Lead Exposures in U.S. Children, 2008: Implications for Prevention

1Some recent tragedies have evinced a more complicated risk pattern for pediatric lead exposures in the United States than had previously been considered:

221 April 2000, New Hampshire: A 2-year-old Sudanese refugee died from exposure to lead paint, the first U.S. child known to die from lead poisoning in 10 years.

3July 2002, New York City: A 1-year-old’s elevated blood lead level was traced to ceramic dinnerware without visible signs of wear.

423 July 2003, Massachusetts: A lead-coated copper wall and roof were identified in a child’s condominium where dust lead levels were 224,377 μg/ft2 (Brown MJ, unpublished memo to the Consumer Product Safety Commission, 2004).

52004, Oregon: A child was hospitalized after ingesting a necklace made with lead, resulting in voluntary recall of 150 million pieces of children’s jewelry.

623 March 2006: Minnesota: A 4-year-old died from lead poisoning after swallowing a charm with 99% lead content received with a purchase of shoes.

7The implications of these and similar events drove members of core federal agencies to jointly construct a more complete picture of potential lead exposures than had previously been compiled.

8Lead is corrosion-resistant, dense, ductile, and malleable and has been used since at least 3500 BCE. Atmospheric lead levels increased more than six orders of magnitude over the past six millennia accompanying population and economic growth (Figure 1). Blood lead levels (BLLs) of U.S. children rose sharply between 1900 and 1975 as increased lead emissions caused widespread contamination. Changes in federal laws have reversed this trend, including eliminating leaded gasoline from on-road vehicles, banning the sale of leaded house paint, and prohibiting lead solder in public water systems, plumbing components, and food and drink cans. The sharp reduction in children’s BLLs between 1976 and 1989 demonstrates that these policies have been effective. However, children continue to be exposed to lead. In 1999–2002, an estimated 310,000 (1.6%) U.S. children had BLLs ≥10 μg/dL, and 1.4 million had BLLs of 5–9 μg/dL (almost 14%).

9The adverse health effects of lead—including death, insanity, nervous system damage, and sterility—have been reported since the second century BCE. Even low lead exposure affects children’s intellectual development and lifetime achievement. Since the 1980s, studies have linked BLLs < 10 μg/dL in children 1–5 years of age with decreased IQ and cognition, with demonstrated effects evident at about 2 μg/dL. No threshold for effects has been demonstrated.

10In 2000, the United States adopted the goal of reducing all exposures to lead and eliminating elevated blood lead levels (EBLs; BLLs ≥10 μg/dL) in children by 2010. However, projections of future decreases in the number of children with EBLs assume a funding schedule that is not fully actualized. The nation’s goal to eliminate childhood BLLs > 25 μg/dL by 2000 was not met. The 2010 goal may fall short without augmented investment.

11Screening children for lead and abating lead paint hazards in homes of children with EBLs must continue. But given ubiquitous lead contamination, merely reducing hazards in residences of children identified with EBLs will not suffice. Childhood lead poisoning prevention programs (CLPPPs) must consider current and past uses of lead as well as behaviors that leave specific populations vulnerable to excessive lead exposures. To be effective, CLPPPs must shift to primary prevention.

12Deteriorating lead paint and contaminated dust and soil are the primary, but not the only, causes of EBLs among U.S. children. Lead is used in thousands of applications, all of which constitute potential exposure sources. Recent data indicate that ≥30% of children with EBLs do not have an immediate lead paint hazard. For example, in 2004 in Arizona, soil was the most common identified proximate exposure source, accounting for about 24% of pediatric EBL cases, followed by paint (17%), folk remedies and pottery (17%), dust (15%), and miscellaneous other sources (19%). In 8% of cases, no lead source was identified.

13Nonpaint lead exposure sources are insufficiently characterized, and their importance is often underestimated. When a child with an EBL is reported, investigators look for lead paint in places where s/he spends time, exploring alternative lead exposure sources only when no paint hazards are found. Thus, for some children, significant nonpaint sources may be missed. Evidence also suggests that for children with BLLs < 10 μg/dL, no single exposure source predominates.

14The United States is the third largest lead producer, producing about 450,000 tons in 2003. In 2003, the United States consumed about 1.5 million tons of lead. Facilities using lead can raise exposures for adjacent populations. Not all sources are obvious, and many users are exempt from reporting. In Massachusetts in 2003, for instance, 252 facilities used nearly 9.3 million pounds of lead, with the largest releases reported by municipal waste combustors (Table 1).

15During the 20th century, leaded gasoline was the predominant source of airborne lead. Today, industrial emissions predominate. In 2001, the U.S. Environmental Protection Agency (EPA) reported that industrial emissions accounted for 78% of air lead, fuel consumption accounted for 10%, and the transportation sector accounted for 12%. In 2004, four waste treatment plants were among the 20 largest dischargers of lead submitting data to the Toxics Release Inventory (TRI) of the U.S. EPA (U.S. EPA 2007d).

16After declining for > 25 years, U.S. air lead levels rose in 2004–2006 (Figure 2). The highest air concentrations of lead are found near smelters and battery manufacturers. At present, these are the only violations of the national air lead standards. However, national air lead emission data cannot accurately portray local lead emissions or their risk for proximate populations. Exposure modeling at the U.S. EPA indicates that for the 20 highest air emitters, local emissions are significantly related to local BLLs (.

17Not all sources of lead are listed in the U.S. EPA TRI. Municipal incinerators, small operations such as auto repair shops, off-road vehicles including NASCAR, and propeller aircraft using aviation gasoline (avgas) are exempt from reporting, fall below reporting quantities, or choose not to report; nonetheless, they can contaminate surrounding communities. For example, at one airport where many airplanes used avgas, average and maximum air lead levels were 0.030 and 0.302 μg/m3, respectively, versus background levels of 0.007 and 0.018 μg/m3. Another study showed that even at an airport with few planes using avgas, air lead levels were higher downwind than upwind.

18Demolition of old buildings contributes to local air lead levels and can increase BLLs in children.

19Lead binds tightly to soils, and eight decades of leaded gasoline combustion and past industrial emissions have left a legacy entrained in soil. Peeling lead paint on residences also contaminates soil, especially in distressed neighborhoods. Because of higher traffic levels and denser housing, the soil in urban areas can average 800–1,200 μg/g. Soil from play areas has a larger impact on children’s BLLs than soil from other areas. Lead tire weights that fall off are quickly abraded and ground into tiny pieces by traffic, resulting in high dust-loading rates, especially in urban areas. Lead exposure also occurs through produce grown in contaminated soil.

20Children living near mining and smelting sites are at risk for EBLs. Studies find effects even 20 years after smelter closing.

21Historical research to uncover past commercial activities can identify current sources of exposure. For instance, a Washington State study found that homes near locations where lead arsenate was used as a pesticide between 1905 and 1947 had significantly higher soil and indoor dust levels.

22Elevated soil lead levels are found at more than two thirds of Superfund sites in all 50 states. Lead is the chemical most frequently released from uncontrolled hazardous waste sites; in 1997, the ATSDR identified lead contamination in 59% of the sites monitored. Numerous historical mining and smelting districts are now Superfund sites.

23BLLs can rise 1–5 μg/dL for every 1,000-ppm increase in soil lead.

24Dusts are composed of fine particles of soil, paint, and industrial or automotive emissions. They accumulate on exposed surfaces and are trapped in clothing and carpet fibers. Ingesting dust particles is the typical route of lead exposure for children. Dust is absorbed more readily than either paint or soil; house dust levels best predict children’s BLLs. Consequently, regulations for lead abatement and remediation have included dust clearance standards that quantify lead concentrations.

25BLLs can rise 1–5 μg/dL for every 1,000-ppm increase in dust lead.

26The sources of lead in food may be natural or anthropogenic, and contamination can occur at any point in processing through contact with metal implements, solder, pigments, glazes, or packaging. Lead also enters food from drinking water, serving utensils, and household dust. Dietary exposures in the United States are 1–4 μg lead per day, and have remained fairly constant during the past decade. Foreign manufacturers who fail to meet U.S. standards can produce contaminated food.

27Lead in breast milk is related to current maternal exposures and to past exposures mobilized from lead stored in bones. Even low levels of lead in breast milk strongly influence an infant’s BLL. Calcium supplementation can reduce lead in breast milk. In a randomized trial, calcium supplements lowered BLLs in lactating women with past high lead exposure and low dietary calcium intake. The benefits of breastfeeding outweigh concern for lead at BLLs common among U.S. women.

28Lead is unlikely in source water but contaminates tap water through the corrosion of plumbing materials containing lead. Lead pipes are more likely to be found in older homes. In new homes, legally “lead-free” plumbing components can contain up to 8% lead. New plumbing leaches lead more readily than older fixtures, where mineral scale covers internal surfaces. The largest unaddressed sources of lead in water are brass or chrome-plated fixtures and illegal use of lead solder.

29Cases of pediatric lead poisoning have been associated with drinking water. BLLs correlate with drinking water lead levels even in populations with low exposures. Sampling drinking water to determine exposure is difficult, and it is easy for sporadic or short-term elevations to go undetected. Hence, exposure to lead from drinking water may be underestimated.

30Changing or introducing secondary disinfection practices (to kill waterborne pathogens) can affect lead levels in drinking water. After Washington, DC, switched disinfection agents, children in homes with lead service lines did not experience the almost 70% decrease in BLLs > 5 μg/dL experienced by other children. Children with lead service lines also had considerably higher BLLs (32% >5 μg/dL vs. 23% citywide). Another study of changing disinfectants found that both water lead and BLLs increased.

31Lead levels in school drinking water can rise because long periods of nonuse (overnight, weekends, vacation) are followed by heavy consumption. The U.S. EPA has developed guidelines to help schools manage lead in their drinking water.

32Drinking water contributes an estimated 10–20% of the total lead exposure of the general population; formula-fed infants can have higher exposures. Drinking-water lead levels > 15 ppb are associated with a 14% increase in the percentage of children with BLLs > 10 μg/dL.

33Lead levels in chocolate products exceed those in other foods. In 1980, the market basket Total Diet Study (TDS) by the FDA found lead levels in chocolate milk more than three times those in whole milk, and levels in milk chocolate candy approximated those in canned foods. In the 2004 TDS, chocolate bars had the highest lead levels of the 280 items surveyed. A 2005 study comparing lead concentrations and isotopic compositions of cocoa beans grown in Nigeria with finished candy products found levels 60 times higher in finished candy versus cocoa beans. No single source of lead was identified; levels rose at each stage of production.

34Candy imported from Mexico is found repeatedly with high lead levels. Both candy and wrappers printed with lead ink have been cited. Lead-contaminated candy has also been imported from the Philippines and from Asian and Latin American countries. EBL cases have been reported in California, New York, North Dakota, Oklahoma, and Texas. In California, in 2001, candy was identified as a possible lead source for > 150 children with EBLs. In November 2006, the FDA reduced its recommended maximum lead level for candy consumed by children from 0.5 ppm to 0.1 ppm.

35Foods and packaging produced outside the United States can contain high lead levels. Several spices, especially Hungarian paprika, have been contaminated. Food coloring also has been implicated in children’s EBLs. In 2006, California sued PepsiCo and Coca-Cola Co. concerning lead in the labels of bottles brought to the United States from Mexico.

36An assessment of 84 dietary supplements found lead in all, with 11 samples exceeding the tolerable dietary lead intake level. These results correlate with other FDA data. Other herbal supplements associated with high levels of lead include nettle and supplements to treat hair loss.

37The Dietary Supplement Health and Education Act prevents the FDA from requiring premarket safety approval for supplements; hence, they require neither proof of safety nor efficacy. The FDA recently proposed good manufacturing practice regulations to help ensure the safety of dietary supplements and is developing a final rule.

38Leaded crystal contains 24–32% lead oxide. Crystal decanters and glasses can release high amounts of lead in a short time, especially with cola. The FDA has cautioned that children and pregnant women should avoid frequent use of crystal glassware and should not use lead crystal baby bottles.

39Ceramic pottery and other dinnerware containing lead glazes can be important exposure sources. Numerous reports of EBLs associated with homemade or low-fired ceramics from Mexico, southern Europe, North Africa, and the Middle East exist. Relatively new, commercially manufactured ceramic dinnerware has also been cited. The FDA has established criteria for leachable lead in ceramics ranging from 0.5 to 3.0 μg/mL, depending on the product.

40Glassware with decals or painted surfaces can also contain lead. In 1979, the FDA and the U.S. glassware industry established a voluntary quality control program for decorated glasses that contain lead. Since 1994, the FDA has exempted ornamental ceramicware from lead-leaching requirements if it contains a permanent marking warning “for decorative use only”. A complete listing of dishware restricted for importation is available.

41The U.S. FDA advised manufacturers and suppliers that lead in soft vinyl lunchboxes may transfer to food. Thus, it could be deemed an unsafe food additive (under Section 409 of the Federal Food Drug and Cosmetic Act) and adulterated within the meaning of Section 402(a)(2)(C) of the statute and subject to regulation.

42According to the Consumer Product Safety Commission (CPSC), lead is the most frequently recalled substance that could result in poisoning. Many products associated with childhood lead poisoning are imported and do not meet U.S. standards. A listing of all CPSC-recalled items is available. Products containing wood, metal, plastic, ceramics, and paper have been found with high lead concentrations.

43Consumer goods with high lead content are found regularly. One study showed that 94% of plastic bread bags contained lead in the printing ink; a survey of families found that 16% reused bags to package children’s lunches. In March and April 2007, CPSC issued recalls of 2,500 children’s painting easels, 128,700 toy sets, 400,000 key chains, 58,000 children’s necklaces, and 4 million children’s bracelets because of lead content. In August and September 2007, Mattel Inc. alone recalled 2.8 million lead-contaminated toys. All of these items were made in China.

44A study of toy jewelry found lead concentrations ≥ 50% in 40% of samples; when wiped, 70% of these samples released at least 1.0 μg lead, enough to cause high exposure with little handling. The scope and frequency of the recalls suggest that the current nonregulatory approach to controlling lead in children’s products could be strengthened.

45Lead salts are used to stabilize polymers to avoid degradation from heat, sunlight, and wear. Although several studies demonstrate that dangerous lead exposures can occur with normal use of PVC products after extended use or exposure to sunlight, initial evaluation by CPSC found that lead in PVC products posed few risks to children.

46An investigation of vinyl miniblinds found that they contaminate house dust and contribute significantly to lead toxicity in children. Because about 30 million sets are sold annually and the polymers degrade under normal conditions, this might be a lead exposure source for millions of children, particularly those living in manufactured housing commonly equipped with miniblinds.

47Since 1977, the water pipe market has more than doubled, and 80% of new drinking water and wastewater pipes are plastic, mostly PVC. Early tests of PVC pipes showed that lead contamination could be high. Despite a standardized testing procedure for plastic pipes to reduce the potential for high lead exposures, reports of dangerous exposures from plastic pipes continue.

48Artificial Christmas trees made of PVC also degrade under normal conditions. About 50 million U.S. households have artificial Christmas trees, of which about 20 million are at least 9 years old, the point at which dangerous lead exposures can occur. High lead levels have also been found in telephone cords.

49Synthetic turf is currently used on about 3,500 playing fields throughout the United States. Rubber infill or crumbs made from recycled tires keep the turf blades upright, and this rubber can contain lead. The exposure potential, especially on older fields that have accumulated dust and where the materials are deteriorating, is a research gap.

50Candles with a lead metal core contribute to lead in the home. Exposure occurs both from air and from hand-to-mouth activity. However, to date, no children’s EBLs traceable to candles have been reported. In 2002, the CPSC banned candlewicks containing > 0.06% lead.

51Approximately 38 million homes had lead-based paint (LBP) in 2000. Of those, an estimated 24 million units had deteriorated lead paint, dust lead, or bare soil contaminated with lead. Of those with LBP hazards, 1.2 million units housed low-income families with children < 6 years of age. A relatively small number of properties may account for large numbers of children with EBLs.

52Housing units with LBP hazards are not evenly distributed. In 2000, for households with incomes ≤ $30,000—the federal poverty level at that time—35% of the housing units had LBP hazards compared with 19% of all housing units. Northeast and Midwest housing has twice the prevalence of LBP hazards compared with housing in the South and West. Although the prevalence of LBP hazards increases with the age of the building, most painted surfaces, even in older housing, do not have lead paint; only 2–25% of building components have LBP.

53Children in units with LBP are almost 10 times more likely to have an EBL than children in similar housing without lead paint. Addressing lead paint hazards significantly reduces the risk of identifying another child with an EBL in a unit where one was previously identified.

54Mean BLLs of children whose housing was abated show a 38% decrease over a 2-year period after lead hazard control. Nonetheless, disturbing lead painted surfaces can increase the BLLs of children living in those units during repair work unless appropriate controls are instituted, especially dust clearance levels. Studies of well-conducted renovation activities show that although lead hazard interventions reduce most children’s BLLs, about 10% of the time BLLs significantly increased; young children (< 18 months of age) are at highest risk of increases. BLLs of children who continued to live in the house or relocated for less than the full work period also were significantly more likely to increase than those of children who relocated for the entire renovation. Consequently, remediation and abatement activities that disturb lead paint must be followed by specialized cleaning and dust-lead testing to determine whether the unit is safe for re-occupancy.

55Between 1976 and 2002, the National Health and Nutrition Examination Surveys (NHANES) identified a constellation of risk factors for EBLs among children. Previously undocumented risk factors continue to be uncovered in urban areas and within particular subpopulations. Nationally representative samples do not identify or characterize local risks. The CDC recommends that states target communities with the highest risk for lead exposure, using established risk factors.

56Children’s BLLs peak around 15–24 months of age. This age dependence persists even as average BLLs have decreased. Given the pervasive lead contamination of our environment, it is not surprising that normal hand-to-mouth behaviors result in high exposures among toddlers. Young children also absorb lead more readily than do older children and adults. Exposures with little effect on adults cause high levels in young children.

57The NHANES show an association between BLLs and race/ethnicity (Figure 3). In 1976–1980, the geometric mean BLL for all U.S. children was 16 μg/dL versus 21 μg/dL for black children. Data from 1999–2002 show similar patterns: 46.8% of non-Hispanic black children and 27.9% of Mexican-American children exceeded 5 μg/dL compared with 18.7% for white children. Fortunately, the gap is narrowing. The most recent national data show that non-Hispanic black children had the largest decline in BLLs (72%) of all racial and ethnic groups, reducing the differences between subpopulations (Jones R, personal communication).

58Folk medicines and remedies from many cultures can contain high lead levels. Traditional Mexican remedies were the earliest focus, but poisonings in six states and one death have been linked to Ayurveda, a traditional South Asian medicine. Imported herbal remedies are available at many local markets. Ethnic and imported cosmetics and other goods have also been associated with high lead exposures.

59Refugee, internationally adopted, and recent immigrant children are more likely than U.S.-born children to have EBLs, both on arrival in the country and later. Many foreign children enter the United States with EBLs resulting from lead sources in their native countries. Their BLLs rise after resettlement because of both lead contamination in their new environments and continued use of imported products containing lead. Existing health burdens and cultural, language, and economic barriers compound the risk for lead poisoning after resettlement. For example, iron deficiency, prevalent among refugee children, increases lead absorption through the gastrointestinal tract. Exposure to small amounts of lead can result in very high BLLs in iron-deficient children.

60An increased risk for EBLs has been documented among refugee and immigrant children from Africa, Cuba, China, Russia, Thailand, and other countries. For instance, although there were only 46 cases of EBLs in Manchester, New Hampshire, in 1997, there were 88 in 2004; all the additional EBLs were among African-born children. In 2003, the CDC found that 45% of refugee children had elevated BLLs a few months after resettlement. BLLs are often elevated in school-age and teenage foreign-born children. The CDC recommends testing refugee and immigrant children on entry to the United States and again 3–6 months later, mirroring policies established by New Hampshire’s CLPPPs after a fatality in 2000. The CDC also recommends nutritional evaluation and intervention for deficiencies.

61Children with EBLs are more common in communities with many households below the federal poverty level, independent of housing age or proportion of black children. In 1976–1980, children with the lowest family income had an average BLL of 20 μg/dL versus 16 μg/dL nationally. In Massachusetts in 1991–1992, the 15 communities with > 25% of children ≤ 5 years old living in poverty accounted for 71% of children with BLLs ≥ 25 μg/dL.

62Income-based disparities of EBLs in children have narrowed. In 1991–1994, the percent of children with EBLs was 4.5% in the lowest income group versus 0.7% in the highest income group. By 1999–2002, the difference between the percent of Medicaid-enrolled children with EBLs and the general population was not statistically significant (1.7% vs. 1.3%, respectively). However, the geometric mean BLL for Medicaid-enrolled children exceeds unenrolled children, indicating continued disparity in lead exposures (2.6 μg/dL vs. 1.7 μg/dL) (CDC, unpublished data).

63Housing built before the 1978 ban on lead paint is a significant risk factor for exposure. Forty-two percent of children living in housing built before 1946, and 39% of children in housing built between 1946 and 1973 had BLLs ≥5 μg/dL versus 14% of children in housing built after 1973.

64Children 1–5 years of age living in the 10 largest U.S. cities accounted for 46% of EBLs reported to the CDC in 2003 but only 7% of the population that age (CDC, unpublished data). Usually, EBL cases are clustered within cities. A 2001 study of seven cities found that 50% of children with EBLs lived in 11% of the ZIP codes in those cities.

65Lead contamination typically is greater in urban versus rural areas. Although long-distance transport of lead does occur, many studies show that most of the lead emitted in urban areas remains there. The discrepancy between BLLs of urban and rural children has remained constant despite the decline in overall lead exposures for U.S. children since the late 1970s.

66Lead dust from work inadvertently carried by parents settles on surfaces and workers’ clothing, where it can be ingested or inhaled by young children. Children of lead-exposed workers have disproportionately higher BLLs. Based on 1981–1983 survey data, an estimated 48,000 families with children < 6 years of age had a household member who worked with lead. Concern for take-home exposure is not new; two studies from the early 1900s identified severe poisonings of workers’ families, including case histories from 1860.

67Many occupations with potential high lead exposures are exempted from Occupational Safety and Health Administration workplace protections, including transportation workers, most public employees, and self-employed workers in industries such as battery reclamation, automobile repair, pottery and ceramics, and stained glass. Undocumented workers are particularly vulnerable because of limited access to exposure monitoring and protective measures.

68BLLs are significantly higher in warm weather in both national and local studies. The relation persists despite the decline in lead exposure. Several factors may explain seasonal variations: greater exposures to soil lead, dispersion of dust when lead-painted windows are opened and shut, and remobilization of lead on interior surfaces as air moves through open windows and doors. In warmer weather, children’s longer hours outdoors may increase exposure to airborne and soil lead and contribute to seasonality in BLLs. Changes in Vitamin D exposures during the warmer weather may also account for some of the seasonality observed.

69Having a smoker in the house has been associated with higher BLLs in children for 30 years. Cotinine levels still correlate positively with BLLs.

70The current CDC advisory level for intervention in individual children is 10 μg/dL. It is not a safe level; studies show strong and long-lasting effects with BLLs as low as 2 μg/dL. Therefore, the CDC recommends primary prevention—that is, that all lead sources in children’s environments be controlled or eliminated before children are exposed.

71Achieving the Healthy People 2010 objective—to reduce BLLs as much as possible and to eliminate childhood lead poisoning— will require collaboration by all levels of government. This cannot succeed without enforcing all existing standards, ensuring that ambient lead levels continue to decline, and reversing recent trends of increased lead exposures, such as air lead and imported consumer goods. Table 2 summarizes federal authorities for regulating lead.

72Lead-based paint in housing remains the most common high-dose source of lead in children’s environments. Reducing lead hazards in housing requires

73Data to be shared across organizational boundaries

74Local and state regulatory requirements for lead-safe housing

75Strengthened enforcement of existing laws, especially cleanup

76Greater public and private investment for lead hazard control.

77Some of the most hazardous residential units may not be eligible for HUD’s Lead Hazard Control program because they are uninsured, have outstanding taxes, have other serious code violations, or because the owner cannot be located. In this case, emergency funds are needed to raze buildings that cannot reasonably be made safe. Evidence that primary prevention is effective is mounting. For example, a project initiated in 1998 by HUD, assisted by the Department of Justice, the CDC, and the U.S. EPA, to enforce Title 1018 of the Toxic Substances Control Act has resulted in commitments to make over 185,000 high-risk properties lead-safe by 2006 (Gant J, HUD, personal communication).

78Local CLPPPs remain the frontline in identifying lead exposure sources. As particular lead paint hazards are controlled or eliminated, other lead sources assume greater importance and visibility. The CDC recommends that when children with EBLs are identified, CLPPPs identify all sources of lead in the child’s environment. Research is needed on effective intervention strategies for children with BLLs above average but < 10 μg/dL to prevent dangerous exposures.

79Creating lead-safe communities can occur only with the active involvement of all levels of government—local, state, and federal—and will depend on several strategies. Foremost are systems that monitor and evaluate all children’s potential lead exposures. Other keys to institutionalizing primary prevention are requirements for lead-safe housing and work practices, dust- and soil-lead testing after repairs in older housing, identification of all lead sources for children with EBLs, elimination of products with dangerous lead levels, and timely mechanisms to share information about lead sources, including toxic properties, across government agencies.

80State and local officials should evaluate whether their existing primary prevention efforts sufficiently protect children.

81Federal agencies should support local and state efforts by

82Monitoring lead in air, drinking water, food, and consumer products

83Enforcing laws that control lead contamination

84Educating specific populations about lead and controlling exposures

85Improving exposure modeling techniques, accounting for all sources of exposure

86Conducting research and ongoing evaluation of lead poisoning prevention activities.

87The Healthy People 2010 objective to eliminate BLLs ≥ 10 μg/dL is within our grasp. The course is clear. We must identify and address all existing lead hazards and be vigilant in preventing new hazards. Recent research describes the enormous societal benefits to be reaped from preventing lead exposure in children, with total annual estimates of $43–110 billion or more. The overall reduction of lead in the environment will benefit all U.S. children—and adults, too.

88In “Sources of Lead Exposure,” the percentages given for types of sources were incorrect in the manuscript originally published online. They have been corrected here.