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PEDIATRICS Vol. 107 No. 3 March 2001, pp. 581-583
The clinical recognition of lead toxicity
in children in the United States has changed drastically over the past
50 years. Accordingly, both medical management and public policy in
such cases needs to be modernized in keeping with these changes. Fifty years ago lead poisoning in children was often only recognized in the
severe acute phase (acute lead encephalopathy). Today this condition is
rare, and children are detected in screening programs most often in the
asymptomatic phase. The removal of lead additives from gasoline and the
removal of lead solder from food and beverage cans has greatly reduced
the background level of lead absorption during the past
decade.1 The changes in exposure to lead and its clinical
presentation mandate that we change the approach to the management of
childhood lead toxicity. We must place reduced emphasis on chelation
therapy and major emphasis on the environmental history to identify the source(s) of lead in the child's environment and steps to separate the
child from these sources. The primary source of lead in childhood lead
toxicity 50 years ago was deteriorating lead paint in old housing: it
remains the primary source in the United States today. Reduction of
exposure is the single most important modality of long-term management,
as it has been for >50 years.
THE BENEFITS AND LIMITATIONS OF When chelating agents first appeared It is now clear that chelating agents promote the mobilization and
excretion of lead primarily from blood and soft tissues. Thus, we find
evidence of reversal of acute renal injury and impairment of heme
synthesis is beneficially affected by chelation therapy.9
The acute toxic effects of lead In 1991 the Food and Drug Administration approved the use of
meso-2,3-dimercaptosuccinic acid ([DMSA], succimer) for treating lead
poisoning. It is now probably the most widely used chelating agent in
the management of low level increase in blood lead. However, experimental studies in rats13 have shown that although
lead concentrations in the soft tissues, including the brain, are
temporarily reduced by DMSA, the agent has no effect on the
concentration of lead in bone. Woolard et al14 has
recently reported that DMSA does not remove lead from brain in
primates. In children the concentration of lead in blood rebounds close
to pretreatment levels after DMSA therapy, even if the child's environmental sources of lead are removed. Thus, a major source of lead
in blood, during this follow-up period is the bone.12
Whether even multiple courses of DMSA in early childhood will have any
long-term benefit in asymptomatic cases is under study,15
but remains doubtful. Thus, we must look to environmental interventions to prevent lead toxicity, especially at current levels of exposure. In
the future it is likely that chelating agent will have only limited
use.
LEAD IN DUST
In 1904, Gibson16 showed in Brisbane, Australia, by a
simple experiment that the major route of lead into children's bodies was from the lead in the form of dust (powder) that came from the lead
painted woodwork in their homes that got onto their hands and their
fingers, which they sucked. This observation lay fallow for about 70 years. In 1970, emphasis was first placed on automotive exhaust as the
major source of lead in dust.17 With regard to children,
it was Sayre et al18 in 1974 in Rochester, New York, who
rediscovered household dust as probably an important source of lead for
children. This was further documented by others,19
including Bornschein et al,20 who showed by statistical
analysis that the lead paint on the walls entered into the household
dust as did lead in soil brought in from the outside. The direct route
was from the interior household dust to the blood. There was no
statistically significant direct link between lead in paint on the
walls or surfaces or lead in the outside soil to the child's blood.
Most recently, Manton et al12 have demonstrated, by
elegant stabile isotope ratio studies using thermal ionization mass
spectroscopy, that dust is the major source of lead in children's
blood today. Diet has improved so much, primarily from changes in
canning and reduction in lead, that it now makes no measurable
contribution to lead in blood in these studies. They also noted the
long persistence of lead in blood and urine in young children, perhaps
related to the rapid turnover and growth of bone in children. Thus,
there can be no doubt that lead in household dust as derived from paint
and exterior soil is the major direct source of lead in blood and urine
today, as originally shown by Gibson.16 Some physicians
and others continue in the mistaken belief that a child must eat large
chunks of lead paint to be poisoned. This has never been the case.
In 1977, on the recommendation of the National Research
Council,21 the US Consumer Product Safety Commission
(CPSC)22 finally banned the use of lead additives in paint
intended for interior or exterior residential surfaces. Specifically,
the CPSC banned the transport of such paint in interstate commerce and ruled that there should be no deliberate addition of lead to paint intended for residential purposes. By the time this was done, in 1978, titanium dioxide had largely replaced lead as the major white pigment
in paint. The consumption of white lead had decreased substantially to
about 3000 tons per annum21 from a peak in the 1920s, to
about 170 000 to 180 000 tons of lead per annum in white paint.
ENVIRONMENTAL AND MEDICAL MANAGEMENT
The total removal of lead paint from old housing in the United
States has long been rejected by the authorities as too expensive. In
the words of Barltrop23: "It is likely that children
will continue to be employed as biological indicators of substandard
housing." This must stop! Although the ultimate goal of primary
prevention is the eradication of lead paint in the house, interim steps
can be taken to reduce exposure as we work our way systematically
toward the ultimate goal of primary prevention. This is the only
"treatment" that is likely to be successful. Today a team approach
is required involving the physician, public health nurse, social
service worker, and environmental inspector. It is quite clear that
poor residents in dilapidated housing, armed with mops and buckets, are
not able to do and maintain a satisfactory clean-up.24 An
initial professional clean-up, incorporating a high-efficiency particle
accumulator (HEPA) vacuum24-26 is needed along with
stabilization or removal of lead painted surfaces. This has been
studied intensively under Farfel27 at the Kennedy
Institute. We have found, depending on the condition of the house, that
simple repair of minor defects plus a thorough professional cleaning
will substantially reduce the lead in household dust, at least
temporarily. More intensive work involves replacement of defective
windows with vinyl replacement windows and making the floors cleanable
with a smooth linoleum or vinyl surface. Under these conditions we have
found that residents, with ordinary cleaning techniques can maintain
substantially reduced dust lead levels in the child's home for at
least 3 years. (This study is still in progress).
It is important to evaluate any steps to reduce environmental exposure
primarily based on dust lead levels. Follow-up blood lead levels serves
only as a secondary indicator, inasmuch as blood lead is responsive to
the slow release of lead from bone as well as new input from the
environment. The replacement of old windows with new vinyl windows and
making floors more easily cleanable by covering with either vinyl or
linoleum has cost up to $7500 in recent years in small rowhouses. As
modern low-cost lead-free housing becomes more available, a
concentrated effort should be made to relocate the child out of the old
contaminated neighborhood into newer housing wherever possible. Often
this is not feasible for these poor families without a rent subsidy. For example, the requirement that Section 8 housing be made lead-safe should be enforced. Furthermore, the house-by-house approach to abatement is poor policy; rather, whole areas need to be either gut-rehabilitated or replaced. Under these circumstances the child can
then reside in a neighborhood without risk of significant lead
exposure.
COMPREHENSIVE CAPITATION GRANTS
We may now compare the costs of environmental interventions with
medical cost. Medical treatment in a lead-safe environment is going to
cost even more than interim repairs to a house, particularly if the
child is hospitalized in a general hospital, where the cost may be
$1000 a day or more. For the past several years, the Kennedy Krieger
Institute in Baltimore, Maryland, has operated a Lead Safe House and
has contracted with some health maintenance organizations to undertake
a comprehensive approach. These contracts covered not only the cost of
professional cleaning, minor repairs, and moving, but also direct
medical cost and brief residence at the Kennedy Krieger Lead Safe
House, while repair work was being done. Unfortunately, managed care
has recently put an end to this. Some of the more extensive work in
recent years has been covered by grants from the State of Maryland
Department of Housing and Community Development and the US Department
of Housing and Urban Development. A recent federal
report28 has set forth the programs of various federal
agencies to eliminate lead paint in housing including proposed funding
over the next 10 years. In the past, if a child was hospitalized on a
general pediatric service, for up to 3 weeks, that could add up to
$30 000. Many houses could be repaired for that. Indeed, in 1984 review of data from the State of Maryland showed that the State and
Medicaid spent, approximately $4 000 000 per year for medical
management of lead poisoning, not to mention the excess cost for
special education attributed to lead. We may say that this money was
ill-spent, because drug therapy alone is not likely to have significant
long-term benefit, whereas the removal or stabilization of lead paint
in the house would benefit all children who might ever reside in the
house.
Primary prevention is achievable. That this can be done has been
documented by Farago et al.29 They studied children in
Landskrona in Sweden, the site of the only secondary smelter for the
recovery of lead from 85% of the lead acid batteries in all of
Scandinavia. In this city there was no lead paint in the houses.
Controls were introduced at the smelter 10 years ago, so that the
emissions of lead were reduced from 2.25 tons per annum to less than a
half ton per annum. Also, it has been a long-standing custom throughout
Scandinavia to remove one's shoes when one enters the house and to
replace them with house slippers. During 1999 the average blood lead
concentration in young children living in that city was 3.05 ug Pb/dL
compared with 6.5 ug Pb/dL earlier.
When one considers the number of children treated with chelation
therapy during the past 50 years and all of the associated cost, proper
environmental control would have had a much longer lasting benefit to
our population. As we move toward primary prevention,30
the ultimate goal, one should not shy from introducing interim measures
that will be effective for 3 years at least and thereby protect
thousands of children until we can eliminate this preventable disease
altogether.
CHELATION THERAPY
2,3-dimercapto-1-propanol
(BAL)2 in 1946 and calcium disodium
ethylenediaminetetraacetate
(CaNa2EDTA)3 in 1950childhood lead
poisoning was recognized clinically only in the severe acute phase.
These agents alone reduced the mortality of severe acute lead
encephalopathy from 66% to approximately 25% to 30%.4
Subsequently, it was found that these agents given in
combination5 reduced mortality to about 1% to 2%. They
were not effective in reducing the neurologic sequelae.6
Ongoing prospective studies conducted now to at least 101/2
years of age have shown what appears to be a greatly increased risk of
long-lasting, if not permanent, cognitive and neurobehavioral deficits7 in asymptomatic children with blood lead levels
during infancy <25 ug Pb/dL.8 Despite this, there are
many physicians who still consider chelation therapy the mainstay of
treatment, even in the asymptomatic phase including low blood lead
concentrations.
vomiting, abdominal pain, and encephalopathyare related to the concentration of lead in blood and
soft tissues, which normally contains no more than about 5% of the
total body burden of lead.10 During the acute clinical
episodes this proportion may be somewhat higher. The remaining 90% to
95% of lead is sequestered in bone. We have no chelating agents that
remove any significant amount of lead from bone, where the half-life in
adults is estimated at 16 to 20 years.11 In children
recent data shows the average half-life of lead in blood is from 20 to
38 months.12 Bone can be a source of lead in blood for
years.
Kennedy Krieger Institute
Baltimore, MD 21213
FOOTNOTES
Address reprint requests to (J.J.C.) Kennedy Krieger Institute, 3001 E Biddle St, Baltimore, MD 21213.
Received for publication Jun 6, 2000; accepted Jun 6, 2000.
ABBREVIATIONS
DMSA, meso-2,3-dimercaptosuccinic acid; CPSC, US Consumer Product Safety Commission.
REFERENCES
XX: Proceedings of University of Missouri's 20th Annual
Conference; June 1986; University of Missouri, Columbia, MO; pages
322-332This article has been cited by other articles:
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  E. K. Silbergeld MERCURY, VACCINES, AND AUTISM, REVISITED Am J Public Health, August 1, 2008; 98(8): 1350 - 1350. [Full Text] [PDF]
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D. R. Buchanan and F. G. Miller Justice and Fairness in the Kennedy Krieger Institute Lead Paint Study: the Ethics of Public Health Research on Less Expensive, Less Effective Interventions Am J Public Health, May 1, 2006; 96(5): 781 - 787. [Abstract] [Full Text] [PDF]
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 H H Ang, E L Lee, and K Matsumoto Analysis of lead content in herbal preparations in Malaysia Human and Experimental Toxicology, August 1, 2003; 22(8): 445 - 451. [Abstract] [PDF]
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