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Preventing Lead Poisoning in Young Children: Chapter 2

Chapter 2. Background


The blood lead level considered to indicate lead toxicity has progressively shifted downwards.

In general, children are more at risk for lead exposure than adults.

Large numbers of children in the united states continue to have blood lead levels in the toxic range.

This Chapter describes the health effects of lead on children and fetuses, the metabolism of lead, and the demographics of lead exposure in the United States. It explains why the definition of childhood lead poisoning is being revised.


Effects of Lead on Children and Fetuses

  • Lead affects virtually every system in the body.
  • The blood lead level considered to indicate lead poisoning has fallen steadily since the 1970s.
  • Blood lead levels at least as low as 10 µg/dL are associated with adverse effects.
  • Although the effects of low-level lead exposure may not seem severe in the individual child, on a population basis they are extremely important.

Lead is a poison that affects virtually every system in the body. It is particularly harmful to the developing brain and nervous system of fetuses and young children. The adverse effects of lead on children and adults are summarized in Figure 2-1.

The risks of lead exposure are not based on theoretical calculations. They are well known from studies of children themselves and are not extrapolated from data on laboratory animals or high-dose occupational exposures.

Levels of Concern

Since 1970, our understanding of childhood lead poisoning has changed substantially. As investigators have used more sensitive measures and better study designs, the generally recognized level for lead toxicity has progressively shifted downward. Before the mid-1960s, a level above 60 µg/dL was considered toxic (Chisolm and Harrison, 1956). By 1978, the defined level of toxicity had declined 50% to 30 µg/dL. Figure 2-2 shows how the federal definition of an elevated blood lead level has changed over the years.

Range of Effects of Lead

Very severe lead exposure in children (blood lead levels > or = to 380 µg/dL) can cause coma, convulsions, and even death. Lower levels cause adverse effects on the central nervous system, kidney, and hematopoietic system. Blood lead levels as low as 10 µg/dL, which do not cause distinctive symptoms, are associated with decreased intelligence and impaired neurobehavioral development (Davis and Svendsgaard, 1987; Mushak et al., 1989). Many other effects begin at these low blood lead levels, including decreased stature or growth (Schwartz et al., 1986; Bornschein et al., 1986; Shulka et al., 1989), decreased hearing acuity (Schwartz and Otto, 1987), and decreased ability to maintain a steady posture (Bhattacharya et al., 1988). Lead's impairment of the synthesis of the active metabolite 1,25-(OH)2 vitamin D is detectable at blood lead levels of 10-15 µg/dL. Maternal and cord blood lead levels of 10-15 µg/dL appear to be associated with reduced gestational age and reduced weight at birth (ATSDR, 1988). Although researchers have not yet completely defined the impact of blood lead levels <10 µg/dL on central nervous system function, it may be that even these levels are associated with adverse effects that will be clearer with more refined research.

Studies of Low-Level Lead Effects on the Central Nervous System

The concern about adverse effects on central nervous system functioning at blood lead levels as low as 10 µg/dL is based on a large number of rigorous epidemiologic and experimental studies. In particular, recent cross-sectional and prospective studies have provided new evidence about the association between low-level lead exposure and child development.

Several well-designed and carefully conducted cross-sectional and retrospective cohort studies in many different countries have been conducted (Lansdown et al., 1986; Fulton et al., 1987; Fergusson et al., 1988; Silva et al., 1988; Bergomi et al., 1989; Hansen et al., 1989; Hatzakis et al., 1989; Winneke et al., 1990; Lyngbye et al., 1990; Needleman et al., 1990; Yule et al., 1981; Lansdown et al., 1986; Hawk et al., 1986; Schroeder et al., 1985). Figure 2.3 shows the mean intelligence quotient (IQ) scores (in most cases adjusted for potential confounding factors) achieved by children with different blood lead levels from several of these studies. Some inconsistencies can be found in the results of these studies, but the weight of the evidence clearly supports the hypothesis that decrements in children's cognition are evident at blood lead levels well below 25 µg/dL. No threshold for the lead-IQ relationship is discernable from these data.

Most investigators report lower IQ scores among the more highly exposed children but these differences have not uniformly reached statistical significance (that is, p<.05). One way to synthesize the data from different studies is meta-analysis. Recent evaluation of 24 major cross-sectional studies provides strong support for the hypothesis that children's IQ scores are inversely related to lead burden (Needleman and Gatsonis, 1990).

Although available evidence is not sufficient to conclude that lead-associated deficits are irreversible, a recent followup study reported that the educational success of a cohort of young adults was significantly inversely associated with the amount of lead in teeth they shed as first and second graders (Needleman et al., 1990). In this study, dentine lead levels above 20 ppm were associated with a seven-fold risk of not graduating from high school, a six-fold risk of having a reading disability, deficits in vocabulary, problems with attention and fine motor coordination, greater absenteeism, and lower class ranking. Although dentine lead levels did not correspond in any simple way to blood lead levels, the available preschool blood lead levels of the more highly exposed children averaged 35 µg/dL (Needleman et al., 1979). Increased circumpulpal dentine lead levels (>16 ppm) have been linked to higher rates of learning disabilities in a recent Danish study as well (Lyngbye et al., 1990).

To address methodological limitations of cross-sectional studies of lead and child development, a number of prospective studies were begun during the 1980s. Blood lead measurements were begun during the prenatal period and continued for several years, along with assessment of development. In several but not all cohorts, prenatal exposures have been associated with slower sensory-motor and delayed early cognitive development (Bellinger et al., 1987; Bellinger et al., 1991; Dietrich et al., 1987; Ernhart et al., 1986; Dietrich et al., 1991). With low postnatal exposures and favorable socioeconomic conditions, some of these early associations may attenuate as children grow older (Bellinger et al., 1991). In addition, several studies have noted that children's cognitive performance in the preschool period may be associated with early postnatal lead exposures (McMichael et al., 1988; Bellinger et al., 1991). It will be necessary for these prospective studies to follow their respective cohorts into the school-age years in order for the full implications of these early patterns to become clear.

Questions are frequently raised about the practical significance of the difference frequently observed between the IQ scores of more exposed and less exposed children. For the previously described population of children studied by Needleman et al. (Needleman et al., 1979), a shift in mean IQ score of 4-6 points as a result of lead exposure was associated with a substantial increase in the prevalence of children with severe deficits (that is, IQ scores less than 80) (Figure 2-4). Similarly, in this population the shift was associated with an absence of children who achieved superior function (that is, IQ scores greater than 125).

Absorption of Lead

Children are at higher risk for lead exposure because

  • They have more hand-to-mouth activity than adults.
  • They absorb more lead than adults.

Many factors can affect the absorption, distribution, and toxicity of lead. Children are more exposed to lead than older groups because their normal hand-to-mouth activities may introduce many nonfood items into their gastrointestinal tract (Lin-Fu, 1973). The efficiency of gastrointestinal absorption of lead in food and beverages in children has been estimated to be around 40% (Ziegler et al., 1978). From experimental studies, gastrointestinal absorption of lead from nonfood sources is decreased in the presence of food (Rabinowitz, 1980). Efficiency of absorption is probably also affected by the particle size and form of lead (Barltrop and Meek, 1979). Deficiencies in iron, calcium, protein, and zinc are related to increased blood lead levels and perhaps increased vulnerability to the adverse effects of lead (Mahaffey, 1981; Mahaffey and Michaelson, 1980).

Blood Lead Levels In The United States

  • Large numbers of children continue to have blood lead levels high enough to cause adverse effects.
  • Substantial progress has been made, however, in reducing blood lead levels in the United States.
  • Lead-based paint remains the major source of high-dose lead poisoning in the United States.

The Agency for Toxic Substances and Disease Registry estimated that in 1984, 17% of all American preschool children had blood lead levels that exceed 15 µg/dL (ATSDR, 1988). Although all children are at risk for lead toxicity, poor and minority children are disproportionately affected. Lead exposure is at once a by-product of poverty and a contributor to the cycle that perpetuates and deepens the state of being poor.

Substantial progress has been made in reducing blood lead levels in U.S. children. Perhaps the most important advance has been the virtual elimination of lead from gasoline. Close correlations have been demonstrated between the decline in the use of leaded gasoline and declines in the blood lead levels of children and adults between 1976 and 1980 (Annest, 1983) (Figure 2-5). Levels of lead in food have also declined significantly, as a result both of the decreased use of lead solder in cans and the decreasing air lead levels.

Lead-based paint remains the major source of high-dose lead poisoning in the United States. Although the Consumer Products Safety Commission (CPSC) limited the lead content of new residential paint starting in 1978, millions of houses still contain old leaded paint. The Department of Housing and Urban Development estimates that about 3.8 million homes with young children living in them have either nonintact lead-based paint or high levels of lead in dust (HUD 1990).


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