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Current Trends Childhood Lead Poisoning -- United States: Report to the Congress by the Agency for Toxic Substances and Disease Registry


The long-term consequences of unabated exposures to environmental leadsources can be serious, particularly for children. Recent scientific studies have shown a progressive decline in the lowest exposure levels of lead at which adverse effects can be reliably detected in children. In recognition of this, Congress directed the Agency for Toxic Substances and Disease Registry (ATSDR), in consultation with the Environmental Protection Agency (EPA), to examine the nature and extent of childhood lead poisoning in the United States. The study was to address such areas as the long-term health implications of environmental lead exposure in children, the extent of lead intoxication of children in terms of geographic areas and sources of lead in the United States, and methods and strategies for removing lead from the environment of U.S. children. This article summarizes the key findings of the report (1).*


The degree of exposure to children was classified by blood lead (Pb-B)levels of 25, 20, and 15 ug/dL. The groupings were based on 1) presence of both 25 ug/dL Pb-B and elevation of erythrocyte protoporphyrin (EP)**; 2) the corresponding value of 20 ug/dL used recently by the World Health Organization** for the European Economic Community; and 3) findings of EPA's Clean Air Scientific Advisory Committee,** which concluded that 10-15 ug/dL of lead is associated with the onset of effects that "may be argued as becoming biomedically adverse" (2). Levels of 25, 20, 15, and 10 ug/dL were used for grouping pregnant women and women of reproductive age when estimating fetal lead exposure and potential adverse health effects (2-4).


Infants and young children are at highest risk for the adverse health effects of lead (2,3). Exposures of women of childbearing age are also a concern because lead is directly transferred across the placenta; therefore, the developing fetus is exposed at levels proportional to maternal lead stores (5-7).

The toxic effects of lead in children (Table 1) are evident across a broad range of exposures, and some occur at Pb-B levels previously considered noninjurious (i.e., less than 25 ug/dL) (4). Further follow-up studies are needed before the impact and persistence of the low-level neurobehavioral effects are fully known.


Valid estimates of the total number of lead-exposed children according to standard metropolitan statistical areas (SMSAs) or other appropriate geographic units smaller than the nation as a whole are not possible. The only national data set for Pb-B levels in children comes from the National Health and Nutrition Examination Survey II (NHANES-II). Using this data set, ATSDR quantified the numbers of lead-exposed children (ages 6 months to 5 years) living in all SMSAs according to 30 socioeconomic and demographic strata and selected Pb-B levels.

These estimates for 1984 were projected from data collected in 1976-1980 (the years of NHANES-II). The degree of error in these estimates is difficult to quantify since sources of both overestimation and underestimation are present. In addition, Hispanic, Asian, and other subgroups are omitted because no data are available; however, no economic or racial subgrouping of children is exempt from the risk of sufficiently high Pb-B levels to cause adverse health effects.

For all SMSAs, about 400,000 fetuses are exposed to maternal Pb-B levels of more than 10 ug/dL and are therefore at risk for adverse health effects.

Of the estimated 2,380,600 children exposed to lead at levels above 15 ug/dL (about 17% of the total 13,840,000 children within SMSAs), an estimated 715,500 (5.2%) and 199,700 (1.4%) children have Pb-B levels greater than 20 ug/dL and greater than 25 ug/dL, respectively.


The most current data for lead screening results came from an ATSDR survey conducted in December 1986. All data for 1985 screening programs were voluntarily reported. There was no centrally administered data collection and assessment. Of 785,285 children screened by those programs in 1985, 11,739 (1.5%) had lead toxicity as determined by one of two CDC definitions (1978 criteria: a Pb-B level of 30 ug/dL and an EP level greater than or equal to 50 ug/dL; 1985 criteria: a Pb-B level 25 ug/dL and an EP level greater than or equal to35 ug/dL).

Based on examination of 1980 census data for children and their housing in the 318 SMSAs, for 35 SMSAs, greater than or equal to50% of the children were at high risk of exposure to leaded paint because their housing was built before 1950. For all 318 SMSAs, 4.4 million children were at potential risk because they lived in older housing with high lead content paint.


The ATSDR estimates of children exposed to lead by source are shown in Table 2. Because of the interrelating pathways of exposure, the numbers of children exposed to lead on a source-specific basis can only be estimated. In addition, since the type and availability of data for each lead source vary considerably, exposure category definitions are different for each of the major lead sources, i.e., paint, gasoline, stationary sources, dust/soil, water, and food. Since the estimated numbers of children for each source and category are comparable, they cannot be used to rank the severity of the lead problem by source of exposure.

The total of approximately 12 million children exposed to leaded paint is for children less than 7 years of age; the estimated 5.9 million children in the oldest housing were less than 6 years of age. Of the estimated 1.8 to 2.0 million children living in old and deteriorated housing, approximately 230,000 would be expected to have Pb-B levels greater than 30 ug/dL and 1.3 million greater than 15 ug/dL because of leaded paint exposure.

The estimate of 5.6 million children less than 7 years of age potentially exposed to lead at some level from gasoline are derived for the number of children in the 100 largest urban areas in the United States where vehicular traffic could be expected to figure significantly in childhood lead exposure. This estimate takes into consideration the phase-down of lead in gasoline required by EPA regulations.

Although data are very limited, an estimated 233,000 children are exposed to lead from stationary sources of all types (8).

Dust/soil lead is lead that has settled from leaded paint, gasoline, and stationary sources; therefore, exposure estimates can only be roughly calculated as the sum of these three categories. Dust/soil lead is the primary long-term repository for lead exposure; this pathway is a major contributor to overall lead exposure because of the hand-to-mouth activity of children.

Children are exposed to lead in drinking water primarily from contamination of the supply system (e.g., from lead pipes or from leachable lead solder). EPA recently estimated that 241,000 children less than 6 years of age have Pb-B levels greater than 15 ug/dL because of elevated concentrations of lead in drinking water, including 100 with Pb-B levels greater than 50 ug/dL, 11,000 with levels 30-50 ug/dL, and 230,000 with levels 15-30 ug/dL (9).

Because the use of lead-soldered food cans has decreased dramatically in recent years, lead in food is a declining source of exposure. Nonetheless, dietary exposure remains sufficient to add measurable amounts to the total Pb-B levels of as many as 1 million U.S. children.


Primary environmental lead abatement has been most effective for gasoline, stationary lead sources, and food. Activities are now under way to bring significant reductions of lead in water. Despite the marked reductions of lead in new paint (in 1977, the Consumer Product Safety Commission mandated the reduction of lead in paint to 0.06%), exposure to lead paint in old housing remains an important problem. In addition, lead from other sources that has been deposited in dust and soil is recognized as an important problem.

Abatement of secondary environmental lead exposure is closely linked to childhood lead-screening programs. These efforts involve environmental evaluation and abatement of exposure for children with recognized lead toxicity. Early screening and detection of exposure and toxicity have reduced the rates of severe lead poisoning. Such effective screening programs will reduce the toxicity and costs of lead poisoning. The success of screening programs in the past has been limited by the 1) difficulty of locating all children with lead toxicity; 2) inability to identify remediable sources of lead for many lead-poisoned children; and 3) incomplete removal of lead from the children's environments. Some methods of removing and disposing of lead from homes and other sites are relatively crude and can endanger both abatement workers and occupants.


Recommendations contained in the ATSDR report include the needs to

  1. integrate comprehensive approaches to controlling lead exposure in high-risk areas of the United States, 2) establish and maintain effective and efficient screening programs, 3) develop environmental measurement techniques for field use, and 4) conduct research on childhood lead poisoning and develop effective legal sanctions. Reported by: Agency for Toxic Substances and Disease Registry and Center for Environmental Health and Injury Control, CDC.

    Editorial Note

Editorial Note: In the past 2 decades, knowledge of the effects of lead poisoning has changed substantially. When national childhood lead poisoning prevention programs were instituted in the early 1970s, lead encephalopathy and other manifestations of severe overt lead poisoning were common. Today these outcomes are rare--to a great extent because of childhood lead-screening programs in high-risk areas and reduction of lead in the environment (particularly for gasoline, air, and food).

Despite these reductions, childhood lead poisoning is not disappearing. The ATSDR lead report documents three critical developments in lead poisoning (1). First, long-term effects (particularly neurobehavioral, cognitive, and developmental) are increasingly being observed in studies of children with lead levels much lower than previously believed harmful. Second, the numbers of children exposed to lead at these new lower levels of concern (corresponding to Pb-B levels approximately greater than or equal to 15 ug/L) are estimated at several million. This estimate is largely based on projections from the data in NHANES-II; NHANES-III will provide updated data in the coming decade. Third, the remaining important sources of lead in the environment (primarily lead paint in older housing and lead in dust and soil from past deposition and from deteriorating housing) will be difficult and expensive to remedy.

Childhood lead poisoning is one of the most common environmental diseases of children in the United States. In concept, it is a totally preventable disease--remove the lead from the child's environment and the disease will disappear. In practice, eliminating childhood lead poisoning will require substantial commitment.


  1. 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: US Department of Health and Human Services, Public Health Service, 1988; DHHS document no. 99-2966.

  2. Environmental Protection Agency. Air quality criteria for lead. Research Triangle Park, North Carolina: US Environmental Protection Agency, Office of Health and Environmental Assessment; EPA report no. EPA-600/8-83/028aF-dF.

  3. CDC. Preventing lead poisoning in young children: a statement by the Centers for Disease Control, January 1985. Atlanta: US Department of Health and Human Services, Public Health Service, 1985; DHHS publication no. 99-2230.

  4. World Health Organization. Air quality guidelines for Europe. Copenhagen: World Health Organization, Regional Office for Europe, 1987:242-61.

  5. Rabinowitz MB, Needleman HL. Temporal trends in the lead concentrations of umbilical cord blood. Science 1982;216:1429-31.

  6. Alexander FW, Delves HT. Blood lead levels during pregnancy. Inter Arch Occup Environ Health 1981;48:35-9.

  7. Barltrop D. Transfer of lead to the human foetus. In: Barltrop D, Burland WL, eds. Mineral metabolism in paediatrics: proceedings of a symposium held at Greenford in 1968. Philadelphia, Pennsylvania: Davis Co., 1969:135-51.

  8. GCA Corporation. Estimated numbers of children residing near lead paint sources. Research Triangle Park, North Carolina: US Environmental Protection Agency, Office of Air Quality Planning and Standards, 1985; contract no. 68-02-3804.

  9. Environmental Protection Agency. Reducing lead in drinking water: a benefit analysis. Washington, DC: US Environmental Protection Agency, Office of Policy Planning and Evaluation, 1986; EPA report no. EPA-230-09-86-019. *The complete report is available on request from ATSDR, Mailstop F38, Atlanta, Georgia 30333. **References are available on request from the Office of the Associate Administration, ATSDR, Mailstop F38, Atlanta, Georgia 30333.

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