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, the Australian physician J. Lockhart Gibson concluded that lead paint in the home was responsible for poisoning children.  Despite Gibson’s work, and subsequent confirmation of it in the US medical literature, lead was not banned from US household paints until 1978.
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.  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.  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. In 1991, the Centers for Disease Control and Prevention (CDC) defined blood lead levels (BLLs) ≥10 µg/dL as the “level of concern” for children aged 1–5 years.  This level, which was originally intended to trigger community-wide prevention strategies, has often been misinterpreted as a definitive toxicologic threshold. In fact, no safe BLL threshold has been identified. Studies have indicated intellectual impairment in children with BLLs of less than 10 µg/dL. [5, 6]
In May 2012, the CDC replaced the term “level of concern” with an upper reference interval value defined as the 97.5th percentile of BLLs in US children aged 1–5 years from two consecutive cycles of the National Health and Nutrition Examination Survey (NHANES). By this method, the BLL upper reference value was calculated as 5 µg/dL. 
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 of lead can 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. 
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, welding, and electronic scrap recycling.  Workers should be instructed to change their working clothes at work.
According to the Centers for Disease Control and Prevention (CDC), the percentage of confirmed blood lead levels (BLLs) ≥10 µg/dL in US children younger than 72 months fell from 7.61% in 1997 to 0.56% in 2013. Nevertheless, the CDC estimates that at least 4 million US households have children living in them that are being exposed to high levels of lead, and approximately half a million US children age 1-5 years have 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.
Lead continues to be a significant public health problem in developing countries. In general, children with heavy exposure to automobile exhaust (in countries where leaded gasoline is still sold), lead-based paint, or home-industry manufacture of batteries, ceramics, or painted artifacts have high lead burdens. [9, 10] Children living in rural areas who are not engaged in manufacturing pursuits do not usually have high lead burdens.
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 10 μg/dL.  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. 
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.
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Mohamed K Badawy, MD, FAAP Assistant Professor of Emergency Medicine and Pediatrics, University of Texas Southwestern Medical School; Associate Medical Director, Division of Emergency Medicine, Children’s Medical Center Dallas
Disclosure: Nothing to disclose.
Gregory P Conners, MD, MPH, MBA, FAAP, FACEP Director, Division of Emergency Medicine, Children’s Mercy Hospital; Associate Chair of Pediatrics, Professor of Pediatrics and Emergency Medicine, University of Missouri-Kansas City School of Medicine
Gregory P Conners, MD, MPH, MBA, FAAP, FACEP is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, American Pediatric Society, Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children’s Hospital of Wisconsin
Disclosure: Nothing to disclose.
Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children’s Medical Center
Disclosure: Merck Salary Employment
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Pediatric Lead Toxicity
Research & References of Pediatric Lead Toxicity|A&C Accounting And Tax Services