Hong
Kong Med J 2017 Dec;23(6):616–21 | Epub 13 Oct 2017
DOI: 10.12809/hkmj176214
© Hong Kong Academy of Medicine. CC BY-NC-ND 4.0
REVIEW ARTICLE
Childhood lead poisoning: an overview
KL Hon, MD, FAAP1; CK Fung, MB, ChB2;
Alexander KC Leung, FRCP(UK), FRCPCH3
1 Department of Paediatrics, Prince
of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong
2 Department of Anatomical and
Cellular Pathology, United Christian Hospital, Kwun Tong, Hong Kong
3 Department of Pediatrics, Alberta
Children’s Hospital, University of Calgary, Calgary, Alberta, Canada
Corresponding author: Prof KL Hon (ehon@cuhk.edu.hk)
![](https://www.hkmj.org/sites/default/files/mjimage/pdficon.png)
Abstract
Childhood lead poisoning is a major public health
concern in many countries. In 2015, the Hong Kong SAR Government and its
citizens faced a major public health crisis due to the presence of lead
in the drinking water of a number of public housing estates.
Fortunately, no child was diagnosed with lead poisoning that required
treatment with chelation. Lead is a ubiquitous, naturally occurring
material that exists in air, dust, soil, and water. It is also widely
present in industrial products including petrol, paints, ceramics, food
cans, candies, cosmetics, traditional remedies, batteries, solder,
stained glass, crystal vessels, ammunition, ceramic glazes, jewellry,
and toys. It can also be found in human milk. There is no safe blood
lead level and it may be impossible to completely eliminate lead from
any city. Hence routine measurement of blood lead levels is not
considered useful. Acute poisoning, especially with encephalopathy,
deserves immediate medical treatment in hospital. Chelation therapy is
recommended if blood lead level is 45 µg/dL or higher. For blood levels
between 20 and 45 µg/dL, treatment is indicated if the child is
symptomatic. For blood levels below 20 µg/dL in otherwise asymptomatic
children, the principle of treatment is to provide long-term
neurodevelopmental follow-up and counselling. In all cases, immediate
removal of the source of lead exposure is vital. Even low levels of lead
exposure can significantly impair learning, educational attainment, and
neurodevelopment.
Introduction
Childhood lead poisoning is a major public health
concern in many countries as it may result in serious health consequences.
In general, children absorb a greater percentage of lead from the
gastrointestinal tract than adults.1
2 Fasting, iron deficiency, and
calcium deficiency may further increase gastrointestinal absorption of
lead.1 2
In Hong Kong, food safety has become a major public concern in recent
years. In 2015, the Hong Kong SAR Government and its citizens faced a
major public health crisis due to the presence of lead in the drinking
water of a number of public housing estates. Fortunately, no child was
diagnosed with lead poisoning and hence did not require chelation therapy.
This review discusses the possible sources of lead
exposure and poisoning in children, public health implications, medical
management, and neurodevelopmental outcomes with a focus on the situation
in Hong Kong. References were searched in January 2017 using keywords:
((“toxicity”) OR (“poisoning”) AND “lead”) AND ((“lead toxicity”) OR
(“lead poisoning”) AND “Hong Kong”) in PubMed, limited to ‘human’, with no
filters for article type or date of publication. Discussion is based on,
but not limited to, the search results.
Possible sources of lead exposure and poisoning in
children
According to the World Health Organization, lead is
a ubiquitous, naturally occurring material that exists in air, dust, soil,
and water. It is also widely present in industrial products including
petrol, paints, ceramics, food cans, candies, cosmetics, traditional
remedies, batteries, solder, stained glass, crystal vessels, ammunition,
ceramic glazes, jewellry, and toys.3
4 5
6 7
It is also found in human breast milk.8
In the US, lead-containing paint in old houses is one of the main sources
of lead exposure or poisoning in children. In many industrialising
countries including China, smelters, refineries, mines, soil
contamination, and use of lead gasoline are important sources of lead
exposure.
Water supply can be contaminated with lead.9 10 11 12 A recent
example is the drinking water crisis that occurred in the post-industrial
city of Flint in Michigan, US.11
In this situation, lead in drinking water is absorbed to a greater extent
than lead in food and may account for more than 50% of the lead ingested
by children.13 The US
Environmental Protection Agency recommended taking actions when lead in
drinking water exceeds 15 parts per billion, including taking further
steps to optimise their corrosion-control treatment (for water systems
serving 50 000 people who have not fully optimised their corrosion
control), educating the public about lead in drinking water and actions
consumers can take to reduce their exposure to lead, replacing the
portions of lead service lines (lines that connect distribution mains to
customers) under the water system’s control.14
Most incidents of lead contamination of household water were caused by
copper plumbing with lead solder. Occasionally, lead pipes may also be
responsible although they are now rarely used.
No review article about lead toxicity in Hong Kong
was found on MEDLINE/PubMed at the time of writing. Nevertheless discrete
reports from different institutes about local lead toxicity are available,
with the earliest report dated 1969, when 121 Gurkha soldiers investigated
for ‘epidemic myalgia’ were found to have lead poisoning due to curry
powder contaminated with lead chromate.5
Later in 1977, a 4-month-old girl presented with a grand mal seizure after
ingestion of Chinese herbal medicines containing lead.3 In 1991, a case of acute lead poisoning with cerebral
oedema and death was reported in a 2-month-old girl.15 Two other case reports described a total of four
adult patients who had lead poisoning following ingestion of two different
Chinese herbal pills. They had variable clinical presentations ranging
from relatively asymptomatic to end-organ complications.16 17 In 2014,
a middle-aged woman who presented with motor neuron disease was found to
have a raised blood lead level after consumption of ashes from burnt
Chinese talismans (Dao religious handwriting believed to have the power to
expel evil).18 Hong Kong is a
commercialised city with very few industries and factories. The main
sources of lead are contaminated food, toys, adulterated medicines,
traditional remedies, and batteries. A study of children with eczema
revealed that disease severity and quality of life correlated with blood
lead level, and patients who had used traditional herbal remedies
generally had a higher blood lead level.19
Contaminated water in public housing estates was first described in 2015
in Hong Kong.20
Potential public health implications
There is no screening programme for lead or other
heavy metals in Hong Kong. Guidelines about lead screening, however, are
available worldwide. In 2013, nearly 30 questionnaires were available,
designed as a preliminary screening tool for paediatric lead poisoning.
They showed variable sensitivity and specificity based on systematic
reviews.21 22 According to the latest guideline in 2012 from the
Centers for Disease Control and Prevention (CDC)’s Advisory Committee on
Childhood Lead Poisoning Prevention (ACCLPP), clinicians should perform an
environmental assessment before screening children for lead poisoning.13 23 This
changed the practice of universal screening of all children for elevated
blood lead levels2 23 24 to
targeted screening after mathematical simulations suggested that such
screening among 1-year-old children may not be cost-effective, especially
in communities with a lower prevalence of lead poisoning.25 At the same time, with reference to the level of
‘lead toxicity’ in children, ACCLPP eliminated the term ‘level of concern’
for blood lead level (previously defined as 10 µg/dL) and replaced it with
a reference level of 5 µg/dL, based on the 97.5th percentile of the
population blood lead level in children aged between 1 and 5 years.2 13 24 This was supported by the American Academy of
Pediatrics who acknowledged that even the lowest degree of lead exposure
might harm children,13 23 26 and
echoed the European Food Safety Authority who concluded that there is no
known safe exposure to lead as evidenced by international studies in
Europe.27 28 29 In other
words, there is no safe or ‘non-toxic’ blood lead level.
A systematic review of the effectiveness of
interventions to reduce lead exposure from consumer products and drinking
water in Germany concluded that the limited quantity and quality of the
evidence derived from measuring blood lead level and associated health
outcomes suggested an urgent need for more robust research into the
effectiveness of interventions to reduce lead exposure from consumer
products and drinking water, especially for regulatory interventions.6 The dilemma is that there is no safe lead level, and it
is impossible to completely eliminate lead from any city. Hence routine
measurement of blood lead level is not considered useful for management.
Clinical manifestations/complications of lead poisoning
Lead is a potent neurotoxin. Neurotoxicity is more
prominent in children and infants in-utero than in adults because of the
incomplete blood-brain barrier.8 30 31
Despite this, the majority of children with lead poisoning is
asymptomatic. Neurological manifestations/complications of lead poisoning
include acute encephalopathy, peripheral neuropathy, hearing loss, and
neurobehavioural deficits such as hyperactivity, withdrawal, developmental
delay, lower intelligence quotient, higher academic failure, and lower
overall life achievements.32 33 34
Meta-analysis of 19 studies with a total of 8561 children suggested that
lead exposure is positively related to conduct problems.35 The causal effect of lead exposure on these
behavioural problems, however, cannot be proven as poor housing, poverty,
and other stressors are significant confounding factors.36 According to the American Academy of Neurology, the
clinical correlation of mildly elevated but non-toxic levels of blood lead
with developmental status remains controversial.
Lead lines at the junction of the gums and teeth,
if present, suggest severe and prolonged lead exposure. Other clinical
manifestations/complications include colicky abdominal pain, constipation,
growth retardation, vitamin D deficiency, anaemia, and nephropathy.1 2 24 Rarely, lead poisoning may also lead to hypertension,
immunodeficiency, osteoporosis, changes in serum level of sex hormones and
thyroid hormones, premature delivery, pre-eclampsia, infertility, and
malignancy.30 37 38
Exposure versus poisoning
Despite the potential harmful effects of lead on
humans, lead exposure is not synonymous with lead toxicity. According to
the Agency for Toxic Substances and Disease Registry, exposure is defined
as contact with a substance by swallowing, breathing, or touching the skin
or eyes. Exposure may be short-term (acute exposure), of intermediate
duration, or long-term (chronic exposure). A toxic agent is a chemical or
physical (eg radiation, heat, cold, microwaves) agent that, under certain
circumstances of exposure, can cause harmful effects to living organisms (https://www.atsdr.cdc.gov/glossary.html).
In
other words, it is the lead toxicity per se not lead exposure that
necessitates treatment. Although there is no definitive toxic level for
blood lead, the affected child should be continuously monitored to ensure
medical intervention if necessary.
Screening of children for lead poisoning
The American Academy of Neurology suggests
screening of children with developmental delay for lead toxicity. This
should target those with known identifiable risk factors for excessive
lead exposure, including children aged 1 to 2 years living in housing
built before 1950, exposure to lead-containing folk remedies, child
immigrants from countries where lead poisoning is prevalent, children with
iron deficiency, children with developmental delay with pica disorder,
victims of neglect, and children of low-income families.39
The CDC’s ACCLPP has updated its guidelines for
blood lead screening among children eligible for Medicaid by providing
recommendations to improve screening and information for health care
providers, state officials, and others interested in lead-related services
for Medicaid-eligible children.40
Because state and local officials are more familiar than federal agencies
with local risks for elevated blood lead levels, the CDC recommends that
state and local officials have the flexibility to develop blood lead
screening strategies that reflect local risk. Rather than provision of
universal screening to all Medicaid children, which was previously
recommended, state and local officials should target screening towards
specific groups of children in their area at higher risk. The updated CDC
recommendations provide strategies to (1) improve screening rates of
children at risk of an elevated blood lead level, (2) develop surveillance
policies that are not solely dependent on blood lead level testing, and
(3) assist states with evaluation of screening plans.
Neurocognitive impairment in children is a grave
concern as it may be irreversible. The current policy in Hong Kong is to
perform lead exposure risk assessment in citizens with a borderline raised
blood lead level, and carry out developmental assessment in affected
children under the age of 12 years, while continuously monitoring all
citizens with raised blood lead levels. The threshold for further
management for children under 18 years, pregnant women, and lactating
mothers is lower than that for the general adult population. This strategy
correlates with the targeted screening promoted by the ACCLPP.
Medical management protocol for childhood lead
poisoning
The protocol of management according to blood lead
level, adopted from ‘Care plan for residents of public estates with
elevated lead level in drinking water’, was last updated on 28 August 2015
by the Centre for Health Protection, Hong Kong SAR.41
Management of patients with lead exposure involves
not only the pharmacological management of toxicity, but also strategies
for intervention and prevention of further exposure. Once an elevated lead
level is found, the local health department should be notified and a home
risk assessment performed to determine the need for abatement strategies.
With the gradual lowering of the ‘blood lead level of concern’ by the CDC,
the threshold for action has also decreased. The Pediatric Environmental
Health Specialty Units have made recommendations for further evaluation
and/or intervention based on the blood lead level.42
In all cases, identification and immediate removal
of the source of lead exposure from the child’s environment is crucial to
the successful management of the patient. Medical treatment of lead
poisoning is relatively straightforward.40
43 44
45 46
There is no benefit in prescribing activated charcoal for lead ingestion
since it binds lead poorly. Gastric lavage may be performed although the
American Academy of Clinical Toxicology stated that there is no evidence
to show that its use improves clinical outcome. Whole bowel irrigation has
a theoretical benefit for decontamination of heavy metal ingestion but
there are insufficient data at present to support or exclude its use.
For blood lead level between 20 and 45 µg/dL, the
minimum medical management for children is to decrease their exposure to
all sources of lead, to correct any iron deficiency and maintain an
adequate calcium intake, and to test frequently to ensure that the child’s
blood lead levels are decreasing. Although not approved by the CDC, some
clinicians prescribe D-penicillamine for children within this range of
blood lead level. Otherwise the patient should have a confirmatory venous
blood lead level measured within 1 to 4 weeks as a venous sample is
subjected to less contamination than a capillary one. A capillary blood
sampling protocol has also been documented by the CDC, and is more
practical than venous blood sampling, especially in infants. For blood
lead level of <20 µg/dL in otherwise asymptomatic children, the
principle of treatment is to provide long-term neurodevelopmental
follow-up and counselling as well as periodic blood sampling to ensure
lead level is not increasing and to continue until the level is <5
µg/dL.40 43 44 45 46 For
symptomatic patients with blood lead level of <20 µg/dL, sequential
measurements of blood lead level along with review of the child’s clinical
status should be done at least every 3 months. Iron deficiency should be
treated promptly. Children with blood lead levels in this range should be
referred for environmental investigation and management. Identifying and
eradicating all sources of excessive lead exposure is the most important
intervention for decreasing blood lead levels.
Chelation therapy is recommended if the patient has
a blood lead level of ≥45 µg/dL. Before starting therapy, the blood lead
measurement must be repeated immediately for confirmation but treatment
should not be delayed while awaiting the result if encephalopathy is
suspected. Chelation therapy, especially in the setting of encephalopathy,
can be complicated. The patient must be admitted to a hospital with at
least a physician who has proficiency with chelation therapy and
management of childhood lead poisoning. The decision as to which agent
should be used depends on the blood lead level, the symptomatology, and
the environmental lead burden. Intravenous fluids should be given if
necessary to ensure adequate urine output to permit chelation and
excretion of lead in the body.2 47 Fluid intake and output should
be monitored to permit early detection of inappropriate antidiuretic
hormone secretion.
Succimer (dimercaptosuccinic acid) is a
water-soluble, oral chelating agent that is appropriate for asymptomatic
children with a blood lead level of 45 to 69 µg/dL. The recommended dose
is 10 mg/kg or 350 mg/m2 three times per day.47 D-penicillamine is a second-line oral chelating agent
because of its potential for significant side-effects (thromobocytopenia,
leukopaenia, urticaria, angioedema, abnormal liver function,
Stevens-Johnson syndrome, and nephrotic syndrome).47
Calcium disodium edetate (CaNa2 EDTA) is
a chelating agent that is preferably given by continuous intravenous
infusion. The recommended dose is 35 to 50 mg/kg/day or 1000 to 1500 mg/m2/day.47 It should not be used as the
sole agent in patients who manifest features of lead encephalopathy,
because it does not cross the blood-brain barrier and can potentially lead
to exacerbation of lead encephalopathy. Rather, dimercaprol (also referred
to as British anti-Lewisite), which does cross the blood-brain barrier,
should be used in combination with CaNa2 EDTA. Dimercaprol is a
parenteral chelating agent of choice for patients with lead
encephalopathy; the recommended dose is 3 to 5 mg every 4 hours given by
deep intramuscular injection. Combination therapy with CaNa2
EDTA and dimercaprol or succimer should be instituted in symptomatic
children with blood lead level of 45 to 69 µg/dL.2
47 Children whose blood lead level
is ≥70 µg/dL should be treated as medical emergencies, preferably with
intravenous therapy. A combination of intramuscular dimercaprol and
intravenous CaNa2 EDTA should be used for children with blood
lead level of 70 to 99 µg/dL if there are features of lead encephalopathy
or with a blood lead level of ≥100 µg/dL even in the absence of features
of lead encephalopathy. Features of lead encephalopathy include persistent
lethargy, persistent vomiting, headache, afebrile seizures, or coma.
Chelation therapy has its own limitations. With
chronic lead ingestion, lead can be incorporated into the skeletal system
and can be an endogenous reservoir of lead exposure that is hard to
eliminate.2 47
Neurodevelopmental outcomes: who and for how long
should at-risk children be monitored?
Lead poisoning in childhood produces long-term
problems with learning, intelligence, and earning power.48 Asymptomatic lead poisoning has a far better
prognosis. Given that there is no safe blood lead level, the CDC stresses
the importance of regular follow-up of children with elevated blood lead
levels. A monitoring programme should include nutritional support (such as
ensuring sufficient intake of calcium, vitamin D, vitamin C) to minimise
lead absorption, preventive measures to avoid household lead exposure, and
education of caregivers about sources of lead exposure, prevention of
exposure, and ways to decrease intestinal absorption.40 44 45 46 Affected
children should be followed up continuously at least until environmental
sources of lead have been identified and eliminated, and thereafter until
blood lead level has declined to <15 µg/dL for at least 6 months, while
other objectives of the management plan are achieved. Long-term
neurodevelopmental monitoring is also advised after a case is closed, in
view of many of the neurological deficits that manifest late in life. Any
surveillance should be continued until a child reaches 6 years of age, an
age of critical learning transition points and elevated risk exposure,
although the definitive duration of follow-up is unclear.40 43 44 45 46 Likewise, no end-point of follow-up is recommended by
the Centre of Health Protection in Hong Kong.
Conclusion
It has been established that even low-level lead
exposure can significantly impair the learning and educational attainment
and neurodevelopment of a child.49
50 51
52 53
54 In-utero exposure to lead can
adversely affect the infant’s neurodevelopment, independent of postnatal
blood lead level. With no safe limit of blood lead level, rigorously
reducing the amount of lead in the environment is imperative for young
children and unborn babies.13
Declaration
All authors have disclosed no conflicts of
interest.
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