Pediatric Lead Toxicity 

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 mental retardation and growth failure. (See Epidemiology and Prognosis.)

Lead is a ubiquitous and versatile metal. It has been extensively used since ancient times, and the history of public exposure to lead in food and drink is extensive. Lead poisoning was common in Roman times because of the use of lead in water pipes and in wine containers.

Lead poisoning became common among industrial workers in the 19th and 20th centuries, when workers were exposed to lead in smelting, painting, plumbing, printing, and many other industrial activities. Following the advent of motor vehicles at the beginning of the 20th century and the introduction of leaded gasoline, environmental lead contamination substantially increased. (See Etiology.)

In 1904, Gibson concluded that lead paint in the home was responsible for poisoning children. Despite this, lead was not banned from American household paints until 1978. Other common sources of lead exposure include batteries, putty, cement, imported canned food, cosmetics, jewelry, leaded glass artwork, farm equipment, and illicit intravenous drugs.

Children are more susceptible than adults to the adverse effects of lead exposure.^[1] 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 to the effects of lead. (See Etiology.)

Lead poisoning in children has been the focus of many researchers. The American Academy of Pediatrics (APP) currently defines lead poisoning as a venous BLL equal to or higher than 10μg/dL (0.50 µmol/L).^{[2, 3]} This level, which was originally intended to trigger community-wide prevention strategies, has often been misinterpreted as a definitive toxicologic threshold. Studies have indicated intellectual impairment in children with BLLs of less than 10 µg/dL. (See Treatment and Medications.)^{[4, 5]}

However, the lack of a specific BLL cutoff for adverse effects, the rather small sample size of these studies, and the absence of effective clinical or public health interventions that reliably and consistently lower BLLs that are already less than 10 µg/dL have made the Centers for Disease Control's (CDC's) Advisory Committee on Childhood Lead Poisoning Prevention keep the current level of concern at BLLs equal to or higher than10µg/dl. (See Treatment and Medications.)^{[6, 7]}

Patient education

For patient education information, see Poisoning.

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. Ingestion is the most common source of lead poisoning in children because of their normal hand-to-mouth activities. Inorganic lead absorption occurs via the mechanisms involved in absorption of essential elements, such as calcium and iron, and depends on the following factors:

• Solubility - Lead salts are more soluble in acidic media
• 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
• Nutritional deficiencies -Iron, calcium, zinc, copper, and protein deficiencies result in greater lead absorption
• Dietary fats and oils - Excess intake results in increased lead absorption
• Other dietary components - Dietary components such as phytates, found in leafy green vegetables, bind lead particles and increase their elimination

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.

Inhalation adds little lead burden to the body in children. Lead particles are frequently large and coughed up. However, because children do not expectorate well, these particles are likely to travel up the mucociliary system and be swallowed, allowing for some absorption. Lead toxicity may also develop in adolescents who sniff leaded gasoline recreationally.

Absorbed lead is attracted to sulfur, nitrogen, and oxides. Its toxicity is elicited by inhibiting sulfhydryl-dependent enzymes. Most of the lead is sequestered in the bone, and the rest is distributed in the blood and soft tissues. Lead interferes with hematopoiesis at several steps. This results in less heme synthesis and the accumulation of toxic products (eg, aminolevulinic acid, protoporphyrin). The half-life of lead in the soft tissues and blood is approximately 30-70 days. Conversely, lead deposits in the bones for several years. Lead is primarily excreted by glomerular filtration.

As previously stated, children are more susceptible than adults to the adverse effects of lead exposure. Toddlers often place objects in their mouths, resulting in dust and soil being ingested and, possibly, an increased intake of lead. Physiological 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, rendering them more susceptible to the effects of lead.

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, and welding. Workers should be instructed to change their working clothes at work.

Occurrence in the United States

According to the National Health and Nutrition Examination Survey (NHANES), from 1999-2002, the overall prevalence of elevated blood lead levels (BLLs) for the US population aged 1 year or older was 0.7%, a decrease of 68% from 2.2% in the 1991-1994 survey. In addition, the prevalence of elevated BLLs in children aged 1-5 years of age, who had the highest prevalence, was 1.6%, a decrease of 64% (from 4.4%) in the 1991-1994 survey. Children who belong to minority populations or low-income families or who live in older homes are particularly at risk.

International occurrence

Lead continues to be a significant public health problem in developing countries. In general, children with heavy exposure to automobile exhaust, lead-based paint, or home-industry manufacture of batteries, ceramics, or painted artifacts have high lead burdens. Children living in rural areas who are not engaged in manufacturing pursuits do not usually have high lead burdens.

Race- and age-related demographics

Overall, from 1999-2002, non-Hispanic blacks and Mexican Americans had higher percentages of elevated BLLs (1.4% and 1.5%, respectively) than did non-Hispanic whites (0.5%). Lead poisoning chiefly affects children younger than age 6 years and adults in lead-risk occupations.

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 10μg/dL.^[4] 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.^[8]

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.