Childhood Lead Poisoning in Galveston, Texas: Background

Transcription

B ackground
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What Is Lead?
Lead (Pb) is a heavy, low melting, bluish-gray metal that
occurs naturally in the Earth’s crust (7). It is actually a
relatively uncommon metal, compared with the two most
abundant metals: aluminum and iron (7), and is usually
found combined with two or more other elements to form
lead compounds. Most commonly it is found in its +2
oxidation state, combined with other substances to form
compounds such as galena (PbS), anglesite (PbSO4) and
cerussite (PbCO3) (154).
Because of its wide availability, durability, malleability, and
low melting point (low enough to melt in a camp fire), humans
have been using lead for numerous purposes since ancient times
(166). Indeed, environmental lead levels have increased more
than 1,000-fold over the past three centuries alone, with the
greatest increase occurring between the years 1950 and 2000—
reflecting the increasing worldwide use of leaded gasoline (7).
Currently the U.S. leads the world in the production of
refined lead (one third of the world’s reserves are in North
America), as well as in the consumption of lead, using 1.3
million tons of lead in 1980—approximately 40% of the
worlds supply. In 1986, lead was the fifth most used metal in
the U.S. (286). Most lead used by industry comes from mined
ores (“primary”) or from recycled scrap metal or batteries
(“secondary”). In the U.S., lead is mined primarily in Alaska
and Missouri. However, most lead today is “secondary” lead
obtained from lead-acid batteries. It is reported that 97% of
these batteries are recycled (7).
History of Lead Use and Regulation
Lead has been used for more than 2000 years (7,166). The
Romans, for example, used lead to build their aqueducts and
water pipes, sweeten food and preserve wine (171), and the use
of leaded type in the 15th century made mass printing possible.
In more recent history, lead has been used extensively
in the U.S. and elsewhere. Lead and lead alloys are
commonly found in pipes, storage batteries, weights, shot
and ammunition, cable covers, and radiation sheets. The
largest use for lead is in storage batteries in cars and other
vehicles. Lead was also added to most interior and exterior
oil house paints for most of the 20th century as pigment and
to increase durability and coverage. Lead tetroxide is a strong
red pigment, often used as a primer to control rust and in
fireworks. Lead chromate is a strong yellow pigment still used
for highway stripes. Prior to 1950, paints contained as much
as 50% lead by dry weight. Lead compounds are also used as
a pigment in dyes, and ceramic glazes and in caulk, although
the amount of lead used in these products has been reduced
in recent years. Tetraethyl lead and tetramethyl lead were once
extensively used in the U.S. as gasoline additives to increase
octane rating and to “reduce engine knocking.” Lead is still
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C H I L D H O O D L E A D P O I S O N I N G I N G A LV E S T O N , T E X A S
used in gasoline in many developing countries. The use of
lead in ammunition, which is the largest non-battery end-use,
has remained fairly constant in recent years. Lead, generally
as lead arsenate, has also been used as a pesticide especially
in orchards (7). A more detailed discussion of the sources
of exposure is addressed in the section, “Sources of Lead
Exposure,” beginning on page 14.
“Environmental lead levels have increased more
than 1,000-fold over the past three centuries alone,
with the greatest increase occurring between the
years 1950 and 2000—reflecting the increasing
worldwide use of leaded gasoline.”
Despite its known toxicity and increasing levels of lead
in the environment, efforts to curb its use have been slow.
Indeed, its usefulness, profitability and sweet taste appear
to have contributed to the Romans—and others much more
recently—consciously minimizing its known adverse health
effects, despite mounting medical evidence about lead’s
extensive and often irreversible toxicity. Nriagu and others
have suggested that lead poisoning, also called “plumbism,”
contributed to the downfall of the Roman empire. He
estimates that Roman aristocrats ingested roughly 180
µg of lead daily (219). If accurate, this level of lead would
have had significant physiological consequences, including
anemia, neurological symptoms, depressed sperm count, and
impaired pregnancy and fetal development.
The characteristic features of acute lead poisoning—anemia,
colic, neuropathy, sterility and coma—were first described by
Hippocrates and Nicander during the 5th and 2nd centuries
BC, respectively (219). In 1904, an Australian physician, J.
Lockhart Gibson, published the first warnings of the toxic
effects of lead-based paint in children (106), and five years later
France, Belgium and Austria became the first countries to ban
leaded paint. Most other European nations as well as Cuba and
Australia phased out lead-based paint in the 1920s and 1930s.
In 1922, League of Nations members signed an agreement
forbidding the use of white lead interior paint. The U.S. did
not join in the prohibition. Massachusetts banned lead paint
that year, but the lead industry helped to engineer a repeal.
The National Lead Company and other white-lead producers
continued to maintain that lead paint was not harmful. During
the 1920s, these companies produced 200,000 tons of white lead
a year, making the U.S. the world’s largest lead producer. In 1928,
to combat undesirable publicity about lead’s health hazards,
the companies formed the Lead Industries Association, a trade
group of white-lead manufacturers to promote and defend its
use. “It’s very clear from the lead industry’s own documents
that it did everything it could to obscure the dangers associated
with lead in paint and gasoline for as long as it possibly could,
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and it was very successful,” says Dr. Jerome Paulson, associate
professor of pediatrics and public health at George Washington
University and co-director of the Mid-Atlantic Center for
Children’s Health and the Environment (225).
In 1977, the U.S. Consumer Product Safety Commission
(CPSC) issued a final ban on lead-containing exterior and
interior residential paint and lead-based paint on toys and
furniture (Table 1). This regulation, which went into effect
in 1978, lowered the allowable amount of lead in paint to
0.06 percent, a level conforming to the maximum amount
permissible under the Lead-Based Paint Poisoning Prevention
Act. This Act, administered primarily by the Department
of Housing and Urban Development (HUD), prohibits
application of lead-based paint to housing constructed or
rehabilitated with federal assistance. Exempted from the ban
are mirrors backed with lead-containing paint that are part of
articles of furniture, artists’ paints, certain agricultural and
industrial coatings, touch-up coatings for appliances and lawn
and garden equipment, graphic arts coatings, roadway paint,
and certain coatings for powered model aircraft. In 1992, the
U.S. Congress passed the Residential Lead-Based Paint Hazard
Reduction Act of Title X of the Housing and Community
Development Act, expanding on previous efforts (166).
In addition, the Federal Hazardous Substance Act (FHSA)
bans children’s products containing hazardous amounts of
lead. The recent realization that many children’s vinyl lunch
boxes had significant levels of lead added as a stabilizer to the
vinyl is an example of a non-paint children’s product covered
under the FHSA. See also “Sources of Lead Exposure: Other
Sources” on page 20.
Table 1 - Year lead banned in household paint, in order by year,
in various countries.
Country
Austria
Belgium
France
Greece
Tunisia
Czechoslovakia
Great Britain
Sweden
Poland
Spain
Yugoslavia
Cuba
United States
*Maximum allowable 0.06%.
Year of Ban
1909
1909
1909
1922
1922
1924
1926
1926
1927
1931
1931
1934
1978*
Many countries, however, continue to manufacture and
sell lead-based paints that would be prohibited in the U.S.
and in many other countries. One study found that more
than 75 percent of the consumer paint tested from countries
without controls on lead paint—representing more than 2.5
billion people—had levels exceeding U.S. regulations. About
50 percent of the paint sold in China, India and Malaysia
had lead levels 30 times higher than U.S. regulations would
allow. Children’s toys and other items imported from these
countries can have high lead levels.
In 1923, tetraethyl and tetramethyl lead were introduced
as a gasoline additives. In addition to increasing the octane
of gasoline, leaded gasoline also protected exhaust valve
seats, in vehicles designed to operate on leaded gasoline, from
excessive wear. Despite the president of the National Lead
“One study found . . . that about 50 percent of
the paint sold in China, India and Malaysia
had lead levels 30 times higher than U.S.
regulations would allow. Children’s toys and
other items imported from these countries can
have high lead levels.”
Company acknowledging in 1921 that lead is toxic (147), and
despite the deaths of 15 workers involved in the manufacture
of the gasoline additive in 1924, the U.S. Surgeon General
found insufficient evidence to support a ban on leaded
gasoline (171). It was not until the early 1970s that researchers
were able to demonstrate conclusively that exposure to
airborne lead from gasoline combustion was a public health
threat. In 1973, the U.S. Environmental Protection Agency
(EPA) ordered a gradual phase-out of leaded gasoline, which
led to a complete ban of the use of leaded gasoline in on-road
vehicles by 1996. In 1979, cars released 200 million pounds of
lead into the air in the U.S. In 1989, when the use of lead was
limited but not banned, cars released only 4.8 million pounds
to the air. Current U.S. EPA rules still allow fuel containing
lead to be sold for off-road use, including aircraft, racing cars,
farm equipment, and marine engines. Figure 1 demonstrates
the significant impact of the phase-out of lead from gasoline
on lead exposure in the U.S. population.
Lead contamination of drinking water in the U.S. has also
been recognized as a significant health problem and a series
of regulations have been enacted to provide guidelines for the
states and to reduce the likelihood of contamination (180).
The early federal efforts to keep lead out of drinking water,
most of which were part of the 1975 National Interim Primary
Drinking Water Regulations, were largely ineffective as they
controlled lead at the distribution source rather than at the
consumer’s tap. Subsequent research demonstrated that most
contamination occurred between the source and the tap, often
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in association with corrosion along the distribution system.
The first major initiative to address lead in tap water was the
“Federal Lead Ban,” a set of amendments to the Safe Drinking
Water Act that were signed into law in December 1986. These
amendments banned the use of solders and flux containing
more that 0.2% lead (solders and flux were typically composed
of 40% to 50% lead), and restricted the amount of lead in
any brass in contact with drinking water to 8%. A flurry of
medical research in the 1980s established that the lead levels
commonly found in U.S. drinking water were sufficient to
contribute to lead poisoning, especially in children (33).
In 1988 the U.S. “Lead Contamination Control Act” (LCCA)
was passed. This legislation required the U.S. EPA to assist
schools in reducing lead contamination, particularly in water
coolers, many of which were lined with lead. However, leadcontaminated point-of-use water, i.e., the water coming out of
the tap in homes, continued to be a problem with no federal
or state agencies having the authority to regulate water quality
within homes. In 1991, the U.S. EPA issued the “Lead and
Copper Rule,” which requires each public water supply system
to assess the severity of lead contamination in higher-risk
residences and to take action if more than 10% of residences
exceed a concentration of 15 µg/L. Between 1996 and 1999, in
part in response to a California lawsuit against faucet makers,
virtually all North American and European faucet makers
reformulated their faucets to be no-lead (0.1% to 0.2% lead as
an incidental impurity) or low-lead (typically 2.0% to 2.5%
lead). Federal law still allows up to 8% lead in faucets and most
faucets before 1996 were made from alloys containing 5% to
7% lead. Because the degree of lead-leaching is linked to the
corrosivity of the water, currently all large water suppliers in
110
16
100
15
90
14
80
13
70
12
60
11
Blood-Lead Levels
Lead Used in Gasoline
50
10
Average Blood-Lead Levels (µg/dL)
Lead Used Per 6-Month Period (1,000 tons)
Figure 1
the U.S. are required to reduce lead corrosivity of their finished
water, although the methods to reduce corrosion and lead
leaching in water systems may vary. To combat the corrosivity,
municipal water systems add chemicals such as zinc
orthophosphate, sodium hydroxide and silicates. Although the
effect is not always predictable (180), anticorrosives such as
orthophosphate generally work by forming a protective coating
inside pipes that decreases the amount of lead that leaches
from lead service lines and customers’ plumbing systems.
See also “Sources of Lead Exposure: Water” (page 17) and
“Reducing Exposure: Water” (page 70).
Dietary lead exposure, mainly through food and beverage
cans containing lead solder, also came into focus in the
1970s. During this time, manufacturers of baby foods
changed from cans to glass jars while various other industries
voluntarily stopped using lead solder in cans (86). In 1995,
the U.S. Food and Drug Administration (FDA) issued a ban
on lead-soldered cans. In the 1990s, the FDA also took steps
to increase awareness about lead-contaminated candy and
the use of lead-foil capsules on wine bottles. As a result of
these measures, dietary lead exposure among the entire U.S.
population has decreased significantly since the 1970s (34).
The U.S. Occupational Safety and Health Administration
(OSHA) requires employers of workers who are occupationally
exposed to lead, including construction workers, to keep
lead levels ≤ 50 micrograms per cubic meter of air (µg/m3),
averaged over an 8-hour period. If the lead level is ≥ this level,
BLLs must be monitored and an employee with a BLL ≥ 50
µg/dL must be relocated (7). A number of investigators, based
on growing medical evidence in adults exposed to lead, are
pressuring OSHA to re-evaluate these regulations (245).
Table 2 lists current federal standards for lead in different
media and in different populations. States and municipalities
have enacted additional regulations that vary greatly across
the U.S. in the degree to which they protect residents—
especially children—from exposure to lead. In some areas
federal regulations and guidelines are poorly enforced,
whereas in other states and municipalities additional
regulations have been enacted that are considerably more
protective than federal laws.
Sources of Lead Exposure
In the U.S. today, ingestion is the most common route of lead
absorption. Before leaded gasoline was banned, however,
inhalation of airborne lead was a major source of exposure.
Ambient Air
1976
1977
1978
1979
1980
Relationship between the phase-out of leaded gasoline in onroad vehicles and the decline in blood-lead levels in the U.S.
Redrawn from Pirkle et al (227).
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According to the U.S. EPA, atmospheric emissions of lead
have decreased 93% between 1982 and 2002 (7). The highest
levels are generally observed near stationary sources, such as
lead smelters. Levels of lead in ambient air range from about
7.6 x 10-5 μg/m3 in remote areas such as Antarctica to > 10 μg/m3
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Table 2 - Standards and regulations for lead in the U.S.
Agency
Media
Level
Comments
CDC
Blood (population)
10 µg/dL
Action level for individual management*
OSHA
Blood (workplace)
40 µg/dL
50 µg/dL
Written notification and medical exam**
Medical removal from exposure**
ACGIH
Blood (workplace)
30 µg/dL
Indicates exposure at the TLV*
OSHA
Air (workplace)
50 µg/m
30 µg/m3
PEL (8-hour average)**
Action level**
CDC/ NIOSH
Air (workplace)
100 µg/m3
Maximum REL*
ACGIH
Air (workplace)
150 µg/m3
50 µg/m3
TLV/TWA guideline for lead arsenate*
TLV/TWA guideline for other forms of lead*
EPA
Air (ambient)
1.5 µg/m3
NAAQS (3-month average)**
EPA
Dust
40 µg/ft2 (floors)
250 µg/ft2 (window sills)
Includes carpeted floors*
Interior window sills*
EPA
Soil (residential)
400 ppm (play area)
1,200 ppm (non-play area)
Soil screening guidance level;* requirement
for federally funded projects (40 CFR Part
745, 2001)**
EPA
Water (drinking)
15 µg/L
0 µg/L
Action level for public supplies**
MCLG*
FDA
Food
Various
Action levels for various foods;** example:
lead-soldered food cans now banned
CPSC
Paint
600 ppm (0.06%)
Maximum allowable by dry weight**
Lead-based paint is defined as paint with
lead > 1 mg/cm2 or > 0.5% by weight
3
* Advisory or recommendation or guideline (not enforceable); ** Regulation (enforceable)
Abbreviations: ACGIH = American Conference of Governmental Industrial Hygienists; CDC = U.S. Centers for Disease Control
and Prevention; CPSC = U.S. Consumer Product Safety Commission; EPA = U.S. Environmental Protection Agency; MCLG =
maximum contaminant level goal; NAAQS = National Ambient Air Quality Standard; NIOSH = National Institute for
Occupational Safety and Health; OSHA = U.S. Occupational Safety and Health Administration; PEL = permissible exposure level;
REL =recommended exposure level; TLV = threshold limit value; TWA = time-weighted average
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near point sources or along major roadways where lead is
generally still present from leaded gasoline. The EPA national
ambient air quality standard for lead is 1.5 μg/m3, averaged
over 3 months. In the 8-county Houston-Galveston ozone
nonattainment area, monitoring of air lead levels is no longer
required as results over several years found no exceedances.
Air levels may be elevated near heavy traffic, where particulate
matter is kept airborne, but no monitoring is currently done
close to area roadways. See also “Sources of Lead Exposure:
Soil,” (this page).
Paint
Deteriorating house paint is the largest single source of lead
exposure and the major source of lead poisoning in children
(223). Housing built before 1950, which makes up 22.3% of
the U.S. housing stock, poses the greatest risk because house
paint contained the highest amount of lead (up to 50% by
weight) prior to this time. In the City of Galveston, Census
2000 data indicate that 77.4% of the housing stock was built
before 1978 (279). Moreover, studies conducted by the CDC
have revealed relatively high BLLs in children who live in
housing built before 1973 (51). Homes built before then,
particularly those in need of repair or renovation, therefore
pose the greatest risk to residents. The U.S. HUD estimates
that 90% of privately owned units built before 1940, 80% of
units built between 1940 and 1959, and 62% of units built
between 1960 and 1979 contain some lead-based paint (283).
Indoors, dust from deteriorating paint dust is generally the
greatest concern, although lead-contaminated dust can also
accumulate to significant levels from tracking contaminated
soil indoors. Lanphear and associates noted that levels of floor
lead dust (10 µg/ft 2) and soil lead (72 ppm) almost 10-fold
lower than EPA guidelines resulted in a mean BLL of 4.6
µg/dL in children (157), emphasizing the role of floor dust
lead. The EPA defines a floor wipe sample of 40 µg/ft 2 and a
window sill wipe of 250 µg/ft 2 as a hazard.
Renovation of older residential buildings without taking
proper precautions can result in not only poisoning the
workers and residents but can seriously contaminate the home
and the area around the home or apartment. One example in
Galveston occurred in 1994 and involved workers who were
asked to sandblast the paint from an older structure. The
GCHD was notified by an emergency-department physician
of a 32-year-old man with a BLL of 111 µg/dL who complained
of symptoms of abdominal pain, vomiting, weight loss,
constipation, headache, memory loss, tinnitus, a metallic
taste, stuttering, arthralgias, and discoloration of the gums
(50). The patient reported that for six weeks in February and
March of that year, he and seven others had sandblasted a
100-year-old five-story building in Galveston and that large
quantities of dust had been created during the process. Followup revealed that one of his co-workers had a BLL of 245 µg/dL.
Subsequent analysis of the worksite found lead levels as high as
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145,000 µg/ft2 along the inner surface of a window pane.
As noted in the previous section, the use of lead-based
household paint in the U.S. was not banned until 1978, and
some uses of lead-based paint continue today. Although
these other uses of lead-based paint, such as highway and
marine paint, are less likely to poison children directly, takehome lead from parental occupations is a significant source
of exposure in some households, and deteriorating paint
from bridges or highways on which lead-based paint was or
continues to be used can contaminate nearby soil around
residences and be tracked indoors. Currently approximately
five billion square feet of nonresidential surface area in
the U.S., including approximately 89% of the nation’s steel
bridges, are covered with lead paint (170).
In addition to exterior and interior house paint and paint
used on commercial and public infrastructure surfaces, leadbased paint can be found on old furniture and toys, as well as
“Currently approximately five billion square
feet of nonresidential surface area in the U.S.,
including approximately 89% of the nation’s
steel bridges, are covered with lead paint.”
some new items imported from countries with less stringent
lead laws. For example, in August 2007, Fisher-Price recalled
83 types of toys—including the popular Big Bird, Elmo, Cora
and Diego characters—because the paint contained excessive
amounts of lead. The worldwide recall involved 96,700 plastic
preschool toys made by a Chinese vendor and sold in the U.S.
between May and August, 2007 (261).
Soil
Lead adheres tenaciously to soil particles and thus lead
contamination from car exhaust, paint dust and lead-based
pesticides persists for decades. Soil may be contaminated around
older wooden homes with exterior lead paint, especially following
improper power sanding to prepare the exterior for painting
(139), which can release significant amounts of lead dust.
In relatively uncontaminated rural areas, soil-lead levels
are usually < 50 ppm, whereas urban soil levels are typically
> 200 ppm. In one study of 169 homes, the mean soil-lead
level near the foundation was 1,022 ppm (157). The EPA
considers a soil-lead level of 400 ppm in a play area to be a
hazard; the level of concern for residential yards is 1,200 ppm
(Table 2). The findings of Lanphear and associates suggest
that, in children with BLLs ≥ 10 µg/dL, lead-contaminated
soil contributes significantly to their lead uptake. They also
estimated that an increase of soil lead from 1 ppm to 1,000
ppm would result in a 2.4 µg/dL increase in blood lead (160).
Sixteen percent of pre-1980 homes have adjacent soil lead
concentrations > 500 ppm, and the chance of having levels
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> 500 ppm is 4–5 times higher if the house has exterior leadbased paint. Indeed, lead in urban soil is increasingly regarded
as a potentially major source of lead poisoning, especially
among children (191,304), and even in lead-safe homes and
schools significant levels of lead can often be found near
entrances where lead is tracked in from outdoors (163).
Galveston, New Orleans and other coastal areas may
face additional sources of soil-based contamination (191).
Soil sediment from flood waters can contaminate coastal
properties with lead and other toxic metals, and coastal
properties may be more susceptible to the erosive effects of sea
wind and salt on exterior lead-covered structures. In a recent
study of New Orleans, Mielke and associates noted that,
prior to Hurricane Katrina, 10 inner city census tracts had
median surface soil levels of lead > 1,000 mg/kg (2.5 times the
U.S. standard), with post-Katrina levels considerably higher.
Mielke’s group estimates, based on a pilot soil remediation
project, that the post-Katrina benefits of reducing soil levels
of lead would significantly outweigh the foreseeable costs
of childhood lead poisoning (annual costs of $76 million in
health, education, and societal harm)(191).
Also, soil along freeways or older roadways is usually
contaminated by past emissions of lead in auto exhaust, with
the levels decreasing with distance from the roadway and
proportionate to traffic volume (112). The Agency for Toxic
Substances and Disease Registry (ATSDR) estimates that
leaded gasoline use left behind 4 to 5 million metric tons of
lead in the environment (304).
Other sources of soil contamination with lead include
sites of previous industrial contamination. An excellent
example in the Houston, Texas, area is the Many
Diversified Interests (MDI) National Priority Listing (NPL)
Superfund site in the Fifth Ward, a predominantly lowincome historical, but not historically protected, AfricanAmerican neighborhood located approximately two miles
east of downtown Houston (288). This 36-acre site was
previously home to several industries, including two steel
casting foundries and a spent catalyst recycling plant that
contaminated the site with lead and several other known
toxins. Significantly elevated levels of lead have been found
at the site, in the groundwater and in the soil of nearby
residential properties. A 1998 Texas Department of Health/
ATSDR study found that 22% of the children in the Fifth
Ward had BLLs ≥ 10 µg/dL, a percentage that has fallen
in more recent years largely to targeted intervention in
the area. Although lead-based paint has been determined
to be a source of exposure in many of the children, the
contaminated soil is a major source as well. Numerous
community and governmental agencies are currently
working with the Fifth Ward to remediate homes and remove
contaminated soil. In 2006, Clinton-Gregg Investments, L.P.,
purchased the site and agreed to clean up the ground and
water contamination with U.S. EPA oversight.
Water
Lead is rarely found in source water, but enters tap water
through corrosion of plumbing materials. In Galveston
County, no cases of elevated BLLs from drinking water have
been reported. Although the number of in-home tap water
sources tested is very low (103), there is a considerable amount
of older plumbing. Exposure to lead from contaminated
tap water is a significant source of body burden in many
communities, and can vary from household to household
based on the type of plumbing and fixtures. Regardless of the
household plumbing, the relative corrosivity of the municipal
water supply plays an important role in determining the
amount of lead that leaches into the tap water.
The U.S. EPA estimated in 1991 that 14% to 20% of total U.S.
lead exposure was from drinking water (180). In most instances
the sources are lead pipes, plumbing fixtures and solder along
distribution lines. In addition, some early water coolers, which
were lined with lead, were also sources of contamination in
schools and businesses. Homes built before 1986 are more likely
to have sources of lead in their plumbing systems. However,
new homes are also at risk as even “lead-free” plumbing may
legally contain up to 8 percent lead. The most common problem
is with brass or chrome-plated brass faucets and fixtures,
which can leach significant amounts of lead into the water.
The degree of leaching is dependent on a number of factors
including pH (acidity); concentrations of sulfate, chloride and
“The U.S. EPA estimated in 1991 that 14%
to 20% of total U.S. lead exposure was from
drinking water. In most instances the sources
are lead pipes, plumbing fixtures and solder
along distribution lines.”
orthophosphate; and the presence of organic matter. Lead levels
in tap water tend to be higher if the water is acidic, heated or has
been sitting in the pipes for some time.
Recent evidence also indicates that the use of silicofluorides
to fluoridate municipal water may increase exposure to lead as
this class of compounds increases water corrosivity. Bloodlead data from nearly 800,000 children in the U.S. suggest that
children who live in communities with fluoridated water are
twice as likely to have a BLL ≥ 10 µg/dL than those who live in
communities without municipal fluoridation (72).
Residential leaded-brass water meters and cut-off values are
two other sources of contamination of household drinking
water. As a result of a lawsuit in California in 1999, only nolead water meters can now be sold in California (180).
Maas and associates argue, based on new health research
suggesting that a disproportionate amount of childhood
neurological damage occurs at BLLs less than 5 µg/dL (see
“What Are the Health Effects: Neurological” beginning on
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page 32), that water—rather than paint—may be responsible
for significant cognitive and behavioral damage (180). They
note that ingestion of only 31.2 µg per day of lead via water—
the equivalent of two liters of water with a lead concentration
of approximately 15 µg/L (the EPA action level for drinking
water)—would produce a BLL of 5 µg/dL.
That lead in tap water is still a concern was highlighted in
2003 by a significant number of water samples in Washington,
D.C., having lead levels above the EPA action level. In this
instance it was found that the chloramines the city began
using in 2001 to disinfect its water increased corrosivity and
lead leaching. In July 2007, EPA received the D.C. Water and
Sewer Authority’s (WASA) most recent report on lead levels
in D.C. drinking water. WASA reported that 90 percent of the
samples had lead levels of 10 µg/L or less (287). Since August
2004 orthophosphate has been added to the entire D.C.
distribution system as a corrosion inhibitor.
Although tap water is the primary concern because of the
large number of residents potentially affected, contaminated
well or ground water, run-off from contaminated sites and
flood waters may occasionally contain significantly elevated
lead levels. Lead is not a common contaminant in well or
ground water. Well or ground water contamination with
lead generally occurs when the water is close to a site of
contamination such as a freeway, lead mine, landfill, smelter
or battery reclamation site. In Houston, Texas, ground
water beneath the MDI Superfund site in the Fifth Ward
near downtown is contaminated due to earlier industrial
activities at the site. Anyone using well water should have the
well regularly analyzed by a reputable laboratory. Studies of
Hurricane Katrina floodwaters and the disturbed sediment
that remained after the floodwaters receded demonstrated
lead levels above public health standards in a number of
areas in New Orleans, usually in areas with elevated soil-lead
levels pre-Katrina. In general, lead-contaminated floodwater
is not considered to be a significant source of exposure as
only miniscule amounts are absorbed through the skin and
large amounts of floodwater are not ingested. However,
sediment from flooding can be contaminated and should be
tested as warranted.
Food and Beverages
Lead-glazed pottery and dishes and leaded crystal can
be a source of poisoning. Both recently produced pottery
produced in other countries and antique dishes and glasses
can present problems. Fiesta ware, like most dishes made
before 1972, contains lead and other heavy metals. It is
especially important not to put acidic foods, such as orange
juice, wine and tomato sauce, in these containers because low
pH causes lead to leach into the food.
Also, certain candies test consistently high in lead. Of
particular concern are various Mexican chile and tamarind
candies, especially Chaca Chaca, Bolirindo by Dulmex,
18
Rollito de Tamarindo by Dumex, and Lucas Limon. In some
instances the lead is found in the seasoning; in others it is in
the ink used for the candy wrappers.
Lead is also readily taken up by plants. This can be used
effectively to reduce soil levels and the tracking of lead
dust into homes. However, it is important that food for
consumption not be grown in contaminated soil or close
to a major source, such as along a major roadway. Lead in
soil especially concentrates in root vegetables and leafy
green vegetables. In Houston, Urban Harvest recommends
that all gardens for edible fruits and vegetables be grown in
raised beds with new soil to avoid lead, pesticide and other
contaminants in food.
Lactation
Mother’s milk is the ideal food for newborns. However,
lactation can also expose infants to elevated levels of lead
if the milk is produced by mothers with current ongoing
exposure to lead or by mothers who have been exposed earlier
in life, due to the redistribution of cumulative maternal
bone-lead stores. For high-risk mothers, both current and
past exposure can contribute to contaminated breast milk.
In a study by Ettinger and associates, breast milk lead
accounted for 12% of the variance of infant BLLs at one
month of age, whereas maternal blood lead accounted for
30% (89). Although the levels of lead in breast milk tend to
be low, a growing awareness of the effects of even low levels
of lead during early windows of neural development has
generated renewed interest in approaches to reduce childhood
exposure from lactational lead. Aside from eliminating
exposure, various nutritional approaches are being examined.
Nevertheless, current evidence continues to suggest that the
nutritional and other benefits of human milk outweigh the
effects of lactational lead except in extreme cases.
Folk Remedies and Cosmetics
Some ethnic folk remedies, such as greta and azarcón, are
70% to 90% lead (47). These remedies are commonly found in
areas of the U.S., such as the Houston-Galveston area, where
there is a large population of Mexican Americans. They are
usually sold in “herberias” and prescribed by “curanderas.”
They are more often used by first generation immigrants and
are commonly administered for “empacho” to infants, who
are also particularly susceptible to their toxicity. South Asian
traditional remedies which contain lead include Balrakshak
Sogati, Triphala Tablet, Zandu Sudarshan Tablet, Balguti
Kaseria, Somva 34, Triphala Guggal, and Balsathi.
Some cosmetics also contain significant amounts of lead.
Of particular importance is a traditional cosmetic called kohl,
which is often applied around the eyes in Asia, Africa and the
Middle East (222). In one study of 22 kohl samples, seven had
lead levels in excess of 50%. In addition, some types of hair
colorants and dyes contain lead acetate.
B ackground
Hobbies
Endogenous Exposure from Bone
Hobbies can be a significant source of lead exposure. Hobbies
involving lead include recreational target shooting, home
remodeling, refinishing furniture, casting bullets and fishing
weights, and making stained glass and ceramics.
In one recent instance, a 64-year-old woman was referred to
her local hospital with a 6-month history of anorexia, weight
loss, and abdominal pain (76). Six months later she presented
with left- and right-sided wrist drops. The clinical suspicion
of lead intoxication was confirmed by a BLL of 146 µg/dL.
A subsequent history revealed numerous potential sources
of lead exposure including a childhood history of making
wooden shoes with her father and subsequently working in
a paint shop. She also had had lead water piping in her home
until recently. However, the key factor was her hobby of flower
arranging: she used large amounts of lead to make decorative
figures around which she arranged the flowers.
Other examples include a case of lead poisoning
experienced by a female art conservator who was involved
in restoring antique Peruvian tapestry, and a case of an
entire family experiencing lead intoxication secondary to the
pottery work by an artist family member (97). Yet another
example involved recreational shooters at indoor firing ranges
where powder charges were employed. Of the 22 marksmen
who used power charges, their BLLs in some cases doubled
over the course of the shooting season (270).
Persons exposed to lead store variable amounts of the
metal in their bodies (see “Storage”, page 21), with bone
and teeth being prime repositories. Under various normal
and disease conditions, lead can be released back into the
blood. In general, little lead is released from teeth; bone,
however, continuously undergoes remodeling and is often
a major source of lead in blood. Plasma levels in children
may be particularly influenced by bone levels as children’s
bones are in continual growth, leading to a state in which
lead in bone is continuously released back into the blood
compartment (17,118). In pregnant women, increased
levels of lead, presumably released from bone, are often
Occupational
In the U.S., an estimated 95% of elevated BLLs in adults
are attributable to occupational exposure (50,54), with
approximately 0.5 and 1.5 million workers exposed to lead
in the workplace (7). Industries that expose workers to lead
include battery manufacturing, painting, rubber products and
plastics industries, municipal waste incineration, soldering,
steel welding and cutting operations, lead compound
manufacturing, nonferrous smelting, radiator repair, brass
and bronze foundries, pottery production, scrap metal
recycling, firing ranges, and wrecking and demolition. In the
smelting and refining of lead, mean concentrations of lead
in air can reach 4,470 μg/m3 ; in the manufacture of storage
batteries, mean airborne concentrations of lead ranging
between 50 and 5,400 μg/m3 have been recorded; and in the
breathing zone of welders of structural steel, an average lead
concentration of 1,200 μg/m3 has been found. In a 1992 study
of a lead mine in Romania, workers had mean BLLs of 77.4
µg/dL. In children living near the lead smelter, a mean BLL of
63.3 µg/dL was found (296). The removal of lead-containing
paint from homes or other structures, such as bridges and
marine vessels, is another common occupational exposure.
Approximately 2–3% of children with a BLL ≥ 10 µg/dL
have been exposed to “take-home” lead, that is, lead brought
home from the workplace on the clothes or in the vehicles of
their adult caregivers.
“Approximately 2–3% of children with a
BLL ≥ 10 µg/dL have been exposed to “takehome” lead, that is, lead brought home from
the workplace on the clothes or in the vehicles
of their adult caregivers.”
found in the mothers’ blood (272). Lead easily crosses the
placenta, exposing the developing fetus to potentially high
levels of lead at a time when exposure may be especially
damaging. Healthcare professionals are currently considering
guidelines for routine screening of high-risk mothers.
In general, a fetus will have BLLs similar to that of the
mother, with studies suggesting that the source of the lead
is approximately two thirds dietary and one third skeletal
(10). Women from Eastern Europe and infants adopted
from these countries sometimes have high levels of lead.
Although not a contraindication to adoption, the BLLs need
to be known at the time of adoption to avoid unnecessary
suspicion of current lead poisoning, to track levels, and to
put in place early support. Increased bone demineralization
in postmenopausal women has also been associated with
elevated lead levels. In a study by Nash and co-workers, factors
related to bone turnover were significant predictors of BLLs,
with postmenopausal women having BLLs approximately
25% higher than premenopausal women, after controlling
for numerous potential confounders (206). Among women
or men with osteoporosis, the release of endogenous lead
and the potential for adverse lead-related health effects in
adulthood are intensified (257,278). Moreover, lead may
worsen the prognosis of osteoporosis since lead is known to
inhibit activation of vitamin D, uptake of dietary calcium,
and several regulatory aspects of bone-cell function (257).
Transfusion
Very premature infants (who need repeated blood
transfusions), together with those who need double-volume
exchange transfusions, cardiac surgery necessitating
19
B ackground
bypass, extra-corporeal membrane oxygenation, or chronic
transfusions, are extensively exposed to donated blood—
which is not currently screened for lead levels.
Bearer and associates studied 19 very premature infants
who received 79 transfusions during the first four weeks of
life in 1991. The mean number of transfusions was 4.2, with
a mean of 15.7 mL/kg packed red blood cells (pRBCs) for a
mean lead dose of 1.56 ± 1.77 µg/dL (19). The mean lead level
in whole blood was 2.5 µg/dL (range 0–10 µg/dL); the mean
lead level in the pRBCs was 5.0 µg/dL (range 0–13 µg/dL).
They found that increases in post-transfusion BLLs in the
infants were linear with doses higher than 1.5 µg/dL. The
authors noted that 64 of the 79 transfusions (81%) in their
study exceeded the California Safe Drinking Water and
Toxic Enforcement Act of 1986 (Proposition 65) guidelines
that require notification in any place of business where
exposure to lead exceeds 0.5 µg per day via any route. They
recommended that blood for very premature babies be
screened and that no infants receive pRBC with a BLL ≥ 3.3 µg/dL
or whole blood ≥ 1.6 µg/dL. They estimated that if all of the
infants who had post infusional BLLs > 5 µg/dL had received
blood with lower lead levels, the lifetime savings for each
child due to lost IQ points would be $143,289 (19).
To ascertain if hazardous concentrations of lead continue to
be present in transfused blood, they measured the BLL of 100
units of blood by atomic absorption spectroscopy in 2001 (18).
The median BLL was 0.07 nmol/L (2.5 µg/dL) and the median
was 0.22 nmol/L (3.9 µg/dL), suggesting little change over the
10-year period and representing an unacceptable hazard of
lead exposure, particularly for very premature infants who
often receive multiple transfusions from the same donor.
Other Sources
Numerous consumer products, such as children’s vinyl lunch
boxes and some cosmetics, may contain small amounts lead.
Daluga and Miller recently tested 40 vinyl lunch boxes and
found that 35% were positive for lead (73). They noted that
many of the boxes were marketed under well-known names.
In the lunch boxes, which were made in China, the lead
was added to the vinyl as a stabilizer. Another unexpected
source of lead is Halloween costumes, with face masks often
containing the highest levels (73). Fireworks are another
source. Although the U.S. bans importation of fireworks
containing lead, enforcement is lax and post-fireworks air
analyses have generally found significant levels of lead in the
combustion particles (174). Jewelry is yet another potential
source of lead poisoning. In June 2007 the U.S., in cooperation
with GeoCentral, of Napa, CA, announced a voluntary recall
of approximately 19,000 “Butterfly Necklaces” manufactured
in China because of high lead content in the clasp. Other
infrequent sources of lead exposure include gunshot wounds,
chewing on crayons with lead, sidewalk chalk, and burning
candles with lead wicks.
20
How Does Lead Get Into and Out of the Body?
Absorption
Some of the lead that enters one’s body comes from breathing
in tiny particles or chemicals that contain lead. Once this
lead is breathed deeply into the lungs, it passes into the
bloodstream and then is distributed throughout the body.
Particles that are too large to enter the deeper recesses of
lungs can be coughed up and swallowed. Lead intake from air
is generally greater in children than in adults, probably due to
their higher rate of breathing, which leads to greater exposure
per kg of weight, as well as to the increased efficiency of
exchange across the air-blood interface in children’s lungs. In
adults, each 1 µg/m3 increase of lead in ambient air has been
found to increase the mean BLL by approximately 1 µg/dL,
whereas in children each 1 µg/m3 increase in ambient air lead
causes a mean increase of 2 µg/dL or more in the BLL (286).
The main route of lead absorption is the gastrointestinal
tract. The amount of lead that enters the blood from the
gastrointestinal tract partially depends on the form of the
lead, dose, age, sex, genetic background, nutritional status,
when the last meal was eaten, how well the lead particles are
dissolved in the stomach juices, and whether the exposure is
short-term or chronic (7). Experiments using adult volunteers
have demonstrated that, in adults who had just eaten, the
amount of lead that entered the bloodstream was about 6%
of the total amount ingested (7). In adults who had not eaten
for a day, about 60–80% of the lead entered the bloodstream.
In general, if adults and children ingest the same amount
“Lead intake from air is generally greater in
children than in adults, probably due to their
higher rate of breathing, which leads to greater
exposure per kg of weight, as well as to the
increased efficiency of exchange across the airblood interface in children’s lungs.”
of lead, a larger proportion will enter the blood in children
than in adults. Young children, especially those with dietary
deficiencies of iron, calcium or zinc, absorb approximately
5–10 times more ingested lead through their gastrointestinal
tract than do adults (115). The amount of lead absorbed
also varies with whether the ingested lead is in food, water,
soil or dust. Studies suggest that, in general, gastrointestinal
absorption of lead in soil is approximately 30% lower than from
food (169), and that the greatest increases in BLLs at low levels
of exposure occur when the exposure is to lead in water (252).
Skin is an effective barrier against lead and only a small
portion of lead dust on the skin will pass through the skin
and enter the blood if it is not washed off. It is easy, however,
B ackground
to ingest lead that is on one’s hands. One can, for example,
accidentally swallow lead that is on one’s hands while eating,
drinking, smoking, or applying cosmetics (for example, lip
balm). Young children can swallow a considerable amount
of lead-contaminated dust when they put their hands and
foreign objects in their mouths. “Pica,” which is the eating of
nonfood items such as dirt or paint chips, is common among
infants and toddlers. If the behavior continues after about
three years of age and is characterized by compulsive cravings
to eat nonfood items, it is considered a disorder. Pica is also
common during pregnancy. Pica may cause elevated BLLs
in children and adults. Damaged skin (for example, scrapes,
scratches, and wounds) also absorbs more lead. Tetraethyl and
tetramethyl lead, gasoline additives not longer allowed in the
U.S., are the only forms of lead that easily penetrate the skin.
Storage
The excretory half-life of lead in blood, in adult humans,
is approximately 30 days. After entering the bloodstream
approximately 99% of circulating lead is initially bound to
red blood cells, which disperse the lead to the soft tissues
such as the liver, kidneys, lungs, brain, spleen, muscles and
heart over the following 4–6 weeks. Tissue distribution
differs among children and adults, with a greater percentage
of lead accumulating in the immature brain in children
than in adults. The rate of excretion is low and much of the
lead, especially in situations of chronic exposure, moves into
the bones and teeth for “storage.” In adults, about 94% of
the retained lead is stored in bone (7) whereas in children
about 73% is stored in bone, resulting in more soft-tissue
lead in children. Bone lead will reenter the blood under
various circumstances (e.g., during pregnancy, during breast
feeding, after menopause in women, after a bone is broken, in
conjunction with certain diseases such as osteoporosis, and in
hormonal imbalances). The half-life in bone is estimated to
range from 3 years in trabecular bone such as the patella to 30
years in dense cortical bone such as the tibia. Due to the slow
turnover and release of lead from cortical bone, bone-lead
levels often increase with age (134). See also “Endogenous
Exposure from Bone” (page 19).
Excretion
Lead does not metabolize to any other form in the body.
Independent of the route of exposure, absorbed lead is excreted
primarily in urine and feces; sweat, saliva, hair and nails, and
breast milk are minor routes of excretion (7). Studies have
shown that clearance is greater for adults than for children.
Following short-term exposure, about 99% of the amount
of lead taken into the body of an adult will leave the body
as waste within a couple of weeks. In children the amount
that is eliminated is only about 32% (7). Under conditions of
continued exposure, the lead will begin to accumulate in body
tissues, especially bone, and the rate of excretion is slower.
How Is Lead Exposure Measured?
Several different methods are used to measure lead exposure
(17). Lead levels measured in blood, bone and teeth are the
most used and validated techniques, with each measuring a
different component of lead sequestration.
Blood
The blood-lead concentration, also known as BLL, is the
most commonly used biological marker of lead dose because
a BLL test is both easy and cheap to perform. BLLs are
expressed in µg/dL. For children, either capillary or venous
blood specimens are collected, whereas adult blood samples
are generally obtained from veins. Because capillary blood
specimens can be contaminated by lead on the skin, national
and state blood lead screening guidelines currently require
that capillary lead levels ≥ 10 µg/dL be confirmed with a
second capillary sample or, preferably, a venous blood sample.
The CDC and TDSHS have published detailed collection
methodology (see “Useful Resources”).
The concentration of lead in blood reflects the equilibrium
between current exposure, excretory loss, and the movement
of lead between other longer term storage sites such as bone
(230). More than 95% of lead in blood is bound to red
cells (201) with a relatively short half-life (35 days) in the
bloodstream. For this reason, BLL is an indicator of relatively
recent exposure (134). Only a small fraction of blood-lead
exists in the plasma in a “free” state (i.e., not bound to red
blood cells), but plasma-lead is considered to be the most
rapidly exchangeable fraction of lead in the bloodstream and
the most bioavailable form for crossing soft tissue membranes
into target organs or across the placenta (17,133). For this
reason, the ratio of plasma-lead to whole blood-lead levels
(% plasma-lead/blood-lead ratio) is sometimes used to
monitor exposure and assess risk in different populations
(17). Data from studies utilizing direct measurements of lead
in plasma suggest that the ratio of lead in plasma to whole
blood lead can vary by a factor of 2 to 3, with bone lead as a
major determinant of plasma lead levels (26,128).
The level of detection (LOD) for lead in blood varies by
methodology and, to a lesser extent, the laboratory used. In
the data received for our geospatial and statistical analysis of
blood-lead levels and predictive variables in Galveston, which
begins on page 44, a number of different laboratories were
used including Quest, LabCorp, and the TDSHS Laboratory.
These three laboratories and most others use graphic furnace
atomic absorption spectroscopy (GFAAS). Although some
sources cite the LOD of GFAAS as reliable down to 1 µg/dL,
the TDSHS reports anything below 3 µg/dL as < 3 µg/dL as
it feels that anything below 3 µg/dL may be unreliable with
this method. A few laboratories still use anodic stripping
voltametry, which has an LOD of 5 µg/dL. Increasingly,
however, laboratories are using inductively coupled plasma/
21
B ackground
mass spectrometry (ICP-MS), which results in determinations
of lead in plasma and serum specimens with a much lower
LOD and with better accuracy (17). ARUP Laboratories (the
preferred laboratory for blood-lead determinations at Texas
Children’s Hospital, Houston) uses ICP-MS. The ARUP
Laboratory in Salt Lake City is capable of a LOD of 0.3 µg/dL.
The CDC’s NHANESs have used ICP-MS since the 2nd
(1999-2000) survey and report 0.3 µg/dL as the LOD (56).
More recently a direct readout portable instrument (LeadCare
Analyzer; ESA Laboratories, Bedford, MA) has become
available that has an LOD of 1 µg/dL (135).
Obtaining the sample, which was done at school, also included
teeth cleaning and a fluoride treatment. The median lead
content was statistically higher in the industrial area (median
169.0 vs. 118.1; P < 0.0001). The authors note, however, that
deeper biopsies would have given more reliable results.
More recently there has been interest in using laser ablation
inductively coupled plasma mass spectrometry (LA-ICP-MS)
to study tooth-lead levels. Although this approach offers the
promise of a historical timeline of exposure, including fetal
exposure, the technique is still being refined and depends on
the collection of exfoliated deciduous teeth (289).
Bone
Other
The half-life of bone lead is much longer than in other tissue
compartments, except for teeth. Cortical bone lead, generally
measured in the tibia, has a residence time of 25 to 30 years,
whereas lead in trabecular or spongy bone (e.g., patella) has
a shorter residence time (7). Thus, bone lead, particularly
tibia lead, is a biomarker for cumulative lead dose and is used
in many epidemiological studies to measure body burden or
chronic lead exposure (134). Bone lead is expressed as µg of
lead per gram of bone mineral. Noninvasive technologies,
such as K X-ray fluorescence (KXRF), have been developed to
measure bone-lead levels.
Several other biomarkers for recent lead exposure or longer
term body burden of lead are occasionally used including
saliva, hair, nail, urine and fecal matter. Although saliva, hair
and nail samples are attractive due to their ease of collection,
all three are affected by a number of external factors that are
difficult to control. No reliable references exist for these three
potential biomarkers at this time, and recent studies have
shown large interlaboratory variations on the same samples.
The determination of lead in urine (urine-Pb) reflects
lead that has diffused from the blood plasma and is excreted
through the kidneys. It is favored for long-term monitoring,
especially for occupational exposures. It is also sometimes
used during chelation when significant levels of lead are
released from red blood cells into the plasma. Because a
spot urine specimen is subject to wide biologic variations,
a creatinine correction is required to adjust for the kidney
filtration rate (17). The collection of childhood fecal samples
over several days has occasionally been advocated as a
measure of total lead intake. However, individual physiologic
variations make this an unreliable measure of exposure.
Teeth
Lead also accumulates in teeth. In some ways teeth may be
superior to bone as a marker of long-term exposure because
teeth are less bioactive and the losses are much slower (17).
Several studies of tooth lead have shown a stronger correlation
than bone lead, as measured by KXRF, with cognitive and
attentional deficits in children (21,189,214). In addition,
deciduous (“baby”) teeth are relatively easy to collect and
analyze, are very stable for long-term storage, and the layered
deposition of lead provides some useful information about
exposure history. Most of the problems with tooth lead as
a biomarker relate to inconsistencies in collection that may
make comparisons difficult. These inconsistencies include the
use of different teeth or teeth from different age children and
failure to differentiate between enamel and dentin (enamel
contains much more lead). Also, the use of deciduous teeth is
only possible after around 6 years of age.
Several other tooth-lead measurement techniques have been
used. Gomes and associates recently refined an enamel biopsy
technique, which consists of the removal of a layer of surface
enamel by acid etching of a limited area on the tooth surface
(114). This technique potentially allows more consistency and
avoids the challenge of collecting exfoliated teeth. However
it is not clear whether a small sample of surface enamel is
sufficient and the technique does require a dental visit. Gomes
and co-workers studied 329 4- and 5-year-old kindergarten
children in Piracicaba, Brazil: 197 who lived far from
industrial sources and 132 who lived in an industrial area.
22
Is There a Safe Level of Lead in the Body?
In the 1960s, the threshold for lead poisoning was set at
≤ 60 µg/dL. However, as more toxic effects of lead were
gradually recognized, the CDC lowered its definition of what
is considered an “acceptable” childhood BLL several times in
the past 47 years. Today, 10 µg/dL, the level set by the CDC
in 1991, continues to be the level for action. However, new
evidence shows that toxic effects, particularly neurotoxicity,
occur at levels below 10 µg/dL with no apparent threshold
(158,249). For this reason, researchers such as Gilbert and
Weiss recommend that the blood-lead action level be reduced
to 2 µg/dL (Figure 2) (108). Currently, most researchers and
clinicians agree that there is no safe level of lead in the body.
CDC’s current “action level,” which is considerably higher
than many feel is prudent (108), is 600-fold higher than the
mean natural pre-industrial BLL in humans, which has been
estimated to have been 0.016 µg/dL (98). See “What Are the
Health Effects: Neurological,” beginning on page 32, for a
B ackground
discussion of some of the deleterious effects that have been
observed at BLLs below 5 µg/dL.
Although blood lead is a good marker of recent exposure,
plasma- and bone-lead levels may be of more importance with
regard to toxicity and chronic exposure and/or effects.
How Common Is Lead Poisoning?
In the late 1970s, the median BLL of U.S. preschool children
was 15 μg/dL, and 88% of children had a level ≥ 10 μg/dL
(183). At the same time, the mean BLL of poor Black children
was 23 μg/dL, and 18.5% of poor Black children had a level
≥ 30 μg/dL. The removal of lead from gasoline (Figure 1),
paint and other products resulted in a significant drop in bloodlead concentrations over the period between the second (1976–
1980) and the first phase of the third (1988–1991) NHANESs.
The percentage of children 1 to 5 years of age with BLLs ≥ 10 µg/dL
decreased from 88% to 8.9% during this period (227,228). The
most recent NHANES results reflect a continuing decrease in
BLLs in young children, with 1.6% of children aged 1 to 5 years
having a BLL ≥ 10 µg/dL in 1999–2002 (53). The geometric
mean BLL for this last period was 1.9 μg/dL.
However, the decrease in elevated BLLs is not uniform
across the country; there are still communities and groups
disproportionately affected by high rates of elevated BLLs.
In Table 3, surveillance data collected by the CDC from
NHANES and state lead-testing programs indicate that the
percentage of children with BLLs ≥ 10 µg/dL is consistently
higher among Black children, although the percentage is
gradually dropping—from 17.7% in 1997 to 8.7% in 2001.
Latino and low-income children are also more likely to have
elevated BLLs (94). NHANES data collected between 1999
and 2002 revealed that among children aged 1 to 5 years,
non-Hispanic Blacks and Mexican Americans had higher
Figure 2
Blood Lead (µg/dL)
70
60
50
40
30
20
10
percentages of BLLs ≥ 10 µg/dL (3.1% and 2.0%, respectively)
and higher geometric mean BLLs (2.8 μg/dL and 1.9 μg/dL)
than non-Hispanic Whites (1.3% and 1.8 μg/dL) (53).
Older communities across the U.S. typically have more
contaminated housing stock and therefore higher BLLs and
bone-lead levels in their residents. Galveston is typical of a
historical community with a higher potential for exposure and
elevated BLLs than in much of the U.S. See “Lead Exposure in
Galveston, Texas” beginning on page 26, for a discussion of the
area and some of its challenges in relation to lead exposure.
In addition, subpopulations of adults working in certain
industries, such as battery manufacturing and housing
“Older communities across the U.S. typically
have more contaminated housing stock and
therefore higher BLLs and bone-lead levels in
their residents. Galveston is typical of a historical
community with a higher potential for exposure
and elevated BLLs than in much of the U.S.”
construction, have disproportionately high percentages of
workers with elevated BLLs. According to workplace lead
standards set by OSHA, an employee must be removed from
exposure when his or her BLL exceeds 50 μg/dL. The CDC’s
Adult Blood Lead Epidemiology and Surveillance (ABLES)
program considers an elevated adult BLL to be ≥ 25 μg/dL
(54). The geometric mean BLL for adults aged 20-59 years
in 1999–2002 was 1.5 μg/dL (53). Approximately 94% of
elevated BLL adult cases are due to occupational exposure
(54). Indirectly, through “take-home” lead as well as exposure
during fetal development either from exogenous maternal
exposure or from leaching of lead stored in bones previously,
children are often exposed to lead via their caregivers.
As noted earlier, the predominant way of reporting “lead
poisoning,” that is, the percentage of children with BLLs
≥ 10 µg/dL often unintentionally suggests that below 10 µg/
dL is safe. In addition, other measures of body lead burden or
bioavailability may be as or more useful than the BLL. Given
what we know today about the long-term effects of lead, the
majority of the U.S. population has levels of lead sufficient
to have an adverse effect on their health. These levels should
gradually fall over the next several generations, especially if
lead is removed from homes.
0
CDC
1960
CDC
1973
CDC
1975
CDC
1985
WHO
1986
EPA
1986
CDC
1990
CDC
2006?
Agency & Year
The guideline for action for elevated levels of lead in the blood has
decreased steadily as the awareness of the lasting deleterious effects
of lead on developing brains and other systems have become better
appreciated. Redrawn from Gilbert and Weiss (108).
Who Is Most at Risk?
A number of factors, including age, race, ethnicity, poverty,
occupation, nutrition, education and genetic susceptibility
result in some people being more at risk than others. In
addition, where one lives is a major factor as lead levels
are generally highest in older urban areas. Within these
23
B ackground
Table 3 - Blood lead
lead levels
levels in
in children
children1–5
1–5years
yearsofofage,
age,by
byrace/ethnicity,
race/ethnicity,ininthe
theU.S.,
U.S.,1997–2001.
1997–2001.
Data from U.S. Centers
Centers for
for Disease
DiseaseControl
Controland
andPrevention
Prevention(57).
(57).
Year
Race / Ethnicity
# Tested
# With BLL ≥ 10 µg/dL
% With BLL ≥ 10 µg/dL
1997
White
Black
Native Am
Asian
Hispanic
Other
Unknown
419,428
359,505
5,951
19,697
151,833
17,861
729,081
15,713
63,458
327
1,562
14,383
1,571
33,498
3.75
17.65
5.49
7.93
9.47
8.80
4.59
1998
White
Black
Native Am
Asian
Hispanic
Other
Unknown
401,830
358,241
6,330
20,984
135,728
16,323
797,472
13,426
54,177
286
1,432
12,132
1,160
33,919
3.34
15.12
4.52
6.82
8.94
7.11
4.25
1999
White
Black
Native Am
Asian
Hispanic
Other
Unknown
408,672
339,813
9,745
19,874
139,028
18,323
874,086
11,391
41,471
251
1,172
10,180
1,002
27,768
2.79
12.20
2.58
5.90
7.32
5.47
3.18
2000
White
Black
Native Am
Asian
Hispanic
Other
Unknown
414,833
325,086
13,717
21,886
154,962
17,029
1,188,419
10,250
34,483
234
1,084
9,685
869
30,952
2.47
10.61
1.71
4.95
6.25
5.10
2.60
2001
White
Black
Native Am
Asian
Hispanic
Other
Unknown
433,317
327,126
15,161
20355
154,723
22,073
1,449,543
8,738
28,291
230
901
8,625
872
27,230
2.02
8.65
1.52
4.43
5.57
3.95
1.88
Abbreviations: Am = American; BLL = blood-lead level; µg/dL = micrograms per deciliter. Data from (1) National Health and
Nutrition Examination Surveys (NHANES) conducted during 1976–1980, 1988–1991, 1991–1994, and 1999–2000; and (2) state
child blood-lead surveillance data collected during 1997–2001
24
B ackground
areas, exposure is often related to regulatory policies
and enforcement which, as has been noted earlier, varies
significantly across the U.S. In similar housing stock, a
person in Texas is more likely to be exposed to lead than, for
example, a person in Massachusetts or Connecticut, where
contaminated housing cannot generally be sold or rented.
Adults have often been viewed as relatively unaffected
by lead exposure, in part because their brains are more
fully developed. Nevertheless, long-term adverse health
consequences of lead exposure in adults are increasingly
recognized (190). See “What Are the Health Effects,”
beginning on page 32.
Another increasing concern is the mobilization of bone
lead during pregnancy or other times of stress. In a clinical
report published June 2007, one woman, whose last exposure
“Adults have often been viewed as relatively
unaffected by lead exposure, in part because
their brains are more fully developed.
Nevertheless, long-term adverse health
consequences of lead exposure in adults are
increasingly recognized.”
to lead occurred seven years previously, was treated for lead
poisoning with a BLL of 81 μg/dL. Since no other exposures
to lead were suspected, doctors believe that her acute increase
in BLL was due to the release of lead from her bone as a result
of her recent pregnancy (233).
Children
Young children are most at risk because their developing
brains and body systems are more vulnerable to damage
caused by lead toxicity. There is increasing evidence showing
that pre- and perinatal exposure results in higher brainlead levels than postnatal exposure, most likely due to an
underdeveloped blood-brain barrier in early life (223). Young
children are also more likely to ingest higher amounts of
lead per body weight because they spend more time playing
on the ground and routinely put their hands and foreign
objects in their mouths, resulting in the ingestion of lead
contaminated dust and soil and, to a lesser extent, paint chips,
which are sweet. In addition, young children, especially those
with dietary deficiencies of iron, calcium or zinc, absorb
approximately 5–10 times more ingested lead through their
intestines than do adults (115).
Pregnant Women
Although fetal exposure from lead released from the
mother’s bone has been noted earlier, pregnant women are
themselves at risk. Rothenberg and co-workers measured the
effect of blood and bone lead on blood pressure in the third
trimester and postpartum among 1,006 women enrolled in
Los Angeles prenatal care clinics between 1995 and 2001.
They found that maternal bone lead levels in the calcaneus
bone were associated with increased systolic and diastolic
blood pressure as well as increased risk of third-trimester
hypertension (240). Mean maternal blood-lead levels in
the study were approximately 2 µg/dL, considerably lower
than the levels associated with hypertension in men or
nonpregnant women.
The Poor and Persons of Color
Ethnicity is also a risk factor as some groups of children,
especially African American children, appear to be
disproportionately affected by lead exposure. A study by John
Hopkins Bloomberg School of Public Health found that nonHispanic Black children, compared with non-Hispanic White
children, were three times more likely to have a BLL ≥ 5 μg/dL
but < 10 μg/dL, 7 times more likely to have a BLL of 10–20 μg/
dL, and 13.5 times more likely to have a BLL ≥ 20 μg/dL (27).
Other socioeconomic risk factors for elevated BLLs among
children include housing built before 1973, poor housing
condition, rental status, and poverty.
Renovators
Anyone living in or doing renovation in a home that contains
lead paint is at risk. Any pre-1978 building should be tested
before beginning by a certified lead inspector, and best leadabatement work practices should be used during the renovation.
In one instance a whole family— including a mother, father,
five-year-old daughter, 20-month-old son, and their dogs—was
poisoned after moving into a Victorian farm house that they
were renovating in upstate New York. Both children required
multiple rounds of chelation and one of the dogs died. The use
of heat guns and power sanders to remove old paint increased
significantly their exposure to lead (184). See the intervention
section (page 62) for guidelines to reduce exposure.
At-Risk Occupations
As noted in the section, “Sources of Lead Exposure:
Occupational” (page 19), certain occupations expose workers
and often the worker’s family as well to elevated lead levels. A
recent series in Environmental Health Perspectives focused on
the lax occupational standards to protect workers from lead
exposure and intoxication (135,245,254,260), noting that the
“lead standards of the OSHA are woefully out of date given
the growing evidence of the health effects of lead at levels of
exposure previously thought to be safe, particularly newly
recognized persistent or progressive effects of cumulative
dose” (245). Increasingly it is realized that any lead exposure
is likely to contribute to adult disease, including age-related
cognitive decline (264), cardiovascular effects (186), and
early death (190).
25
B ackground
The Genetically Susceptible
Genetic factors may explain why uptake and symptoms differ
among people with similar lead exposure and/or similar
BLLs. Recent studies suggest that polymorphisms of the
vitamin D receptor (VDR) and delta-aminolevulinic acid
dehydratase (ALAD) genes may make certain individuals
more vulnerable to lead (221). The VDR is important in
maintaining calcium homeostasis and ALAD is an enzyme
in the heme biosynthesis pathway. See also “Biological
Mechanisms of Harm” (page 39).
Lead Exposure in Galveston, Texas
Founded in 1836, the City of Galveston is a historical town
located in Galveston County off the coast of Southeast Texas.
Prior to the 1900s, the island-city was a thriving metropolis
with prosperous trade and wholesale businesses. From the
1920s to 1940s, Galveston became an entertainment hot
spot filled with casinos and nightclubs that hosted big name
performers such as Frank Sinatra and Duke Ellington. Today,
Galveston continues to be a major tourist destination and is
well known for its historical homes, ships, and landmarks.
Galveston County in general and the City of Galveston in
particular are disproportionately affected by environmental
lead exposure (Figure 3; Table 4). Childhood BLLs in
Galveston are significantly higher than the Texas and national
averages, and have not followed the decreasing trend of
BLLs in most of the nation. Despite the high percentage of
children with elevated BLLs, funding support for outreach,
screening, intervention and lead-abatement from government
sources has not generally been forthcoming, in part because
of the city’s small population, relative to other urban areas.
Blood-lead screening data collected by the GCHD and the TX
Figure 3
Galveston City
35
Galveston County
Percentage
30
Texas (Report Card)
25
15
10
5
0
1997
1998
1999
2000
2001
2002
2003
Year
Percentage of children 6 years of age or younger with blood-lead
levels ≥ 10 µg/dL. Sources: Galveston County Health District and
Texas Department of State Health Services.
26
CLPPP for 2001–2003 show that, of tested children under
6 years of age, 11.5% who lived in Galveston County and 17.8%
who lived in the City of Galveston had lead levels ≥ 10 µg/dL,
compared with 2.8% of Texas children in general (103).
Although the percentages vary somewhat depending on
the source, the sampling methodology and the surveillance
guidelines, they are surprisingly consistent across studies.
“Galveston County in general and the City of
Galveston in particular are disproportionately
affected by environmental lead exposure.
Childhood BLLs in Galveston are significantly
higher than the Texas and national averages,
and have not followed the decreasing trend of
BLLs in most of the nation.”
Javier and associates at the University of Texas Medical
Branch (UTMB) in Galveston reviewed Medicaid leadscreening data collected between January 1993 and December
1994 from 1,571 low-income children age 6 months to 8 years
who lived in the City of Galveston and who were tested at
the UTMB Children’s Clinic (141). They found that 19.1% of
the children had BLLs ≥ 10 μg/dL, with higher levels in east
Galveston (zip codes 77550 and 77553) (141).
In 2003, the Galveston Children’s Report Card gave
the region an “F” for elevated BLLs in children (101). The
numbers in Table 4, from several sources, are comparable to
the data we received from the GCHD, which we analyze in the
section titled “Galveston: Using GIS to Identify Hot Spots,”
beginning on page 44.
The City of Galveston, which accounted for over 80% of
the elevated BLL cases reported in Galveston County from
1992 to 2002 (103), has a number of risk factors including
high percentages of (1) African Americans, (2) children
under the age of 5, (3) households with low incomes, and (4)
older homes. In a study by Javier and associates, researchers
found that prevalence of elevated lead was 23% in African
Americans, compared with 17% in Whites, 13% in Hispanics
and 11% in Asians (141). According to Census 2000, 23.4%
of Galveston’s 57,247 residents are younger than 18 years,
with the distribution nearly equal among Blacks (32.2%),
Hispanics (35.5%) and Whites (27.9%). Galveston also has
a high percentage (35.6%) of children less than 5 years of
age living in poverty, which is of particular concern because
children in low-income households are more likely to have
poor nutrition as well as reside in deteriorated housing.
In addition to socioeconomic risk factors, Galveston has a
large number of older homes and apartments, both historic and
non-historic. Of all the housing units in the city, 77.4% were
built before 1978, according to the U.S. Census Bureau (279).
B ackground
Based on blood-screening data received from the GCHD, we
found that 20% of children with a BLL ≥ 10 μg/dL resided in
properties owned by twelve landowners. All these properties
are located in zip code 77550 or 77551, both of which have a
high density of older housing.
Although the higher cost of lead abatement in historically
designated housing is often cited as a key impediment, this
has been a spur to action in some cities, such as Boston, with
considerably more historical housing. Indeed, Massachusetts
has one of the more comprehensive programs in the U.S. to
protect children from lead exposure. It is nevertheless true
that federal funds are more difficult to secure for sometimes
very expensive historical renovations as the same amount
of money might be used for a dozen or so contaminated
nonhistorical homes.
A number of other factors contributing to the high levels
of lead in Galveston children (and adults) potentially include
contaminated soil from flood waters, coastal deteriorating
housing stock, sea salt spray, island-driven density, marine
paint and sandblasting, and hurricanes. But deteriorating
old housing and improper renovation methods appear to
be the primary causes of the majority of elevated lead levels
measured in Galveston children.
More broadly, the question is why so little has been done in
Galveston to address the problem. Based on our research and
discussions with many key leaders, the primary impediment
appears to be a lack of broad awareness of the seriousness of
the problem, reinforced by lack of adequate funding. There is
a sense of frustration among many healthcare professionals
“More broadly, the question is why so little has
been done in Galveston to address the problem.
Based on our research and discussions with
many key leaders, the primary impediment
appears to be a lack of broad awareness of the
seriousness of the problem, reinforced by lack of
adequate funding.”
who repeatedly find themselves with few or no options when
faced with a child with elevated lead levels. This is because
there are no procedures to require or to assist with leadabatement or moving the child and his or her family into a
uncontaminated home or apartment. In most cases the child
returns to the same environment, with some suggestions on
how to reduce exposure through hand washing and other
efforts to slightly reduce the amount of lead dust ingested.
Additionally, given the seriousness of the situation for
Galveston residents, there is a lack of publicity and guidance
from the city and county to help current and new residents avoid
exposure to lead. The City of Galveston has a lead abatement
Table 4 - Blood-lead levels in Texas children ages 1–5 years by
city, county and state (< 6 yr for Houston and Harris County).
Note that different surveillance guidelines do not allow comparison
of data from different sources. Houston data lists the two zip codes
with the highest percentage of BLLs ≥ 10 µg/dL.
Region
% with BLL ≥ 10 µg/dL
Year
# Tested
1997
1998
1999
2000
2001
2002
2003
-
23.0
19.6
27.4
25.2
18.4
16.4
19.0
2004
2004
2003
1080
1068
-
4.3
4.2
2.9
1997
1998
1999
2000
2001
2002
2003
2004
-
11.1
13.8
16.7
17.6
11.0
10.9
13.9
1.1
1997
1998
1999
2000
2001
2002
2003
1997
1998
1999
2000
2001
1,286
876
937
11,883
173,373
5.4
4.6
4.1
3.4
3.0
3.2
2.4
3.9
2.7
6.5
3.0
1.0
City
Galveston1
Houston2 zip
77011
77009
Texas City1
County
Galveston1
Harris2
State
Texas1
Texas3
Abbreviations: BLL = blood-lead level; µg/dL = milligrams
per deciliter; ≥ = greater or equal to; < = less than.
Sources: 1Galveston County Health District,
2
Texas Child Lead Registry, and
3
Centers for Disease Control and Prevention.
27
B ackground
regulation to limit contamination when removing exterior paint
(see the current lead ordinance for Galveston, beginning on
page 79, under “Intervention: Getting the Lead Out”). Likewise,
the Galveston Historical Foundation has a paint program and
is also renovating a contaminated low-income historically
significant home using best practices. However, currently
neither the City nor the Foundation’s websites about restoring
historical homes include information about potential exposure
to lead and lead safe practices.
Fortunately, a number of recent efforts—including
commission of this report—suggest that there is considerable
“Additionally, given the seriousness of the
situation for Galveston residents, there is a lack
of publicity and guidance from the city and
county to help current and new residents avoid
exposure to lead.”
interest in the community to address this issue in a holistic
way that involves not just the GCHD, but local foundations,
HUD, the Galveston City Council, the Galveston Historical
Foundation, the Galveston Independent School District and
Galveston realtors. Most successful efforts in the U.S. have
utilized a collaborative approach and strong leadership to
make fundamental changes to eliminate lead exposure.
Historical Housing in Galveston
As noted above, Galveston has an impressive number of
historical housing units, some of which are legally protected
and many others which are worthy of preservation. See
“Using GIS to Identify Hot Spots in Galveston: Results”
(page 51) for a map showing the Galveston historical
districts, as well as pre-1950 and pre-1978 housing. Although
the guidelines for historical renovation vary significantly
throughout the city (personal communication, Brian Davis,
Galveston Historical Foundation, August 2007), there are
municipal, foundation-supported and federal programs
in place to help with historical lead abatement. Having a
historical property does not exempt owners from protecting
workers, neighbors and residents from exposure to lead.
Within the City of Galveston, there are six designated
historical districts, most of which are nationally designated
historic districts:
• East End (approximately 463 residential structures),
• Silk Stocking (approximately 203 residential structures),
• The Strand (approximately 45 mainly commercial structures,
with some mixed-use apartments or town homes),
• Lost Bayou (approximately 190 residential structures),
• Cedar Lawn (approximately 98 residential structures), and
• Denver Court (approximately 389 residential structures).
28
The approximately 1,300 residential structures within these
districts must adhere to guidelines prepared by the City of
Galveston to preserve the historic integrity of the structures,
while also ensuring that the buildings are safe for habitation.
The Galveston Historical Foundation notes that all structures
east of 61st street are considered historic, although there
are no enforceable renovation guidelines for structures
outside of those in place for the designated historic districts
and buildings that have been named historic landmarks by
national, state or local authorities. Of the 13,473 residential
structures between 1st and 81st streets included in our
analysis, approximately 10% are legally designated historical
housing units.
What Are the Real Costs of Lead Poisoning?
Many people are aware that exposure to lead is dangerous,
especially to children. They often think that high levels of lead
may reduce a child’s IQ by a few points, but that this is either
inconsequential or reversible once the lead level is reduced.
Many people also think that elevated lead levels are not
common and that BLLs below 10 µg/dL are “safe.” None of
these assumptions is true. As discussed in detail in the “What
Are the Health Effects: Neurological” section (beginning
on page 32), any amount of lead in the body—especially in
children—negatively affects cognition, behavior and health.
The American Academy of Pediatrics (AAP) argues that the
negative effects of lead on academic performance have a major
impact on the child’s future social function, employment and
earnings (10). Some critics, however, are not convinced that a
couple of lost IQ points will negatively affect a child’s future,
claiming that extra schooling and one-on-one tutoring
will compensate for the slower learning pace. First, most
evidence suggests that most of the damage is irreversible.
Second, children with low-level lead poisoning are seldom
even identified, let alone offered extra help. This is especially
true for those most at risk, low-income minority children.
Third, the loss of several IQ points at the population level has
a massive effect on society as a whole. In his essay, “Exposure
to Lead in Children – How Low is Low Enough?,” Rogan
states, “Although critics question the importance of small
decrements in the IQs of individual children . . . relatively
small changes in the mean IQ of a large number of children
will dramatically increase the proportion of children below
any fixed level of concern, such as an IQ of 80, and decrease
the proportion above any “gifted” level, such as 120” (236).
Based on recent data, roughly 50% of the nation’s children
have lead levels high enough to negatively affect school
performance (199).
In addition, lead neurotoxicity does not only affect IQ.
It decreases graduation rates and increases antisocial and
criminal behavior. Lead is strongly linked with numerous
behavior disorders and learning problems including
B ackground
demonstrated that since the early 1900s, the rates of virtually
all types of major crime in the U.S. have followed remarkably
closely to the changes in lead exposure, suggesting a strong
influence of lead exposure on criminal activity (Figure 4)
(215). These recent studies reinforce seminal work published
by Needleman and associates in 1979—nearly 30 years
ago—that found a clear association between elevated levels
of lead in baby teeth in apparently asymptomatic elementary
school children and numerous measures of negative behavior
and overall poor functioning (211).
8000
1.5
7000
1.2
6000
5000
0.9
4000
0.6
0.3
3000
Gasoline Lead
Violent Crime
0
2000
1000
Violent Crime
per 100,000 Inhabitants
Tons of Gasoline Lead
per Thousand Population
Figure 4
41
19 : 19
44 64
19 : 19
47 67
19 : 19
50 70
19 : 19
53 73
19 : 19
56 76
19 : 19
59 79
19 : 19
62 82
19 : 19
65 85
19 : 19
68 88
19 : 19
71 91
19 : 19
74 94
19 : 19
77 97
19 : 20
80 00
19 : 20
83 03
19 : 20
86 06
:2
00
9
0
19
dyslexia, autism, attention deficit disorder, diminished self
esteem, and increased aggression and impulsivity. These
problems undermine achievement and directly or indirectly
affect everyone. Researchers from the CDC and Harvard
University quantified the economic benefits from projected
improvements in worker productivity resulting from the
reduction in children’s exposure to lead in the U.S. since
1976 (116). Based on published studies, they estimated
that IQ scores decrease between 0.185 and 0.323 points for
each 1 μg/dL of lead in the blood, and that each IQ point
raises a worker’s productivity by 1.76%–2.38%. They then
calculated the economic benefit associated with that increased
productivity for each year’s cohort of approximately 3.8
million 2-year-old children between 1976 and 1999, based
on their mean BLL. The authors calculated that the annual
economic benefit of reduced BLLs in 2-year-old children
since 1976 ranged from $110 to $319 billion. In another
study, using an environmentally attributable fraction model,
it was estimated that the present value of economic losses
in the U.S. attributable to lead exposure amounts to $43.4
billion per year in each annual birth cohort (155). More
recently, one study estimated that mild mental retardation
and cardiovascular disease resulting from exposure to lead
amounts to almost 1% of the global burden of disease (96).
Crime
One particularly well studied association is that of childhood
exposure to lead and antisocial behavior, including crime
and/or incarceration in later life (212,213,215,216,268).
Numerous studies have shown that lead-exposure related
effects, such as reduced school performance, attention
deficit and hyperactivity disorder (ADHD) and various
antisocial and aggressive behaviors, contribute to an increased
probability of violence and delinquent activity in later life.
Herbert Needleman, one of the foremost lead experts in the
nation, and associates published one such study in 2002 in
Neurotoxicology and Teratology. His group measured tibia
bone-lead levels in 194 arrested and adjudicated 12–18-yearold delinquents and in 146 non-delinquent teenagers attending
high school (212). They found that the delinquents had
significantly higher bone lead concentrations than the controls
(212). The work of Stretesky and Lynch, two sociologists
at Colorado State University, supports this finding. These
investigators conducted a cross-sectional ecological study
looking at the homicide rates in 3,111 U.S. counties (267).
After adjusting for six sociological and nine air pollutant
factors, they found that the counties with the highest air lead
concentrations had four times the murder rate of the counties
with the lowest air lead concentrations (267). Rick Nevin, an
economist, examined the temporal relationships between the
rates for multiple types of crime and the amount of lead in
gasoline and paint lead, the two major sources of exposure
in the U.S. (215). Using a lag of approximately 20 years, he
Lead Year : Crime Year (23 year lag)
Gasoline lead vs. violent crime. Redrawn from Nevin et al (215).
29

Childhood Lead Poisoning in Galveston, Texas: Background

Transcription

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