Preventing Lead Poisoning in Young Children: Chapter 2
- Table of Contents
- Chapter 1. Introduction
- Chapter 2. Background
- Chapter 3. Sources and Pathways of Lead Exposure
- Chapter 4. The Role of the Pediatric Health-Care Provider
- Chapter 5. The Role of State and Local Public Agencies
- Chapter 6. Screening
- Chapter 7. Diagnostic Evaluation and Medical Management of Children with Blood Lead Levels > or = to 20 µg/dL
- Chapter 8. Management of Lead Hazards in the Environment of the Individual Child
- Chapter 9. Management of Lead Hazards in the Community
- Appendix I. Capillary Sampling Protocol
- Appendix II. Summary for the Pediatric Health-Care Provider
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.
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).
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).
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).
ATSDR (Agency for Toxic Substances and Disease Registry). Case studies in environmental medicine: lead toxicity. Atlanta: ATSDR, 1990.
ATSDR (Agency for Toxic Substances and Disease Registry). The nature and extent of lead poisoning in children in the United States: a report to Congress. Atlanta: ATSDR, 1988.
Annest JL. Trends in the blood lead levels of the US population. In: Rutter M, Jones RR, editors. Lead versus health. Chichester and New York: John Wiley and Sons, 1983:33-58.
Barltrop D, Meek F. Effect of particle size on lead absorption from the gut. Arch Environ Health 1979;34:280-5.
Bellinger D, Leviton A, Waternaux C, Needleman H, Rabinowitz M. Longitudinal analyses of prenatal and Postnatal lead exposure and early cognitive development. N Engl J Med 1987;316:1037-43.
Bellinger D, Sloman J, Leviton A, Rabinowitz M, Needleman H, Waternaux C. Low-level exposure and children's cognitive function in the preschool years. Pediatrics 1991;87:219-27.
Bergomi M, Borella P, Fantuzzi G, Vivoli G, Sturloni N, Cavazzuti G, Tampieri A, Tartoni PL. Relationship between lead exposure indicators and neuropyschological performance in children. Dev Med Child Neurol 1989;31:181-90.
Bhattacharya A, Shulka R, Bornshein R, Dietrich K, Kopke J. Postural disequilibrium quantification in children with chronic lead exposure: a pilot study. Neurotoxicology 1988;9:327-40.
Bornschein RL, Succop PA, Krafft KM, Clark CS, Peace B, Hammond PB. Exterior surface dust lead, interior house dust lead and childhood lead exposure in an urban environment. In: Hemphill DD, ed. Trace substances in environmental health. Columbia (MO): University of Missouri, 1986:322-32.
CDC (Centers for Disease Control). Preventing lead poisoning in young children: a statement by the Centers for Disease Control. Atlanta: CDC, 1985; CDC report no. 99-2230.
Chisolm JJ, Harrison HE. The exposure of children to lead. Pediatrics 1956;18:934-55.
Davis JM, Svendsgaard DJ. Lead and child development. Nature 1987; 329:297-300.
Dietrich KN, Krafft KM, Bornshein RL, Hammond PB, Berger O, Succop PA, Bier M. Low-level fetal lead exposure effect on neurobehavioral development in early infancy. Pediatrics 1987;80:721-30.
Dietrich KN, Succop PA, Berger O, Hammond P, Bornschein RL. Lead exposure and cognitive development of urban preschool children: the Cincinnati lead study cohort at age 4 years. Neurotoxicology and Teratology 1991;13:203-11.
Ernhart CB, Wolf AW, Kennard MJ, Erhard P, Filipovich HF, Sokol RJ. Intrauterine exposure to low levels of lead: the status of the neonate. Arch Environ Health 1986;41:287-91.
Fergusson DM, Fergussen JE, Horwood LJ, Kinzett NG. A longitudinal study of dentine lead levels, intelligence, school performance, and behavior Part II: dentine lead and cognitive ability. J Child Psych Pyschiat 1988;29:793-809.
Fulton M, Raab G, Thompson G, Laxen D, Hunter R, Hepburn W. Influence of blood lead on the ability and the attainment of children in Edinburgh. Lancet 1987;i:1221-6.
Hansen ON, Trillingsgaard A, Beese I, Lyngbye T, Grandjean P. A neuropsychological study of children with elevated dentine lead level: assessment of the effect of lead in different socio-economic groups. Neurotoxicology and Teratology 1989;11:205-13.
Hatzakis A, Kokkevi A, Maravelias C, Katsouyanni K, Salaminios F, Kalandidi A, Koutselinis A, Stefanis C, Trichopoulos D. Pyschometric intelligence deficits in lead-exposed children. In: Smith M, Grant L, Sors A, editors. Lead exposure and child development: an international assessment. Dordrecht: Kluwer Academic Publishers, 1989:211-23.
Hawk BA, Schroeder SR, Robinson G, Otto D, Mushak P, Kleinbaum D, Dawson G. Relation of lead and social factors to IQ of low-SES children: a partial replication. Am J Ment Def 1986;91:178-83.
HUD (U.S. Department of Housing and Urban Development). Comprehensive and workable plan for the abatement of lead-based paint in privately owned housing: report to Congress. Washington (DC): HUD, 1990.
Lansdown R, Yule W, Urbanowicz MA, Hunter J. The relationship between blood-level concentrations, intelligence, attainment and behaviour in a school population: the second study. Int Arch Occup Environ Health 1986;57:225-35.
Lin-Fu JS. Vulnerability of children to lead exposure and toxicity: Part one. N Engl J Med 1973; 289:1229-33.
Lyngbye T, Hansen ON, Trillingsgaard A, Beese I, Grandjean P. Learning disabilities in children: significance of low-level lead exposure and confounding effects. Acta Pediatr Scand 1990;79:352-60.
Mahaffey KR. Nutritional factors in lead poisoning. Nutr Rev 1981; 39:353-62.
Mahaffey KR, Michaelson IA. The interaction between lead and nutrition. In: Needleman HL, editor. Low level lead exposure: the clinical implications of current research. New York (NY): Raven Press, 1980:159-200.
McMichael AJ, Baghurst PA, Wigg NR, Vimpani GV, Robertson EF, Roberts RJ. Port Pirie cohort study: environmental exposure to lead and children's abilities at four years. N Engl J Med 1988;319:468-75.
Mushak P, Davis JM, Crochetti AF, Grant LD. Prenatal and postnatal effects of low level lead exposure: integrated summary of a report to the U.S. Congress on childhood lead poisoning. Environ Res 1989; 50: 11-36.
Needleman HL, Gatsonis CA. Low-level lead exposure and the IQ of children. JAMA 1990:263:673-8.
Needleman HL, Gunnoe C, Leviton A, Reed R, Peresie H, Maher C, Barret P. Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Engl J Med 1979:300:689-95.
Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN. The long- term effects of exposure to low doses of lead in childhood: an 11-year followup report. N Engl J Med 1990;322:83-8.
Rabinowitz MB, Kopple JD, Wetherill GW. Effect of food intake and fasting on gastrointestinal lead absorption in humans. Am J Clin Nutrition 1980;33:1784-8.
Schroeder SR, Hawk B, Otto DA, Mushak P, Hicks RE. Separating the effects of lead and social factors on IQ. Environ Res 1985;38:144-54.
Schwartz J, Angle C, Pitcher H. Relationship between childhood blood lead levels and stature. Pediatrics 1986;77:281-8.
Schwartz J, Otto D. Blood lead, hearing thresholds, and neurobehavioral development in children and youth. Arch Environ Health 1987;42:153-60.
Shukla R, Bornschein RL, Dietrich KN, Buncher CR, Berger OG, Hammond PB, Succop PA. Fetal and infant lead exposure: effects on growth in stature. Pediatrics 1989;84:604-12.
Silva PA, Hughes P, Williams S, Faed JM. Blood lead, intelligence, reading attainment, and behaviour in eleven year old children in Dunedin, New Zealand. J Child Psych Psychiat 1988;29:43-52.
Winneke G, Brockhaus A, Ewers U, Kramer U, Neuf M. Results from European multicenter study on lead neurotoxicity in children: implications for risk assessment. Neurotoxicity and Teratology 1990;12:553 9
Yule W, Lansdown R, Miller I, Urbanowicz M. The relationship between blood lead concentrations, intelligence, and attainment in a school population: a pilot study. Dev Med Child Neurol 1981;23:567-76.
Ziegler EE, Edwards BB, Jensen RL, Mahaffey KR, Fomon SJ. Absorption and retention of lead by infants. Pediatric Research 1978;12:29-34.
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