Some recent tragedies have evinced a more

complicated risk pattern for pediatric lead

exposures in the United States than had previously been considered: 

• 21 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 [Centers for Disease

Control and Prevention (CDC) 2005a]. 

• July 2002, New York City: A 1-year-old’s

elevated blood lead level was traced to

ceramic dinnerware without visible signs of

wear (CDC 2004a). 

• 23 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were 224,377 μg/ft2 (Brown MJ, unpublished memo to the Consumer Product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). 

• 2004, Oregon: A child was hospitalized

after ingesting a necklace made with lead,

resulting in voluntary recall of 150 million

pieces of children's jewelry (CDC 2004b). 

• 23 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 (CDC 2006). 

The 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. 

Introduction

Lead 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) (Davidson

and Rabinowitz 1992). 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 (Mahaffey et al. 1982; Pirkle

et al. 1998). 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%) (CDC 2005b).

The adverse health effects of lead—including death, insanity, nervous system damage,

and sterility—have been reported since

the second century BCE (Major 1945). 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

(Jusko et al. 2008). No threshold for effects

has been demonstrated.

In 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

(Department of Health and Human Services

2000). However, projections of future

decreases in the number of children with

EBLs (Jacobs et al. 2002) 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 (Jacobs and

Nevin 2006). The 2010 goal may fall short

without augmented investment.

Screening 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. 

Sources of Lead Exposure

Deteriorating 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

[U.S. Environmental Protection Agency

Environmental Health Perspectives • VOLUME 116 | NUMBER 10 | October 2008 1285

Review

Address correspondence to R. Levin, U.S. EPA SEP,

One Congress St., Boston MA 02114 USA.

Telephone: (617) 918-1716. Fax: (617) 918-0716.

E-mail: levin.ronnie@epa.gov 

*Current address: National Center for Healthy

Housing, Columbia, Maryland, USA.

We thank J. Matheson, I. Cote, D. Brown,

M. Bolger, J. Bryson, J. Mosby, and our anonymous

reviewers for their assistance. 

This article reflects the opinions of the authors, not

the official positions of the federal agencies listed.

The authors declare they have no competing

financial interests.

Received 7 January 2008; accepted 19 May 2008.

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

Ronnie Levin,1 Mary Jean Brown,2 Michael E. Kashtock,3 David E. Jacobs,4* Elizabeth A. Whelan,5

Joanne Rodman,6 Michael R. Schock,7 Alma Padilla,1 and Thomas Sinks2

1U.S. Environmental Protection Agency, Boston, Massachusetts, USA; 2Centers for Disease Control and Prevention, Atlanta, Georgia,

USA; 3Food and Drug Administration, Washington, DC, USA; 4Department of Housing and Urban Development, Washington, DC, USA; 5National Institute for Occupational Safety and Health, Cincinnati, Ohio, USA; 6U.S. Environmental Protection Agency, Washington, DC,

USA; 7U.S. Environmental Protection Agency, Cincinnati, Ohio, USA

OBJECTIVE: We reviewed the sources of lead in the environments of U.S. children, contributions to

children’s blood lead levels, source elimination and control efforts, and existing federal authorities.

Our context is the U.S. public health goal to eliminate pediatric elevated blood lead levels (EBLs)

by 2010.

DATA SOURCES: National, state, and local exposure assessments over the past half century have

identified risk factors for EBLs among U.S. children, including age, race, income, age and location

of housing, parental occupation, and season. 

DATA EXTRACTION AND SYNTHESIS: Recent national policies have greatly reduced lead exposure

among U.S. children, but even very low exposure levels compromise children’s later intellectual

development and lifetime achievement. No threshold for these effects has been demonstrated.

Although lead paint and dust may still account for up to 70% of EBLs in U.S. children, the U.S.

Centers for Disease Control and Prevention estimates that ≥ 30% of current EBLs do not have an

immediate lead paint source, and numerous studies indicate that lead exposures result from multiple sources. EBLs and even deaths have been associated with inadequately controlled sources

including ethnic remedies and goods, consumer products, and food-related items such as ceramics.

Lead in public drinking water and in older urban centers remain exposure sources in many areas. 

CONCLUSIONS: Achieving the 2010 goal requires maintaining current efforts, especially programs

addressing lead paint, while developing interventions that prevent exposure before children are poisoned. It also requires active collaboration across all levels of government to identify and control all

potential sources of lead exposure, as well as primary prevention.

KEY WORDS: children’s health, environmental health, lead poisoning, primary prevention. Environ

Health Perspect 116:1285–1293 (2008). doi:10.1289/ehp.11241 available via http://dx.doi.org/

[Online 19 May 2008]
(EPA) 2006a]. 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 (Arizona Department of

Health Services 2005). 

Nonpaint 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 (Bernard

and McGeehin 2003). 

Lead in the environment. The United

States is the third largest lead producer, producing about 450,000 tons in 2003 (U.S.

Geological Service 2004). In 2003, the United

States consumed about 1.5 million tons of

lead (Commodity Research Bureau 2006).

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). 

Air. During 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% (U.S.

EPA 2007a). 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). 

After declining for > 25 years, U.S. air

lead levels rose in 2004–2006 (Figure 2) (U.S.

EPA 2007a). 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

(U.S. EPA 2007a). 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 (U.S. EPA 2007b). 

Not 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

(Environment Canada 2000). Another study

showed that even at an airport with few planes

using avgas, air lead levels were higher downwind than upwind (Illinois Environmental

Protection Agency 2002). 

Demolition of old buildings contributes to

local air lead levels and can increase BLLs in

children (Farfel et al 2003; Rabito et al 2007).

Soil. Lead 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

(Duggan and Inskip 1985; Lanphear 1998a).

Soil from play areas has a larger impact on

children’s BLLs than soil from other areas

(Lanphear et al. 1998b; Mielke and Reagan

1998). 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 (Root 2000). Lead

exposure also occurs through produce grown

in contaminated soil (Finster et al. 2004).

Children living near mining and smelting

sites are at risk for EBLs (Maisonet et al.

1997; Murgueytio et al. 1996; Swarup et al.

2005). Studies find effects even 20 years after

smelter closing (Diaz-Barriga et al. 1997). 

Historical research to uncover past commercial activities can identify current sources

of exposure (Eckel et al. 2001). For instance,

a Washington State study (Wolz et al. 2003)

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.

Elevated soil lead levels are found at more

than two thirds of Superfund sites in all 50

states [Agency for Toxic Substances and

Disease Registry (ATSDR) 2005]. 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 (ATSDR 2005).

Numerous historical mining and smelting

districts are now Superfund sites (Spalinger

et al. 2007).

BLLs can rise 1–5 μg/dL for every 1,000-

ppm increase in soil lead (U.S. EPA 2006a).

Dust. Dusts 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 (U.S. EPA

2006a). Dust is absorbed more readily than

either paint or soil; house dust levels best predict children’s BLLs (Lanphear et al. 1998c).

Consequently, regulations for lead abatement

and remediation have included dust clearance

standards that quantify lead concentrations

[Department of Housing and Urban Development (HUD) 1999; U.S. EPA 2006c].

Levin et al.

1286 VOLUME 116 | NUMBER 10 | October 2008 • Environmental Health Perspectives

Figure 1. Increases in lead production and corresponding increases in lead emissions. Data from Davidson

and Rabinowitz (1992) and U.S. EPA (1986).

106

105

104

103

102

101

100

5,500 5,000 4,500 4,000 3,500 3,000 2,500 2,000 1,500 1,000 500 0

Solar years before present

Production worldwide (tons/year)

Discovery of

cuppellation

Rise and fall

of Athens

Roman Republic

and Empire

Introduction of coinage

Lead production

begins in

Germany

Industrial

Revolution

Exhaustion of

Roman silver mines Spanish production

of silver in New World
BLLs can rise 1–5 μg/dL for every 1,000-

ppm increase in dust lead (U.S. EPA 2006a).

Lead in the diet. The 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 [U.S. Food and Drug Administration

(FDA) 2006a], and have remained fairly constant during the past decade. Foreign manufacturers who fail to meet U.S. standards can

produce contaminated food. 

Breast milk. Lead in breast milk is related to

current maternal exposures and to past exposures mobilized from lead stored in bones

(Chien et al. 2006). Even low levels of lead in

breast milk strongly influence an infant’s BLL

(Ettinger et al. 2006). 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 (Hernandez-Avila

et al. 2003). The benefits of breastfeeding outweigh concern for lead at BLLs common among

U.S. women (Lawrence 1997). 

Drinking water. Lead is unlikely in

source water but contaminates tap water

through the corrosion of plumbing materials

containing lead (Chin and Karalekas 1985;

Levin 1986). 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 (Safe Drinking Water Act

Amendments of 1986). 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 (U.S. EPA 2006b). 

Cases of pediatric lead poisoning have

been associated with drinking water (CDC

1994; Cosgrove et al. 1989; Shannon and

Graef 1989). BLLs correlate with drinking

water lead levels even in populations with low

exposures (Lanphear et al. 1998b). Sampling

drinking water to determine exposure is difficult, and it is easy for sporadic or short-term

elevations to go undetected (Schock 1999).

Hence, exposure to lead from drinking water

may be underestimated (Testud et al. 2001). 

Changing 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

(CDC 2004c). Children with lead service lines

also had considerably higher BLLs (32%

> 5 μg/dL vs. 23% citywide) (CDC 2004c).

Another study of changing disinfectants found

that both water lead and BLLs increased

(Miranda et al. 2007). 

Lead levels in school drinking water can

rise because long periods of nonuse (overnight,

weekends, vacation) are followed by heavy consumption (Bryan 2004). The U.S. EPA has

developed guidelines to help schools manage

lead in their drinking water (U.S. EPA 2006d). 

Drinking water contributes an estimated

10–20% of the total lead exposure of the general population (U.S. EPA 1991); formula-fed

infants can have higher exposures. Drinkingwater lead levels > 15 ppb are associated with a

14% increase in the percentage of children

with BLLs > 10 μg/dL (Lanphear et al. 1998b). 

Chocolate. Lead 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 (Pennington 1983). In

the 2004 TDS, chocolate bars had the highest

lead levels of the 280 items surveyed (FDA

2006a). 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 (Rankin et al.

2005). No single source of lead was identified;

levels rose at each stage of production. 

Candy. Candy imported from Mexico is

found repeatedly with high lead levels. Both

candy and wrappers printed with lead ink have

been cited (CDC 2002a; FDA 1995; Lynch

et al. 2000; North Dakota Department of

Health 2004). 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 (FDA 2006b). 

Imported foods. Foods and packaging

produced outside the United States can contain high lead levels. Several spices (Sattar

et al. 1989; Woolf and Woolf 2005), especially Hungarian paprika, have been contaminated (Kakosy et al. 1996). Food coloring

also has been implicated in children’s EBLs

(Vassilev et al. 2005). In 2006, California

sued PepsiCo and Coca-Cola Co. concerning

lead in the labels of bottles brought to the

United States from Mexico (Lifsher 2006). 

Dietary supplements. An assessment of 84

dietary supplements found lead in all, with 11

samples exceeding the tolerable dietary lead

intake level (Dolan et al. 2003). These results

Lead exposures in U.S. children, 2008

Environmental Health Perspectives • VOLUME 116 | NUMBER 10 | October 2008 1287

Table 1. Lead used in Massachusetts manufacturing, 2003. 

Activity/facility type No. of facilities Total use (lb)

Municipal waste combustors 7 2,642,987

Wire and cable manufacturing 21 2,622,713

Rubber and plastics manufacturing 10 1,856,941

Hazardous waste facilities 1 714,118

Fabricated metals manufacturing 22 363,406

Chemicals and allied products 12 304,619

Primary metals manufacturing 8 157,742

Electronic equipment manufacturing 37 119,651

Others 134 503,451

Total 252 9,285,628

Data from Massachusetts Department of Environmental Protection (2005).

Figure 2. Maximum quarterly mean air lead concentrations, 1980–2006, showing 95% decrease 1980–2003

and slight increase 2004–2006; national trend based on 15 sites. Reprinted from U.S. EPA (2007a). 

2.5

2.0

1.5

1.0

0.5

0.0

Concentration (μg/m3)

198019811982198319841985198619871988198919901991199219931994199519961997199819992000200120022003200420052006

National standard

1980–2006: 95% decrease in national average
correlate with other FDA data (Hight et al.

1993; Wong et al. 2004). Other herbal supplements associated with high levels of lead

include nettle (FDA 2002) and supplements

to treat hair loss (Health Canada 2004). 

The 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 (Marcus and Grollman

2002). The FDA recently proposed good

manufacturing practice regulations to help

ensure the safety of dietary supplements

(FDA 2003b) and is developing a final rule. 

Glass and dishes. Leaded crystal contains

24–32% lead oxide. Crystal decanters and

glasses can release high amounts of lead in a

short time, especially with cola (Guadagnino

et al. 2000). The FDA has cautioned that children and pregnant women should avoid frequent use of crystal glassware and should not

use lead crystal baby bottles (Farley 1998). 

Ceramic 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 (HellstromLindberg et al. 2006; Manor and Freundlich

1983; Matte et al. 1994). Relatively new,

commercially manufactured ceramic dinnerware has also been cited (CDC 2004a). The

FDA has established criteria for leachable lead

in ceramics ranging from 0.5 to 3.0 μg/mL,

depending on the product (FDA 2005c). 

Glassware with decals or painted surfaces

can also contain lead (Sheets 1999). In 1979,

the FDA and the U.S. glassware industry

established a voluntary quality control program for decorated glasses that contain lead

(FDA 1992). Since 1994, the FDA has

exempted ornamental ceramicware from leadleaching requirements if it contains a permanent marking warning “for decorative use

only” (FDA 1992). A complete listing of

dishware restricted for importation is available

(FDA 2007b). 

Vinyl lunchboxes. The U.S. FDA advised

manufacturers and suppliers that lead in soft

vinyl lunchboxes (FDA 2006c) may transfer

to food. Thus, it could be deemed an unsafe

food additive (under Section 409 of the

Federal Food Drug and Cosmetic Act) (FDA

2008) and adulterated within the meaning of

Section 402(a)(2)(C) of the statute and subject to regulation. 

Lead in consumer goods. According 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 (CDC 2002a; Geltman et al. 2001).

A listing of all CPSC-recalled items is available

(CPSC 2007). Products containing wood,

metal, plastic, ceramics, and paper have been

found with high lead concentrations.

Children’s products. Consumer 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 (Weisel et al.

1991). 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 (Denver Post 2007). All of these items

were made in China. 

A study of toy jewelry found lead concentrations ≥ 50% in 40% of samples (Maas

et al. 2005); 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. 

Polyvinyl chloride (PVC). Lead 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 (CPSC 1997). 

An investigation of vinyl miniblinds

found that they contaminate house dust and

contribute significantly to lead toxicity in

children (Norman et al. 1997; West et al.

1998). 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. 

Since 1977, the water pipe market has

more than doubled, and 80% of new drinking

water and wastewater pipes are plastic, mostly

PVC (Vinyl News Service 2006). Early tests of

PVC pipes showed that lead contamination

could be high (National Academy of Sciences

Safe Drinking Water Committee 1982).

Despite a standardized testing procedure for

plastic pipes to reduce the potential for high

lead exposures [Mitchener 1992; NSF/ANSI

(American National Standards Institute)

2008; U.S. EPA 2007e], reports of dangerous

exposures from plastic pipes continue (Koh

et al. 1991). 

Artificial Christmas trees made of PVC

also degrade under normal conditions (Maas

et al. 2004). 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 (Abdul-Razzaq et al. 2003). 

Synthetic turf. Synthetic turf is currently

used on about 3,500 playing fields throughout the United States (Claudio 2008).

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.

Candle wicks. Candles with a lead metal

core contribute to lead in the home (Nriagu

and Kim 2000; van Alphen 1999). 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 (CPSC 2003). 

Lead paint in housing. Approximately

38 million homes had lead-based paint (LBP)

in 2000 (Jacobs and Nevin 2006). Of those,

an estimated 24 million units had deteriorated

lead paint, dust lead, or bare soil contaminated

with lead (Jacobs et al. 2002). Of those with

LBP hazards, 1.2 million units housed lowincome families with children < 6 years of age.

A relatively small number of properties may

account for large numbers of children with

EBLs (Korfmacher and Kuholski 2007; Meyer

et al. 2005; Reyes et al. 2006).

Housing units with LBP hazards are not

evenly distributed (Jacobs et al. 2002). 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 (Jacobs

et al. 2002). 

Children in units with LBP are almost 10

times more likely to have an EBL than children in similar housing without lead paint

(Schwartz and Levin 1991). Addressing lead

paint hazards significantly reduces the risk of

identifying another child with an EBL in a

unit where one was previously identified

(Brown et al. 2001a).

Mean BLLs of children whose housing

was abated show a 38% decrease over a 2-year

period after lead hazard control (National

Center for Healthy Housing and the

University of Cincinnati Department of

Environmental Health 2004). Nonetheless,

disturbing lead painted surfaces can increase

the BLLs of children living in those units during repair work unless appropriate controls are

Levin et al.

1288 VOLUME 116 | NUMBER 10 | October 2008 • Environmental Health Perspectives
instituted, especially dust clearance levels

(Amitai et al. 1991; Bellinger et al. 1986;

HUD 1995). 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 (CDC 1997; Clark et al. 2004);

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. 

Risk Factors for EBLs in

U.S. Children

Between 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 (Dignam et al. 2004).

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 (CDC 2003). 

Age. Children’s BLLs peak around 15–24

months of age (Tong et al. 1996). 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 (Faustman et al. 2000). 

Race and ethnicity. The 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 (Mahaffey

et al. 1982). 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 (CDC 2005b).

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). 

Use of ethnic remedies, cosmetics, and

goods. Folk medicines and remedies from

many cultures can contain high lead levels

(Baer and Ackerman 1988; Trotter 1985).

Traditional Mexican remedies were the earliest focus (CDC 2002a), but poisonings in six

states and one death have been linked to

Ayurveda, a traditional South Asian medicine

(CDC 1984, 2004d; Moore and Adler 2000).

Imported herbal remedies are available at

many local markets (Saper et al. 2004).

Ethnic and imported cosmetics and other

goods have also been associated with high

lead exposures (CDC 2005c; Sprinkle 1995).

Immigrant or refugee status. Refugee,

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 (Geltman et al. 2001; Miller

and Hendrie 2000; Tehranifar et al. 2008).

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 (Stauffer et al. 2002;

Weissman 1994). 

An increased risk for EBLs has been documented among refugee and immigrant children from Africa, Cuba, China, Russia,

Thailand, and other countries (CDC 2005a;

Mielke et al. 1984; Trepka et al. 2005). 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 (CDC 2005a). BLLs are often

elevated in school-age and teenage foreignborn 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. 

Income level. Children with EBLs are

more common in communities with many

households below the federal poverty level,

independent of housing age or proportion of

black children (Bernard and McGeehin 2003;

Sargent et al. 1995). In 1976–1980, children

with the lowest family income had an average

BLL of 20 μg/dL versus 16 μg/dL nationally

(Mahaffey et al. 1982). 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 (Sargent et al. 1995). 

Income-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 (Pirkle et al. 1994).

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). 

Age of housing. Housing 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

(Bernard and McGeehin 2003). 

Location of residence. Children 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 (Brown et al. 2001b). 

Lead contamination typically is greater in

urban versus rural areas (National Research

Council 1993; U.S. EPA 2006a). Although

long-distance transport of lead does occur,

many studies show that most of the lead emitted in urban areas remains there (Flegal et al.

1989). The discrepancy between BLLs

of urban and rural children has remained

Lead exposures in U.S. children, 2008

Environmental Health Perspectives • VOLUME 116 | NUMBER 10 | October 2008 1289

Figure 3. Percentage of U.S. children, 1–5 years of

age, with EBLs ≥ 10 μg/dL (95% confidence intervals), by race/ethnicity. Data from CDC (2005b).

100

80

25

20

15

10

5

0

Percent

NHANES II

1976–1980

NHANES III

phase I

1988–1991

NHANES III

phase II

1991–1994

NHANES

1999–2002

Non-Hispanic black

Mexican American

Non-Hispanic white
constant despite the decline in overall lead

exposures for U.S. children since the late

1970s (Brody et al. 1994). 

Parental occupations. Lead dust from work

inadvertently carried by parents settles on surfaces and workers’ clothing, where it can be

ingested or inhaled by young children (Hipkins

et al. 2004). Children of lead-exposed workers

have disproportionately higher BLLs (Chan

et al. 2000; Whelan et al. 1997). 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

(Roscoe et al. 1999). 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

(Holt 1923; Oliver 1914). 

Many 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. 

Other risk factors. Season of the year.

BLLs are significantly higher in warm weather

in both national and local studies (Kaufmann

et al. 2000; U.S. EPA 2007c). 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 (Haley and Talbot 2004),

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 (Yin et al. 2000). Changes in

Vitamin D exposures during the warmer

weather may also account for some of the

seasonality observed (Kemp et al. 2007).

Tobacco smoke. Having a smoker in the

house has been associated with higher BLLs

in children for 30 years (Willers et al. 1988;

Zielhuis et al. 1978). Cotinine levels still correlate positively with BLLs (Mannino et al.

2003). 

Implications for Lead

Poisoning Prevention 

The current CDC advisory level for intervention in individual children is 10 μg/dL (CDC

1991). 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. 

Achieving 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. 

Addressing lead paint hazards. Leadbased paint in housing remains the most

common high-dose source of lead in

children’s environments. Reducing lead hazards in housing requires

• Data to be shared across organizational

boundaries 

• Local and state regulatory requirements for

lead-safe housing

• Strengthened enforcement of existing laws,

especially cleanup

• Greater public and private investment for

lead hazard control.

Some 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). 

Identifying all sources of lead exposure.

Local 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 (CDC 2002b). 

Research is needed on effective intervention

strategies for children with BLLs above average

but < 10 μg/dL to prevent dangerous exposures.

Levin et al.

1290 VOLUME 116 | NUMBER 10 | October 2008 • Environmental Health Perspectives

Table 2. U.S. lead regulatory authorities.

Agency Lead source regulated Statutory authority Voluntary 

CPSC Paint /coatings CPSC 1977 None

Candle wicks CPSC 2003 None

Lead in products intended for use by children None CPSC 2008

FDA Food/materials that contact food (domestic) FDA 2004a None

Lead in bottled water FDA 2003a None

Prescription and over-the-counter drugs FDA 2004b None

Dietary supplements Proposed rule (FDA 2003b) None 

Seizure of imported food, drugs, and cosmetics FDA 2003c None

Candy None FDA 2006a

Ceramics/pottery None FDA 2005a

Shellfish None FDA 2005b

Wine None FDA 2007a

Soft vinyl lunchboxes None FDA 2006b

U.S. EPA Drinking water U.S. EPA 1991 None 

Plumbing components, school drinking water U.S. EPA 1988, 2007c U.S. EPA 2008a

Air U.S. EPA 2008b None 

Lead paint disclosure, renovation/repair, and clean up U.S. EPA 1992, U.S. EPA 2006c None 

Waste management, disposal U.S. EPA 1980a, U.S. EPA 1980b None 

HUD Residential lead paint hazards in federally subsidized properties HUD 1999 None

Disclosure of lead paint at property transfer HUD 1992 None

OSHA Worker protection for general industry OSHA 2008a None

Construction industry OSHA 2008b None 

NSF/ANSI Plumbing codes, plumbing components Local and state housing and plumbing codes NSF/ANSI 2008

U.S. EPA 2007e
Maintaining lead-safe communities.

Creating 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. 

State and local officials should evaluate

whether their existing primary prevention

efforts sufficiently protect children. 

Federal agencies should support local and

state efforts by 

• Monitoring lead in air, drinking water,

food, and consumer products

• Enforcing laws that control lead contamination 

• Educating specific populations about lead

and controlling exposures 

• Improving exposure modeling techniques,

accounting for all sources of exposure

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

Conclusions

The 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 (Grosse et al. 2002; Landrigan et al.

2002; Nevin et al. 2008), 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. 

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