risk for lead exposure in children include [10] :
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Living in poverty
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Member of a racial-ethnic minority group
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Recent immigrant
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Living in older, poorly maintained rental property
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Having parents who are exposed to lead at work.
In children, elevated blood lead levels are most commonly caused by inhalation or ingestion of lead dust and chips of deteriorating lead-based paint. Other sources of exposure include the following [11] :
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Imported or antique toys painted with lead paint
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Imported cookware
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Toy jewelry made of lead
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Contaminated tap water
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Ingested foreign bodies
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Dietary supplements
Transcutaneous absorption of inorganic lead is minimal. However, organic lead, such as tetraethyl lead, may enter through the skin. Tetraethyl lead, the main organic compound in leaded gasoline, is converted in the body to triethyl lead and inorganic lead. While inorganic lead does not readily enter the body through the skin, it can enter the body through accidental ingestion (eating, drinking, and smoking) via contaminated hands, clothing, and surfaces. [9]
Adults are mainly exposed to lead by breathing in lead-containing dust and fumes at work, or from hobbies that involve lead. [9] Toxic lead exposures have also resulted from retained bullets or shrapnel fragments. [12] Intraarticular bullets can fragment and dissolve in synovial fluid, leading to lead absorption and delayed symptomatic lead poisoning. [13]
Inhalation of lead can also occur with exposure to tobacco smoke. Blood lead levels high enough to suggest possible adverse cognitive outcomes have been measured in youths with secondhand smoke exposure. [14]
Several environmental factors expose children to lead hazards, among which are dust, soil, paint chips, folk remedies, and the use of old ceramic cookware. Several parental occupations place children at risk, including lead mining, glass making, printing, welding, and electronic scrap recycling. [1, 9] Workers should be instructed to change their working clothes at work.
Epidemiology
At least 4 million households in the United States have children living in them that are being exposed to high levels of lead. There are approximately half a million children ages 1-5 with blood lead levels above 5 µg/dL, the reference level at which CDC recommends public health actions be initiated.Children who belong to minority populations or low-income families or who live in older homes are particularly at risk. [10]
In 2020, the American Association of Poison Control Centers (AAPCC) reported 2040 single exposures to lead: 931 were in children under the age of 6 years, 136 in children 6 to 12 years old, and 88 in patients 13 to 19 years old; there were 10 major outcomes and no deaths. [15]
According to the Centers for Disease Control and Prevention (CDC), in 2014 the incidence rate of blood lead levels (BLLs) ≥10 µg/dL in US children younger than 5 years old, was 50.66 per 100,000 for children ages 1-5 years and 19.90 for children less than a year old; and, the incidence rate of blood lead levels (BLLs) between 5 and 9 µg/dL in US children younger than 5 years old, was 444.49 per 100,000 for children ages 1-5 years and 148.51 for children less than a year old. [5]
The CDC also reported that 36% of new cases of elevated BLL in 2014 were identified during August–October, more than any other consecutive 3-month period. In warm weather, windows possibly painted with lead-based paint are opened and closed, creating lead dust in the air and on the ground. Repainting and renovation activities also are more common in warmer months. Increased presence and activity of children in and around the home might lead to children having more contact with contaminated dust, surfaces, and soil which can account for the higher BLLs in the late summer and early fall. [5]
Retained bullet fragments (RBFs) are an infrequently reported, but important, cause of severe lead toxicity. During 2003–2012, elevated BLLs associated with RBFs constituted 0.3% of all elevated BLLs and 4.9% of BLLs ≥80 μg/dL. Elevated BLLs associated with RBFs occurred predominantly among males aged 16–24 years in nonoccupational settings. [12]
Lead continues to be a significant public health problem in developing countries. In Africa, children, especially those living in the vicinity of industrial areas, are exposed to the highest levels of lead from different sources, such as heavy exposure to automobile exhaust (in countries where leaded gasoline is still sold), lead released by burning of paper products, discarded rubber, battery casings, and painted wood for cooking and heating. [16] In addition, children exposed to lead-based paint, or home-industry manufacture of batteries, ceramics, or painted artifacts have high lead burdens. [17, 18] Children living in rural areas who are not engaged in manufacturing pursuits do not usually have high lead burdens.
Prognosis
Prognosis depends on the blood lead level (BLL) and whether the patient was symptomatic on presentation. Asymptomatic patients tend to have a better prognosis, and studies demonstrate some improvement in intellectual functions following lowering of the BLL. Severe neurologic damage may follow lead encephalopathy.
Research has demonstrated that cognitive defects may occur at levels below the currently accepted BLL of 10 μg/dL. [3] Lanphear et al found an inverse relationship between blood-lead concentration and all cognitive function scores; this result was observed in math and reading scores for concentrations as low as 2.5 μg/dL. [19]
Lead-related deaths have become extremely rare since the advent of lead screening measures and decreased use of lead. Presently, death from lead encephalopathy is rarely encountered because of the aggressive approach to using chelating agents. However, complications may arise from the chelated lead complex. Therefore, careful monitoring of mental status, cardiovascular function, and renal and hepatic functions are essential parts of the ongoing evaluation.
