Lead Poisoning
Herbert L. Needleman
The clinical picture of childhood lead poisoning (plumbism) has changed dramatically over the past 20 years. Acute symptomatic lead poisoning, once a common problem, now is a rare event. Lead encephalopathy is even rarer. Most pediatric residents will not see a case of acute plumbism during their training; few will encounter the problem in their career. At the same time, epidemiologic studies from around the world on the effects of lead in children have demonstrated behavioral and cognitive deficits in the absence of symptoms, at levels of blood lead once considered harmless. Traditional treatments using chelating agents are ineffective at these levels of lead in blood. As a result, the principal domain of lead toxicity has shifted from the clinic and hospital to the public health arena, where the effects of lead at clinically silent doses on child development remains a major issue.
Lead poisoning, unlike most of the illnesses examined in this textbook, is a manmade disease. The metal’s neurotoxic properties were recognized as least as far back as the second century B.C., when Dioscerides, the author of Materia Medica, wrote that “Lead makes the mind give way.” For centuries, plumbism was thought to be exclusively a disease of workers and drinkers of adulterated wine. (Despite being aware of lead’s toxic properties, ancient Romans used it to counteract the astringent flavor of tannic acid in grapes and thus sweeten wine.) The decrease in fecundity and simultaneous rise in madness in upper class Romans has attracted speculation that the metal played a role in the downfall of the Empire.
Childhood lead poisoning was first reported in 1892, at the Brisbane Children’s Hospital in Australia. In 1914, the first American report of a poisoned child was published. For
decades thereafter, acute childhood lead poisoning was believed to have only two outcomes: death or complete recovery without any residua. The first follow-up study of children who had recovered from acute poisoning was published in 1943, and reported that 19 of 20 recovered cases had severe school problems, behavior disorders, and impaired cognition. This paper established the long-term consequences of acute intoxication, and speculated that undiagnosed lead exposure was among the prominent causes of school and behavior problems.
decades thereafter, acute childhood lead poisoning was believed to have only two outcomes: death or complete recovery without any residua. The first follow-up study of children who had recovered from acute poisoning was published in 1943, and reported that 19 of 20 recovered cases had severe school problems, behavior disorders, and impaired cognition. This paper established the long-term consequences of acute intoxication, and speculated that undiagnosed lead exposure was among the prominent causes of school and behavior problems.
For six decades between 1920 and 1980, symptomatic childhood lead poisoning was relatively frequent, particularly in the eastern United States. Eighty-nine cases were treated at the Boston Infants and Children’s Hospital between 1924 and 1933; 45 of these had encephalopathy, and 11 died. In Baltimore, between 1950 and 1960, 611 cases with 48 deaths were reported. Between 1955 and 1960, in Philadelphia, 223 cases with 41 fatalities were reported. Chicago reported 429 cases and 67 deaths between 1959 and 1961.
The removal of lead from gasoline in the United States, begun in the 1970s and completed by 1991, resulted in a dramatic lowering of blood levels. The mean blood lead level in 1975 was 15.5 μg/dL. At the time of writing, the mean blood lead level is 2 μg/dL, robust testimony to the benefits of sound public health policy. Current data indicates that 2.2% of children under 6 years of age have blood lead levels greater than 10 μg/dL.
The definition of the toxic level of lead in blood, set at 60 μg/dL in the 1960s and 1970s, has, as a result of epidemiologic studies of lead-related cognitive deficits in asymptomatic children, been reduced in steps to 40, 35, and 25 μg/dL. It currently has been set at 10 μg/dL. Recent studies have demonstrated effects on children’s cognition at levels below 10 μg/dL. As a result, modern pediatric attention has shifted from treating symptomatic acute poisoning to finding and preventing effects in asymptomatic children exposed at lower doses.
SOURCES OF LEAD
The major sources of lead for children are old paint, dust, water, and air. Removing lead from gasoline has markedly reduced airborne lead, and blood lead concentrations have correspondingly declined. Airborne emissions from stationery sources such as smelters or battery manufacturing continue to present risks for nearby residents.
Clinicians must consider many less frequent sources of lead when evaluating a poisoned child. Hobbies in the home, such as stained glass making, handloading of ammunition, or ceramics, may introduce lead into household air and dust and raise the body burdens of resident children and adults. Some cosmetics, particularly surma, used by Hindus, and kohl, used by Muslims as eye makeup, have extremely high concentrations of lead. Many folk remedies, such as greta and azarcon, used by Mexicans to treat gastrointestinal disorders, contain large amounts of lead. In some cases, ceramic tableware from foreign countries may release lead into food; some imported toys may be painted with lead-based paints; and some imported plastic Venetian blinds may release substantial amounts of lead after exposure to sunlight.
The concentration of lead in standing water (reservoirs and aquifers) is low. Lead enters drinking water somewhere between the street main and the kitchen tap. Although the use of lead solder in household plumbing has been banned, many older houses have lead solder joints. This can be a hazard if the water supply is soft (of low mineral content) and corrosive. Some brass plumbing fixtures contain lead.
The single greatest contemporary source of lead exposure is household paint. Although lead began to be supplanted by titanium oxide as a pigment in the 1950s, and was banned from household paint in the 1970s, many houses inhabited today were built before 1950 and have leaded surfaces. Many of these surfaces chalk and powder. This liberates lead into household dust and makes it available to the exploring fingers of children. Windowsills and frames are particularly rich sources of lead. Approximately 18 million children under 5 years of age are reported to live in houses built before 1950.
Lead paint has a sweet flavor. Because paint in use before 1950 may contain as much as 50% lead by weight, the ingestion of paint chips is dangerous behavior. Many young children display mouthing behavior, but the seeking and persistent ingestion of nonfood substances (pica) is abnormal and is a strong risk for lead toxicity. The current World Health Organization (WHO) standard for the permissible intake of lead is 25 μg/kg/week. A single 1 gm flake of paint can have as much as 500,000 μg of lead.
Lead dust is a major source of lead for children. It is not necessary for paint to be flaking to contribute to household dust. When paint chalks or powders, or when airborne lead settles, the particles become part of the composite of finely ground, powdered earth and organic material that makes up household dust. A recent pooled analysis of 12 epidemiologic studies found a strong relationship between interior lead-dust loadings and blood lead levels in resident children. Consequently, the Environmental Protection Agency has reduced the household lead-dust standard to 40 μg/ft2, 250 μg/ft2 for windowsills, and 250 μg/ft2 for window troughs.
EPIDEMIOLOGY
The prevalences of blood lead levels above 10 μg/dL over the past 27 years obtained by the National Health and Examination Survey are summarized in Table 123.1. With the removal of lead from gasoline, the prevalence of blood leads above 10 μg/dL declined from 88.2% to 2.2%. The number of children exceeding 10 μg/dL has declined from 13,500,000 in 1976 to 1980 to 434,000 in 1999 to 2000.
Lead is not distributed evenly throughout the population: Low-income families, African American and Hispanic children, and inner city residents have substantially higher blood lead levels. This should not be taken to mean that middle-class white children are spared. The widely held belief that lead exposure does not happen to middle-class white children has obstructed the screening of children in this group, and as a result, many cases of toxicity have been missed. A prevalence of 2.2% has led many to dismiss the problem of lead exposure as solved; however, this prevalence means that in each 1-year cohort of children, 88,000 have unacceptable levels of lead exposure, and that in a clinical practice of 3,000 children, 66 have elevated blood lead levels. Newer data, summarized here, show the effects of lead at serum levels below 10 μg/dL. This increases markedly the number of children now recognized at risk.
TABLE 123.1. BLOOD LEAD LEVELS IN AMERICAN CHILDREN FROM 1976 TO 1999 | ||||||||||||||||||||
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Absorption, Distribution, and Excretion
Lead is taken into the body through the lungs and the gastrointestinal tract. The absorption of inorganic lead through the skin is negligible: Children absorb more lead from the gut (40% to 50%) than adults (20% to 24%). The absorption of respired lead is a function of particle size and respiratory rate. Lead particles of less that 0.5 μM penetrate deeply into the lung, where between 30% and 50% are absorbed directly into the bloodstream. Larger particles are trapped in the upper respiratory tract, migrate up into the pharynx, and are swallowed and absorbed from the gut. Because children are more active and have a higher respiratory rate, they tend to respire and absorb more airborne lead.
Deficiencies of iron, zinc, or calcium increase the amount of lead absorbed from the gut. After absorption, lead enters the bloodstream and is distributed to soft tissues and bone. The residence time of lead differs in these organs. The half-life of lead in blood is 35 days, whereas the half-life in adult bone is approximately 27 years. The half-life of lead in children’s bones has not been measured, but, given the rapid remodeling during childhood, is unquestionably shorter. Lead in soft tissues and the brain has a longer half-life than that in the blood. Most lead in blood is contained within the red blood cell; the concentration of lead in plasma, the transport medium, is generally lower. The largest amount of lead in the body is contained within bone. The various pools of lead within blood, bone, and soft tissue are in active communication and maintain a stasis of lead levels within the entire body. If a child has an elevated blood lead concentration, treatment by chelation will reduce the serum concentration abruptly; however, after treatment has ended, blood lead levels gradually rise as a transfer occurs from the lead pools in soft tissue and bone pools back into the blood.
Lead is excreted primarily through the gut and kidney. Chelating agents enhance urinary excretion by altering the solubility of lead. Small amounts of lead also are excreted in the bile, hair, nails, and sweat. Ninety-five percent of the adult body burden of lead is in bone, where it is relatively biologically inactive. Under certain conditions, bone lead is remobilized. These include fractures with immobilization and hyperthyroidism. Lead is mobilized from bone during pregnancy and is transferred across the placenta to the fetus. With aging, the demineralization of bone takes place, thus releasing lead into the bloodstream. Postmenopausal women have higher blood lead levels than premenopausal women, and lower cognitive test scores in postmenopausal women have been reported in association with blood lead levels. The question of the role of lead in cognitive impairment and dementia in older subjects is intriguing but unstudied.
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