DOI: 10.12809/hkmj177078
© Hong Kong Academy of Medicine. CC BY-NC-ND 4.0
COMMENTARY
Lead poisoning—an aetiology not to be missed
MF Ip, FHKAM (Medicine); SH Li, FHKAM (Medicine);
TY Wai, FHKAM (Medicine)
Department of Medicine, North District Hospital,
Sheung Shui, Hong Kong
Corresponding author: Dr MF Ip (faifaimk@yahoo.com.hk)
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Lead is ubiquitous in the environment. Workers in
industries such as plumbing, mining, and manufacturing of metals,
plastics, or batteries are at risk of exposure through inhalation of
lead-containing dust or fumes. Lead has also been used in many consumer
products, such as gasoline, paints, cosmetics, crayons, ceramic glaze,
cookware, and toys. Children with the eating disorder pica are at risk of
excessive lead ingestion.
In Hong Kong, historical reports of lead poisoning
include an outbreak among Gurkha soldiers exposed to chili powder
contaminated with lead chromate, fisherman and their families who ingested
excessive lead while repairing nets contaminated by lead weights,
consumers of traditional Chinese medicine or processed herbs contaminated
by lead grinders and pans used in the pulverisation process.1 2 There has
also been a case of poisoning due to chronic consumption of ashes from a
Chinese talisman bearing writing in lead tetroxide.3 Although lead poisoning is uncommon in Hong Kong,
clinicians should still have a high index of suspicion, as lead poisoning
has a wide range of clinical manifestations and may present to different
specialities.
Our neurology team recently encountered a
60-year-old man who presented with generalised weakness in all four limbs
and anaemia who later found to have severe lead poisoning. The patient
enjoyed good past health until January 2017, when he reported experiencing
dizziness and a tingling sensation in his extremities. When admitted to
North District Hospital, Hong Kong, on 29 July 2017, the patient was pale
and his speech was confused. His symptoms included bilateral facial palsy,
weak voice dysphonia, dysphagia, dysarthria, generalised muscle wasting,
hypotonia, and areflexia without muscle fasciculation. There was no
apparent sensory-level or sphincter disturbance.
The patient’s signs and symptoms were suggestive of
progressive generalised polyneuropathies with bulbar involvement.
Comprehensive investigations were performed to elucidate the aetiology. On
9 August 2017, the patient’s blood lead level (BLL) was recorded as
markedly elevated to 189 μg/dL, confirming severe lead poisoning
presenting with anaemia, significant sensorimotor axonal polyneuropathy,
and encephalopathy.
The patient was transferred to Toxicology Centre of
Prince of Wales Hospital, Hong Kong, where treatment with
2,3-dimercaptosuccinic acid (DMSA) were initiated. Treatment was changed
to calcium disodium edetate (CaNa2EDTA) with dimercaprol later
for suspected lead encephalopathy. After treatment, the patient’s BLL
dropped to 26.25 μg/dL. Haemoglobin improved to around 10 g/dL. The
patient’s facial weakness, speech, and limb power improved. The patient
has regular follow-ups and repeated courses of DMSA; at his latest review,
in February 2018, his BLL was still elevated to 48.4 μg/dL.
Because of increasing migration to and from
mainland China, clinicians in Hong Kong should be aware that patients may
acquire lead poisoning in mainland. According to a large case series of
childhood lead poisoning in China published in 2017, industrial lead
pollution (43.1%) and folk medicines (41.4%) account for the main source
of lead exposure.4 Our patient
denied using traditional Chinese medicine, over-the-counter medication, or
recreational drugs. He had worked as renovation worker in mainland China
for decades. Therefore, we postulate that the patient’s lead poisoning was
due to contact with lead-containing paint.
Acute high-level lead exposure can lead to
encephalopathy, coma, ataxia, seizure, colicky abdominal pain, nausea, and
vomiting. Acute renal tubular dysfunction presenting with Fanconi-type
syndrome (such as glucosuria, aminoaciduria, phosphaturia) has been
observed in children.5
Chronic lead poisoning causes decline in cognitive
function and neurobehavioural problems such as depression and
irritability. Children are particularly susceptible, owing to an
incomplete blood brain barrier. Chronic lead poisoning in children can
result in lower intelligence quotient, attention deficit hyperactivity
disorder, and impaired learning, memory, speech, and hearing development.6 Mothers may transfer lead to their
developing fetus through the placenta, or to breastfeeding infants through
breast milk. There is no absolute safe BLL. The Centers for Disease
Control and Prevention has lowered the toxic BLL from >25 μg/dL in 1985
to >5 μg/dL in 2010, which correspond to 97.5th percentile of BLL in
children of United States.7
Chronic lead poisoning also causes neuropathies.
Classical lead neuropathy predominantly involves wrist and finger
extensors, resembling radial nerve palsy. This type of motor neuropathy is
more likely to develop following relatively short-term exposure to high
lead concentrations and evolves in a subacute fashion. The mechanism
proposed is lead-induced porphyria rather than its direct neurotoxic
effect. Shobha et al8 described
five patients with lead-related radial neuropathy. All patients had normal
motor conduction velocities, with some demonstrating reduced compound
muscle action potential or mild reduction of sensory nerve action
potential. There is another type of neuropathy with distally accentuated
sensorimotor and autonomic involvement, which evolves more slowly after
many years of exposure. Nerve conduction studies in these patients have
demonstrated normal motor conduction velocities and compound muscle action
potential amplitudes, but prolonged distal motor and sensory latencies.8 9
10 Lead poisoning can also cause
electromyographic abnormalities such as denervation activity and
polyphasic motor unit potentials, mimicking motor neuron disease.11
Chronic lead poisoning also causes anaemia through
increased haemolysis and inhibition of enzymes, such as
delta-aminolevulinic acid dehydratase and ferrochelatase, that are
necessary for haem biosynthesis. The metabolic block results in increased
urinary delta-aminolevulinic acid, coproporphyrin, and erythrocyte zinc
protoporphyrin. Basophilic stippling (caused by inhibition of pyrimidine
5’-nucleotidase and ribosomes aggregates) and ring sideroblasts may be
found.12
Finally, chronic lead exposure causes chronic
interstitial nephritis, increased risk of hypertension, cardiovascular
disease, and cancer.
Acute lead toxicity is confirmed by elevated BLL.
Chronic lead toxicity can be established by measuring red cell zinc
porphobilinogen and by X-ray fluoroscopy of bone.13
Abdominal radiography may demonstrate lead chips in the bowels of children
with pica.
Management of lead poisoning includes
identification of source of exposure, screening of household members, and
determination on the need for chelation therapy. Chelation agents include
DMSA, CaNa2EDTA, and dimercaprol. Adverse effects of these treatments
include rash, neutropenia, liver derangement, gastrointestinal upset, and
haemolysis in glucose-6-phosphate-dehydrogenase deficiency, essential
mineral loss, renal failure, and lead encephalopathy. Whole bowel
irrigation is needed if abdominal radiography demonstrates lead-containing
foreign bodies. Treatment of underlying nutritional deficiencies, such as
iron and calcium deficiencies, helps to reduce lead absorption.14
In conclusion, although legislation controlling
environmental lead exposure has resulted in declining numbers of lead
poisoning cases in most developed countries, clinicians should remain
aware of this diagnosis in patients with both haematological and
neurological manifestations.
Author contributions
All authors contributed to the concept and design
of the study, acquisition of data, and interpretation of data, and
critical revision of the manuscript for important intellectual content. MF
Ip drafted the manuscript.
Acknowledgement
We would like to thank Dr Jones Chun-man Chan,
Toxicology Centre of Prince of Wales Hospital, for his effort in managing
the patient.
Declaration
All authors have disclosed no conflicts of
interest. All authors had full access to the data, contributed to the
study, approved the final version for publication, and take responsibility
for its accuracy and integrity.
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