Review

Lead and mercury exposures: interpretation and action

Elizabeth Brodkin, Ray Copes, Andre Mattman, James Kennedy, Rakel Kling, Annalee Yassi

Abstract
Lead and mercury are naturally occurring elements in the
earths crust and are common environmental contaminants.
Because people concerned about possible exposures to
these elements often seek advice from their physicians, clinicians need to be aware of the signs and symptoms of lead
and mercury poisoning, how to investigate a possible exposure and when intervention is necessary. We describe 3
cases of patients who presented to an occupational medicine specialist with concerns of heavy metal toxicity. We use
these cases to illustrate some of the issues surrounding the
investigation of possible lead and mercury exposures. We review the common sources of exposure, the signs and symptoms of lead and mercury poisoning and the appropriate use
of chelation therapy. There is a need for a clear and consistent guide to help clinicians interpret laboratory investigations. We offer such a guide, with information about population norms, lead and mercury levels that suggest exposure
beyond that seen in the general population and levels that
warrant referral for advice about clinical management.
CMAJ 2007;176(1):59-63

DOI:10.1503/cmaj.060790

xposure to environmental contaminants, including

heavy metals, continues to be a widespread problem
in Canada, and patients concerned about possible exposures often seek advice from their physicians. Heavy metals are a well-established cause of severe illness, and these
concerns need to be addressed. However, although clinically significant exposures to heavy metals still occur in
Canada, a substantial proportion of patients who present
with concerns of heavy metal toxicity do not have true poisoning. Physicians need to be aware of not only the signs and
symptoms of heavy metal poisoning but also what investigations are appropriate, how to interpret the results, when intervention is necessary and when it is unwarranted. Alternative health care providers are also investigating and treating
heavy metal exposures; therefore, it is helpful to be familiar
with the treatments they are offering and some of the pitfalls their patients may fall into.
In this review, we describe 3 cases of patients referred to an
occupational medicine specialist with concerns of heavy metal
toxicity. One was referred with symptoms of severe poisoning
from an unknown source, the others with significant anxiety
about possible occupational exposures and conflicting laboratory investigations. One patient had already consulted and had

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received treatment from an alternative health care provider.

These cases have been chosen to illustrate some of the issues
that commonly arise around concerns of exposure to heavy
metals, in particular lead and mercury. We also provide a
guide to interpreting laboratory investigations to assist clinicians with investigating concerns and advising their patients.

Cases
Case 1
A 54-year-old East Indian man consulted his family physician
because of fatigue, abdominal pain, nausea, headaches and
weight loss. Investigations ordered by the family physician included measurement of the hemoglobin concentration, which
was 73 g/L. The pathologist who reviewed the laboratory test results commented on the low mean cell volume and coarse basophilic stippling of the red blood cells. The blood lead level
was therefore measured and found to be markedly elevated, at
4.15 (reference range < 1.93) mol/L. It was eventually determined that the patient had been taking traditional medicines
imported from India for over 2 years. Analysis revealed that they
contained 13%14% (130 000 g/g) lead and 1% (10 000 g/g)
mercury by weight. The patient was referred to a clinical toxicologist and underwent chelation therapy, with substantial improvement of his symptoms and anemia. At follow-up several
months after his last chelation treatment, his blood lead level
was 1.34 mol/L and hemoglobin concentration 129 g/L.

Case 2
A 35-year-old dentist presented with a 1-year history of a fine
resting tremor in his hands. This is a serious occupational disability for him, because it interferes with his ability to perform
the fine motor tasks required in dental practice. He was assessed
by a neurologist, who diagnosed benign tremor. The patient became concerned about possible mercury toxicity because of
some occupational exposure to mercury and asked his family
physician to arrange for testing. Results from tests conducted at
a laboratory in Quebec City revealed that his blood mercury level
was 18 (reference range < 15) nmol/L, and his mercury level in a
24-hour urine collection was reported as normal. The patient
began reducing his exposure to mercury amalgam and requested
a consultation with an occupational medicine specialist to discuss chelation therapy. Repeat testing at a laboratory in Vancouver revealed a blood mercury level of 19 (reference range < 29)
nmol/L and a mercury level in a 24-hour urine collection of 29

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Review
(reference range < 50) nmol/d. The patient was not reassured by
these results, since he found the different reference ranges used
by the 2 laboratories confusing.

Case 3
A 44-year-old woman worked for 10 months in a car dealership
and service centre. In the course of her work, she was exposed
to vehicle emissions and other substances present in the service
area. There was no established exposure to heavy metals. The
woman developed a variety of symptoms, including pain and
tingling in one hand, abdominal pain and bloating, diarrhea
and constipation, increased bruising, varicose veins and fatigue. After 10 months she left the car dealership. Her symptoms improved, but she remained concerned and consulted an
alternative health care provider. He arranged testing for blood
lead and blood mercury levels and a 24-hour urine toxic metals test, which entailed challenging the patient with a chelating agent and subsequently measuring the levels of various
heavy metals in her urine. Her blood lead level was 0.1 (reference range < 1.93) mol/L and her blood mercury level 10 (reference range < 29) nmol/L. However, the results of the toxic
metals test were presented in such a way as to suggest lead and
mercury toxicity. The alternative health care provider diagnosed
heavy metal poisoning from her working at the car dealership
and started the patient on chelation therapy. The patients family physician questioned this course of action and arranged for
consultation with an occupational medicine specialist.

Lead
Lead is used in many industries, including lead smelting and
processing, the manufacturing of batteries, pigments, solder,
plastics, cable sheathing, ammunition and ceramics, and battery recycling.1 In the United States, most cases of lead poisoning in adults result from occupational exposure, although lead
exposure in the general population is primarily through diet.2
Whether the same is true in Canada is uncertain, since population-based surveillance of exposure to lead or other environmental contaminants is not performed in this country. In addition to diet as a source of exposure, there is ongoing lead
exposure in the general population from old lead-based paint.3
Average blood lead levels in the northeastern and midwestern
United States are higher than those in the southern and western regions, in part because of the increased presence of lead in
older homes.4,5 Heavy metals, including lead, are used in the
manufacture of Ayurvedic medicinal products, and nonstandardized manufacturing may result in high levels remaining in
the final product.6 A recent study of Ayurvedic medicinal products sold in the Boston area revealed that 20% contained heavy
metals.7 These products are commonly imported from India,
both for resale and for private use. Reductions in the use of lead
in food processing, the removal of lead additives from gasoline
and the reduction of lead in paint have resulted in marked declines in lead exposure in the North American population. Data
from the United States show that the mean blood lead level in
the US population decreased from 0.71 to 0.07 mol/L (14.6 to
1.5 g/dL) between 1976 and 2001/02.3,8

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Inorganic and organic forms of lead are absorbed through

the lungs and gastrointestinal tract; organic lead compounds
may also be absorbed through the skin. In occupational settings, exposure through inhalation is more common, whereas in the general population it is largely through ingestion.9
Following absorption, lead is taken up in the blood and deposited in soft tissues (brain, liver, kidney, bone marrow) and
bone. Excretion is primarily via the kidneys, and the half-life
of lead in the blood is about 30 days. Up to 94% of the body
burden of lead is in bone, where it has a half-life of years to
decades.3,9 Pregnancy, lactation, menopause, osteoporosis
and other events that lead to increased bone resorption will
lead to an increase in blood lead levels in people who have
substantial amounts of lead stored in bone, and it can be an
unexpected source of lead poisoning.9
Signs and symptoms of lead poisoning in adults may include abdominal pain, anorexia, nausea and constipation,
headache, joint and muscle pain, difficulties with concentration and memory, sleep disturbances, anemia with basophilic
stippling, peripheral neuropathy and nephropathy.3,9
The blood lead level is the most widely used and most reliable measure of lead exposure. It primarily measures exposures that have taken place in the previous few weeks10 but is
a poor indicator of lead accumulated in bone. Bone lead levels
are theoretically the best indicator of total body burden; however, measurement is difficult. X-ray fluorescence can be used
to monitor lead in the skeleton, but the technique is not
widely available and is generally used only for research.11
Contamination of blood and urine specimens during collection and storage is a potential problem when screening for
heavy metals, and adherence to strict guidelines from a reputable laboratory is important. The use of metal-free collection devices and storage tubes is essential.
Interpretating blood lead levels requires an understanding
of reference ranges and how they are derived. Although lead
is toxic and serves no biological purpose, it is a naturally occurring element, and some degree of exposure is universal.
Reference ranges may vary from laboratory to laboratory; in
some cases they are based on levels commonly or normally
seen in a particular population, and in others they are derived
from exposure limits (e.g., benchmark doses) published by
national or international agencies.12 Although symptoms in
adults generally do not appear until blood lead levels reach at
least 1.9 mol/L (40 g/dL), adverse effects from lead exposure in adults can be measured at levels as low as 0.5 mol/L
(10 g/dL), and a definitive threshold below which no adverse
effects will occur has not yet been established.3,9,13 Children
and fetuses are more susceptible and may show lasting
effects from blood lead concentrations below 0.5 mol/L
(10 g/dL).14,15 Case 1 highlights the fact that heavy metal poisoning does occur in Canada and that physicians need to consider the possibility in their differential diagnoses.

Mercury
Mercury exists in elemental (metallic), inorganic and organic
(methylated) forms. The general population is primarily exposed to mercury vapour from dental amalgam and to organic

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mercury from fish consumption. Mercury bioaccumulates up
steady state maternal blood levels as low as 200 nmol/L
the food chain; therefore, large predatory species such as tuna,
(40 g/L).2224 In adults, clinically observable signs of tremor,
shark and swordfish may have high concentrations of mercury
ataxia and paresthesias begin to occur at blood levels of about
in their tissue.1618 Occupational exposure to mercury is gener500 nmol/L (100 g/L).3,16 Case 2 illustrates some of the diffially to mercury vapour and can occur in dentistry, mining, and
culties inherent in interpreting test results. The dentists inithe manufacture of electrical equipment and medical instrutial blood mercury level (18 nmol/L) was measured at a laboments.19 Thimerosal, a mercury-containing preservative, is a
ratory whose reference range (< 15 nmol/L) reflects the
norms seen in the population of the Quebec City area. The
component of some vaccines but has been phased out from
second measurement (19 nmol/L) was measured at a Vancoumost routine childhood vaccinations.20 Mercury can also be
ver laboratory whose reference range (< 29 nmol/L) is set as a
found in Ayurvedic medicinal products.6,7
percentage of the US Environmental Protection Agencys
The route of exposure and efficiency of absorption depends
benchmark dose for mercury (290 nmol/L). Neither the paon the form of mercury. Mercury vapour is well absorbed
tient nor the ordering physician knew what to make of the rethrough the respiratory route, but absorption of elemental
sults, and in the absence of an understanding of how to intermercury is negligible through the oral route. Oral absorption
pret the reference ranges, the patient became concerned that
of inorganic mercury compounds is poor to moderate dependhe was experiencing mercury poisoning. It required several
ing on the precise form. Oral absorption of organic mercury is
additional encounters to persuade the patient that this was
nearly complete. Once absorbed, mercury is distributed prinot the case.
marily to the central nervous system and the kidneys. Elimination is through the urine and feces. The half-life of elemental
Guide to interpreting laboratory results
and inorganic mercury in the blood is 4060 days, and the
half-life of organic mercury in the blood is about 70 days.3,16,17
Signs and symptoms of mercury toxicity vary with the form
There is a need for a clear and consistent guide to assist cliniof mercury and route of exposure but include gingivitis, stomcians in interpretating laboratory test results of lead and meratitis and excessive salivation. Sensory peripheral neuropathy is
cury levels. Such a guide should provide information on popcommon, and central nervous system effects include personality
ulation norms, levels that suggest exposure beyond that seen
changes, irritability, fatigue, tremor (usually intention tremor),
in the general population and levels that warrant consultation
ataxia, difficulties with memory and concentration, sleep disturfor advice about clinical management. Based on a review of
bances and a metallic taste. Renal effects include both tubular
the lead and mercury toxicology literature, available populaand glomerular damage. In the fetus, organic mercury disrupts
tion-based surveys of exposure and experience in clinical folthe cytoarchitecture of the developing brain and has been assolow-up of patients with a history of exposure, we propose the
ciated with neuropsychological changes after birth.3,16,17
guide presented in Table 1.3,13,25
Mercury levels can be measured in both blood and urine.
Interventions
Either form of measurement can be used to assess exposures
to elemental and inorganic forms of mercury, although individuals with a past history of exposure may have elevated
The first step in treating all cases of heavy metal toxicity is to reurine levels without elevated blood levels. Measurement of
duce or remove the source of exposure. In most cases this is all
mercury in whole blood is the preferred test for exposure to
that is required.3,16 Chelation therapy has historically been used
organic mercury, since this form of mercury is excreted prito reduce the body burden of heavy metals in patients with semarily in the feces rather than in the
urine.3,16,21 It is important to choose
Table 1: Guide to interpreting lead and mercury levels
the appropriate test depending on the
suspected source of exposure.
Threshold level for action
As with lead, interpreting mercury
levels requires some understanding
95th percentile
Investigate possible
Refer for advice about
of the reference ranges. Mercury is
Measurement
of adult population*
exposure
clinical management
naturally present in the earths crust,
Blood lead
0.22 mol/L
0.48 mol/L
1.90 mol/L
and some degree of exposure is in(4.6 g/dL)
(10.0 g/dL)
(40.0 g/dL)
evitable. Reference ranges for merBlood mercury
23 nmol/L
50 nmol/L
200 nmol/L
cury may be based on values com(4.6 g/L)
(10.0 g/L)
(40.0 g/L)
monly seen in a particular population
Urine mercury
4.0 nmol Hg per
19.8 nmol Hg per

or they may be derived from benchmmol creatinine

mmol creatinine
mark doses. Data taken from communities inadvertently exposed to
*These levels are derived from the US National Health and Nutrition Survey and represent levels below which
mercury and from populations that
95% of the adult population is expected to fall. Values below these levels can be considered normal.
consume large quantities of seafood
Exposure is significantly beyond that experienced by the general population and should prompt a search for
the source of exposure with a view to reducing it.
suggest that adverse effects in the
Follow-up is not recommended on the basis of the urine level alone; obtain blood mercury level as well.
most vulnerable subpopulation
Values warrant a consultation with a clinical toxicologist for advice about management options.
Insufficient data.
developing fetuses may start at

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vere symptoms and highly elevated circulating levels of heavy
metals.26 It is a process in which heavy metals are removed
from the body with the use of a chelating agent, a charged molecule that binds metals in a stable complex known as a chelate.
The chelate is subsequently excreted in the urine.27 The decision as to which patients should receive chelation therapy is a
matter of clinical judgment. Although the ability of chelating
agents to bind heavy metals and increase elimination of those
metals in the urine is well established, our review of the Cochrane database revealed a significant shortage of controlled clinical trials that have evaluated the benefits of chelation therapy
in reducing symptoms or in preventing long-term effects in
adults with heavy metal poisoning. However, there is evidence
that some patients given a course of chelation therapy may experience a placebo effect.28 There are no specific blood or urine
levels above which treatment with a chelating agent is always
indicated. The decision to proceed requires expert advice and is
based on the duration of exposure, the patients symptoms and
the laboratory test results. Chelation therapy should be carried
out only in a hospital setting by experienced physicians.2,19
Case 1 is an example of a symptomatic patient with a high body
burden of lead who had substantial relief of symptoms from
chelation therapy carried about by an experienced clinical
toxicologist.
The 24-hour urine toxic metals test that the patient in
case 3 underwent deserves further comment. This procedure
is more commonly known as the chelation challenge test or
provocation chelation. It entails measuring urine levels of
heavy metals before and after a single loading dose of a
known chelating agent. It has been used to determine
whether chelation therapy is indicated but is also used by
some alternative health care providers to diagnose heavy
metal poisoning. There is no good evidence supporting the
use of the chelation challenge test for either purpose, and
findings from some studies have suggested that it can lead to
misleading diagnostic advice.29,30 Reference ranges for blood
and urine levels intended for the general population cannot
be meaningfully applied to people undergoing this test. In addition, there have been reports of serious and fatal reactions
to the chelating agent, and findings from animal studies have
suggested that a single dose of a chelating agent will merely
mobilize heavy metals, which will then redistribute to more
vulnerable tissues such as the central nervous system.29,3133
Case 3 illustrates how the chelation challenge test can be
misused. The patients blood lead and blood mercury levels
were normal. However, following the chelation challenge
test, analysis of her urine did show the presence of heavy metals (a normal response to the chelating agent). Her urine levels were compared with those of a normal population under
nonchallenge conditions (people who had not been administered a chelating agent), and on the basis of this invalid
comparison, the alternative health care provider diagnosed
lead and mercury poisoning and the patient agreed to a
course of outpatient chelation therapy. Once the patient was
offered an explanation as to how the result of the chelation
challenge test had been misinterpreted, she discontinued the
therapy. There is no good evidence of benefits from chelation
therapy in cases in which the patient is asymptomatic or

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mildly symptomatic and has blood and urine levels comparable to population norms. It is not only unnecessary and
costly, but it also places the patient at risk of a reaction to the
chelating agent and may bind other positively charged minerals necessary for normal physiologic function.26,31
Heavy metal poisoning is a small but important public
health problem in Canada. Patients who present with concerns of exposure require appropriate investigation. Many will
not have true toxicity, but unless they are offered clear and
comprehensive information, they may seek treatment elsewhere and risk being given misleading advice and potentially
dangerous treatment. For patients who have elevated blood or
urine levels of heavy metals, the problem can usually be managed by simply reducing or removing the source of exposure.
Referral to the local public health unit can assist in identifying
the source of an atypical exposure and may lead to additional
case finding and removal of a source of exposure to the population. A decision to proceed to chelation therapy should be
made only in consultation with an expert.
This article has been peer reviewed.
From the Community Medicine Residency Program (Brodkin), the Departments of Health Care and Epidemiology (Copes, Yassi), Medicine (Copes,
Kennedy), Pathology (Mattman) and Pharmacology (Kennedy), and the Division of Occupational Medicine (Yassi), Department of Medicine, Faculty of
Medicine, University of British Columbia; the BC Centre for Disease Control
(Copes); the National Collaborating Centre Environmental Health (Copes);
the School of Occupational and Environmental Hygiene (Copes, Kling), University of British Columbia; the Department of Pathology and Laboratory Medicine (Mattman), Childrens & Womens Health Centre of British Columbia;
the BC Drug and Poison Information Centre (Kennedy); and the Canada Research Chair in Transdisciplinary and Global Health (Yassi), Vancouver, BC
Competing interests: None declared.
Contributors: Elizabeth Brodkin participated in the conception and design of
the article, drafted the manuscript and was a member of the team that interviewed and worked up the 3 patients referred to in the article. Ray Copes participated in the conception and design of the article. Andre Mattman was responsible for the analysis and interpretation of the laboratory data. James
Kennedy was responsible for the interpretation of the clinical data and
treated one of the patients referred to in the article. Rakel Kling conducted a
substantial portion of the literature review and was a member of the team
that interviewed and worked up the 3 patients referred to in the article. Annalee Yassi participated in the conception and design of the article and led the
team that interviewed and worked up the 3 patients referred to in the article.
All of the authors revised the manuscript for critical content and approved
the final version to be published.

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Correspondence to: Dr. Elizabeth Brodkin, Community

Medicine Residency Program, Department of Health Care and
Epidemiology, Faculty of Medicine, University of British
Columbia, 5804 Fairview Ave., Vancouver BC V6T 1Z3;
[email protected]

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