Toxicology of Heavy Metals

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It’s Not Your Father’s Music:

Toxicology of Heavy Metals

Paul J. Jannetto, Ph.D., DABCC, FACB, MT(ASCP)


Mayo Clinic
Director, Toxicology & Drug Monitoring Laboratory
Director, Metals Laboratory

©2012 MFMER | slide-1


Disclosures
• Relevant Financial Relationships:
• None

• Off Label Usage:


• None

©2012 MFMER | slide-2


Objectives
• After this session, the participant will be able to:
1. Recognize and correlate the physical, clinical laboratory, and
anatomic findings related to the following heavy metal
exposures/toxicities:
1. Arsenic
2. Lead
3. Mercury
2. Identify the appropriate specimen which should be used to detect
exposure to each of the metals listed above
3. Correctly interpret the heavy metal test results and suggest
appropriate follow-up testing
4. Summarize the mechanism of toxicity for the metals listed above
5. List the appropriate treatment/management for heavy metal
toxicities

©2012 MFMER | slide-3


Why Should People Think About Metals?

http://www.myfoxdetroit.com/story/22140893/lipsticks-glosses-contain-toxic-metals-report
©2012 MFMER | slide-4
• February 2006, a boy aged 4 years with a previous medical history
of microcephaly and developmental delay was brought to a hospital
pediatric emergency department in Minneapolis, Minnesota, with a
chief complaint of vomiting
• Charm was 99.1% lead
• The next day, a BLL of 180 µg/dL was reported

©2012 MFMER | slide-5


Case Study #1

©2012 MFMER | slide-6


Case Study #1
• Background:
• 38 yo female presents to PCP over the course of months with
multiple symptoms:
• Nausea and vomiting
• Confusion/dizziness
• Headaches
• Ataxia
• Chest tightness/Shortness of breath
• Lethargy
• Nosebleeds
• Easy bruising and bleeding gums
• Lives w/ husband and 15 yo son
• Occupation:
• Homemaker/Student (on-line)

©2012 MFMER | slide-7


Case Study #1
• Background:
• Medical Hx:
• Migraines (current)
• Past hx physical abuse by high school boyfriend
• Anorexia/Bulimia eating disorder (in remission 10 yrs)
• Abnormal Pap 11 years ago
• Hospitalizations/Surgeries:
• Vaginal delivery x3
• LEEP procedure
• Inpatient treatment for eating disorder
• Medications
• Vicodin (hydrocodone w/ acetaminophen) for headache
• Relpax (eletriptan) for headache

©2012 MFMER | slide-8


Initial Lab Test Results
Hematology Chemistry Urinalysis
CBC Result Sodium 142 Source Clean void
Hemoglobin 14.2 Potassium 4.2 Appearance clear
Hematocrit 42.4 Calcium 9.9 Specific gravity 1.015
Erythrocytes 4.5 Protein, Total 8.6 H pH 6
MCV 94 Glucose 94 Glucose Negative
RDW 11.9 AST 25 Protein 1+
Leukocytes 4.6 ALT 13
Platelets 366 Creatinine 0.6
Auto Diff Albumin 4.7
Neutrophils 61 BUN 13
Lymphocytes 26 Chloride 99
Monocytes 11 Bicarbonate 30
Eosinophils 1
Basophils 1

©2012 MFMER | slide-9


Referral to Otolaryngology
• ENT concerns/complaints:
• Nosebleeds
• Fluid in ears leading to dizziness, imbalance, nausea, and
vomiting

• ENT exam:
• Negative
• Dry nasal mucous membranes
• List of complaints which don’t fit ENT diagnosis
• Nosebleeds, gum bleeding, easy bruising: possible bleeding
disorder; work up through Hematology
• Headache, nausea, imbalance, memory loss; should assess by
Neurology

©2012 MFMER | slide-10


Referral to Neurology
• Neurological complaints (numerous and don’t localize
into one portion of CNS):
• Confusion/forgetfulness
• Balance is off, walks into door frames/furniture – leads to
bruises
• Food tastes like “copper”

• Neuro exam:
• Normal
• Gait and station are unremarkable
• Orientation/memory: appropriate
• Recommend MRI of head and EEG (electroencephalogram)
• Results negative for intracranial hemorrhage, mass lesion or
acute infarction

©2012 MFMER | slide-11


Referral to Hematology
• Hematology complaints:
• Easy bruising
• Bleeding gums/nosebleeds

• Heme exam:
Hematology Chemistry Previous Current Coagulation Previous Current
CBC Previous Current Sodium 142 139 PT ND 8.6
Hemoglobin 14.2 10.5 L Potassium 4.2 3.5 INR ND 1.0
Hematocrit 42.4 30.0 L Calcium 9.9 8.5 APTT ND 23
Erythrocytes 4.5 3.23 L Protein, Total 8.6 H 6.4 TT ND 19
MCV 94 93 Glucose 94 80 Platelet Aggregation ND Normal
RDW 11.9 12.4 AST 25 30
Leukocytes 4.6 6.4 ALT 13 15
Platelets 366 274 Creatinine 0.6 0.6
Auto Diff Albumin 4.7 4.2
Neutrophils 61 59 BUN 13 11
Lymphocytes 26 32 Chloride 99 104
Monocytes 11 8 Bicarbonate 30 29
Eosinophils 1 0
Basophils 1 1

• Recommend ultrasound to check for thrombus or


evolving hematoma
• Results normal (no DVT)
©2012 MFMER | slide-12
Repeat CBC
Hematology
CBC Original Previous Current
Hemoglobin 14.2 10.5 L 12.1
Hematocrit 42.4 30.0 L 35.3
Erythrocytes 4.5 3.23 L 3.77 L
MCV 94 93 94
RDW 11.9 12.4 13.9
Leukocytes 4.6 6.4 6.6
Platelets 366 274 410
Auto Diff
Neutrophils 61 59 78
Lymphocytes 26 32 16
Monocytes 11 8 6
Eosinophils 1 0 0
Basophils 1 1 0

• Patient referred to Mayo for further evaluation

©2012 MFMER | slide-13


Heavy Metal Testing Performed
• 24hr urine results:
Toxicology Result (mcg/spec) Reference Range
Arsenic-24 hr Urine <15 0-35
Lead- 24 hr Urine <1 0-4
Mercury-24 hr Urine 1,817 0-9
Cadmium-24 hr Urine <0.2 0-1.3

• Blood test result:


• Mercury: 111 µg/L (<10 µg/L = normal)

• Referral for Toxicology consult

©2012 MFMER | slide-14


Mercury
• Forms:
• Elemental form (Hg0) shiny, silver-white liquid, crosses blood-brain
barrier/placenta
• Inorganic form (combines with Cl, S, O) is mildly toxic (Hg2+)
• Organic (combine with C)/methylated form (HgMe2) is extremely toxic;
methylation occurs by microorganisms

• Sources:
• Environmental: natural outgassing from granite rock/volcanic activity,
burning coal and waste, mining ore deposits, food (shellfish/fish)
• Home: electrical switches, thermostats, thermometers
• Occupational: paper & pulp industry, latex paint manufacturing
(fungicide), plastic industry, jewelry making
• Miscellaneous: dental amalgam

• Routes of Exposure:
• Inhalation (75-85% Hg0 absorbed)
• Ingestion (Hg0 0.01%, inorganic 20%, HgMe2 100% absorbed)
• Dermal

©2012 MFMER | slide-15


Common Sources of Exposure to Mercury
• Eating fish or shellfish contaminated with methylmercury
• Breathing vapors in air from spills, incinerators, and industries that
burn mercury-containing fuels
• Release of mercury from dental work and medical treatments
• Breathing contaminated workplace air or skin contact during use in
the workplace (dental, health services, chemical, and other
industries that use mercury)

• Practicing rituals that include mercury.


• Latino and Afro-Caribbean traditions use mercury to: attract luck, love,
or money; protect against evil; or speed the action of spells.
• Done through a variety of uses, including wearing in amulets,
sprinkling on the floor, or adding to a candle, oil lamp or cosmetic
products.

©2012 MFMER | slide-16


What is the Source of Mercury for Case#1
• Environmental:
• Dietary: No fish/shellfish intake
• Dental: No fillings
• No mercury rituals

• Occupational:
• At home student/homemaker

• Home:
• Husband reports description of mercury “balling” up in furnace HEPA
filter
• Structural house fire (March)
• Extensive damage/renovations
• Out of house until September
• Furnace destroyed/replaced
• Insurance company limiting what can be replaced vs. left “as is”

©2012 MFMER | slide-17


Symptoms of Acute and Chronic
Mercury Poisoning
Target System Acute Chronic
Neurologic Fatigue, Insomnia, Tremors, Ataxia (lower
Hearing loss, extremities), Delirium
Headache, Confusion,
Lethargy, Seizures,
Ataxia
GI tract Metallic taste, Nausea, Loose teeth, blue gums
Vomiting, Diarrhea

Pulmonary Respiratory distress,


Pneumonitis, Edema

Hematologic Thrombocytopenia,
Anemia

©2012 MFMER | slide-18


Mercury continued
• Mechanism of Action:
• Inorganic mercury (Hg+2) readily binds to sulfhydryl groups on a
protein (which pay an integral part in the structure/function of
most proteins), distorting tertiary configuration and causing loss
of activity
• In addition, tertiary changes may cause some proteins to
become immunogenic, eliciting T lymphocyte proliferation and
Immunoglobulins to bind to the new antigen (collagen tissues
are particularly sensitive)
• Hg(CH3)2 species are lipophilic and avidly bind to lipid-rich
tissues such as neurons (myelin is susceptible to disruption by
this MOA)

©2012 MFMER | slide-19


Treatment/Management of Mercury Toxicity
In the following order, as necessary:
1. Identify and remove the patient from the source of exposure
2. Supportive measures
3. Chelation therapy (reduce body burden):
• 2,3-Dimercaptopropane-1-sulfonate (DMPS)
• D-penicillamine
• Dimercaprol or BAL (contraindicated for elemental and
organic mercury compounds since increases brain
levels)
4. Hemodialysis w/ infusion of a chelator (cysteine, N-
acetylcysteine) in severe cases

©2012 MFMER | slide-20


Case Study #1 Continued
• Advised not to proceed with any chelation therapy, first
identify source of mercury and remove it
• WI Dept Public Health/EPA investigation:
• Sources of exposure:
• Gas Magic Chef range
• Furnace (>40 yr old, destroyed in fire)

• Family given permission to move back home after


removal
• Follow-up blood testing:
• Elimination half-life (20-65 days)
Toxicology Original (May) June July Aug
Mercury-Blood 111 µg/L 44 µg/L 12 µg/L 6 µg/L

©2012 MFMER | slide-21


Case Study #2

©2012 MFMER | slide-22


Case Study #2
• Background:
• Family moved into a 1900’s home 6 months ago
• Father (29 yr)
• Son (4 yr)
• Son (14 months)
• Remodeling house since day 1
• Brought his kids to the family physician for a wellness check

©2012 MFMER | slide-23


Case Study #2 (4 year old)
• Physical Exam:
• General: pleasant, interactive 4 yr old, no acute distress
• Skin: Warm, well perfused
• ENT: Moist mucous membranes, no oral lesions or pharyngeal
erythema
• Heart: Regular rate/rhythm, no murmurs
• Lungs: Clear, no wheezes
• Abdomen: Normal bowel sounds, soft, non-distended, non-tender
to palpitation

• History:
• Father notes child has been hyperactive the past month
• Patient complains of abdominal cramping/pain; difficulty hearing
• No change in appetite

©2012 MFMER | slide-24


Initial Lab Test Results (4 year old)
Hematology Chemistry Urinalysis
CBC Result Sodium 140 Source Clean void
Hemoglobin 12.1 Potassium 4 Appearance amber
Hematocrit 36 Calcium 10.1 Specific gravity 1.02
Erythrocytes 4.3 Protein, Total 8.2 pH 5.5
MCV 80 Glucose 88 Glucose Negative
RDW 10 AST 25 Protein Negative
Leukocytes 4.6 ALT 24
Platelets 320 Creatinine 1
Auto Diff Iron 59
Neutrophils 60 BUN 13
Lymphocytes 30 Chloride 100
Monocytes 10 Bicarbonate 30
Eosinophils 0
Basophils 0

• Lead (Blood): 39.5 mcg/dL (Ref Range: <5 mcg/dL)

©2012 MFMER | slide-25


Case Study #2 (14 month old)
• Physical Exam:
• General: awake, alert and in no apparent distress
• Skin: Warm, pink
• ENT: Moist mucous membranes
• Heart: Regular rate/rhythm, no murmur
• Lungs: Clear
• Abdomen: Normal bowel sounds, soft, non-distended, non-tender
to palpitation

©2012 MFMER | slide-26


Initial Lab Test Results (14 month old)
Hematology Chemistry Urinalysis
CBC Result Sodium 139 Source Clean void
Hemoglobin 10.8 L Potassium 4.2 Appearance amber
Hematocrit 31 L Calcium 9.8 Specific gravity 1.02
Erythrocytes 3.6 L Protein, Total 7.8 pH 5.5
MCV 72 L Glucose 94 Glucose Negative
RDW 10 AST 24 Protein Negative
Leukocytes 5.1 ALT 24
Platelets 360 Creatinine 0.9
Auto Diff Iron 32 L
Neutrophils 58 BUN 13
Lymphocytes 32 Chloride 101
Monocytes 10 Bicarbonate 28
Eosinophils 0
Basophils 0
Basophilic stippling: present

• Lead (Blood): 47.8 mcg/dL (Ref Range: <5 mcg/dL)

©2012 MFMER | slide-27


Lead
• Properties:
• No known biological function
• Ubiquitous (air, food, water, and soil)

• Sources:
• Environmental: paint (up to 1972), gasoline (1978), water, soil near
industrial sites/freeways
• Occupational: battery manufacturers/foundries, plumbers, auto repair,
mining
• Hobbies: glazes/pottery making, target shooting/slugs
• Miscellaneous: cigarettes, folk remedies/cosmetics, moonshine
whiskey

• Routes of exposure:
• Inhalation:
• Ingestion:
- Children (~50%) / Adults (~10%)
- Dermal: (<inhalation/ingestion)

©2012 MFMER | slide-28


Importance of Diet/Nutritional Status
Healthy Foods to Fight Lead

Foods High in Foods High in Foods High in


Calcium Iron Vitamin C
•Milk •Lean red meat •Oranges/Orange juice
•Yogurt •Low-fat pork •Grapefruit/Grapefruit
•Low-fat cheese •Dried beans and peas juice
•Tofu •Raisins •Dark green, leafy
•Low-fat cottage cheese •Iron fortified cereal vegetables
•Evaporated milk •Iron fortified infant •Potatoes cooked in the
•Foods made with milk; formula skin
including soups, •Breast milk •Broccoli
custards, and puddings •Cabbage
•Powdered milk •Strawberries

http://www.health.state.mn.us/divs/eh/lead/faqs.html#Diet ©2012 MFMER | slide-29


Distribution of Lead in the Body

• 95% long bones.


• 4% brain, liver, kidneys.
• 1% blood.

©2012 MFMER | slide-30


Lead Toxicity: Signs & Symptoms
• Symptomatic lead poisoning is uncommon:
• <45 µg/dL in children and <60 µg/dL in adults are usually
asymptomatic

• Signs and symptoms:


• - Severe abdominal pain
• - Fatigue
• - Mental confusion/poor concentration
• - Headache
• - Vomiting
• - Ataxia
• - Weight loss
• - Constipation
• - Seizures
• - Coma/Death

©2012 MFMER | slide-31


Health Effects of Lead

• Concentration related
• IQ/ delinquency related
to total dosage in
childhood

©2012 MFMER | slide-32


Lead Effects Heme Synthesis
ferrochelatase

δ-aminolevulinic acid
dehydrase

©2012 MFMER | slide-33


Laboratory Assessment
• Blood lead level
- Definitive test
- Measured by: ICP-MS or atomic absorption spectrometry
- Venous (gold standard) vs. capillary blood
- EDTA whole blood = specimen of choice
- t1/2 = ~ 30-50 days
- Updated reference ranges: Blood lead levels in the range of 5-9
mcg/dL have been associated with adverse health effects in children
aged 6 years and younger
• Erythrocyte protoporphyrin (EP) or zinc protoporphyrin
(ZPP)
- t1/2 = ~68 days
- Concentration >60 µg/dL is a significant indicator of exposure
• Other technologies
- Anodic stripping voltammetry (ASV)
- K-X-ray fluorescence (measure lead content of bone)
• Hematological (CBC) findings
- Normochromic/normocytic or hypochromic/microcytic
- Basophilic stippling

©2012 MFMER | slide-34


Case Study #2 Continued
• Family sent to ED for follow-up testing:
• 4 yo lead (blood): 33 mcg/dL (previous 39.5)
• 14 month lead (blood): 55 mcg/dL (previous 47.8)
• Father lead (blood): 51 mcg/dL
• Toxicology consult:
• Local health agency contacted to evaluate home
• Paint contained lead; abatement done
• Family stayed outside home until removal and renovations were
complete
• Father’s other labs were normal with the exception of a low iron
(41 mcg/dL)

©2012 MFMER | slide-35


State Regulations for Laboratory Reporting
of BLL (MN 144.9502)
• Reports of blood lead analysis required:
• (a) Every hospital, medical clinic, medical laboratory, other
facility, or individual performing blood lead analysis shall report
the results after the analysis of each specimen analyzed, for
both capillary and venous specimens, and epidemiologic
information required in this section to the commissioner of
health, within the time frames set forth in clauses (1) and (2):
• (1) within two working days by telephone, fax, or electronic
transmission, with written or electronic confirmation within one
month, for a venous blood lead level equal to or greater than 15
micrograms of lead per deciliter of whole blood; or
• (2) within one month in writing or by electronic transmission, for
any capillary result or for a venous blood lead level less than 15
micrograms of lead per deciliter of whole blood.

©2012 MFMER | slide-36


Treatment and Management
Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention

http://www.cdc.gov/nceh/lead/casemanagement/casemanage_chap3.htm#Table 3.1.
©2012 MFMER | slide-37
Case Study #2 Continued
• Treatment:
• Father (51 mcg/dL): No chelation therapy; start multi-vitamin
(Fe)
• Asymptomatic
• Renovations done/exposure source removed
• 4 year old (33 mcg/dL): No chelation therapy
• Renovations done/exposure source removed
• ENT evaluation showed normal hearing
• Monitor blood level (declining) vs. side effects of treatment
• 14 month old (55 mcg/dL): Chelation therapy
• Oral succimer (200 mg @ 0800, 200 mg @ 1400, and 100 mg
QHS)
• Iron (75 mg PO BID)
• Monitor blood lead levels, CBC, Iron, Cr, LFTs

©2012 MFMER | slide-38


Case Study #3

©2012 MFMER | slide-39


Clinical Case Study #1
• 50 yo man admitted to hospital
• Signs/Symptoms:
• Dry, itchy skin, nausea, vomiting, diarrhea, general tiredness, weight loss (25
lbs-past 2 months), garlic-like breath

• History:
• Multiple hospital admissions in the past year:
• Nausea/vomiting but normal abdominal exam
• Neurologic exam: decreased muscle strength in lower extremities
• Cyclic neutropenia, hyperpigmented skin

• Lab results: Previous Visit Current Visit


• Leukocyte count: 1.4 x 103  N.D.
• BUN: 35 mg/dL  55 mg/dL 
• AST: 30 U/L 1520 U/L 
• ALP: N.D. 550 U/L 
• LD: N.D. 840 U/L 
• Creatinine: N.D. 2.8 mg/dL 
• Additional findings on current visit:
• ↑PT, ↑aPTT, Thrombocytopenia
©2012 MFMER | slide-40
Clinical Case Study #1 Continued

©2012 MFMER | slide-41


Arsenic
• Forms: Inorganic (Toxic) Organic (Nontoxic)
Trivalent (As3+) Mono- and di-methyl arsine
Pentavalent (As5+) Arsenobetaine
Arsenocholine

• Sources:
• Pesticides (largest source)
• Occupational: Industrial (copper/zinc/lead) smelting, Electronics industry, Glass
manufacturing
• Misc: Wood preservative, soil, water (most <5 µg/L but some > 50 µg/L), and
food (meats/seafood/veg; 0.04 mg/day).

• Routes of Exposure:
• Inhalation:
• Ingestion: (almost complete absorption)
• Dermal:

• Elimination: Primarily kidney (urine).

©2012 MFMER | slide-42


Arsenic
• Properties:
• Half-life: ~10 hr
• Crosses the placenta
• Garlic-like odor
• Concentrates in hair and nails (Mees Lines).

• 3 Mechanisms of Toxicity:
• Arsenic binds to any hydrated sulfhydryl group on a protein, distorting 3D
configuration and causing loss of activity
• Arsenic covalently binds to dihyrolipoic acid, a necessary cofactor for pyruvate
dehydrogenase, inhibiting the conversion of pyruvate to acetyl coenzyme A
(first step in gluconeogenesis). Results in loss of energy supply to anaerobic
cells. (Predominant MOA on neural cells leading to bilateral peripheral
neuropathy)
• Arsenic competes with phosphate for binding ATP during its synthesis by
mitochondria resulting in the formation of lower energy ADP monoarsine which
leads to a loss of energy supply to aerobic cells. (Cardiac cells sensitive to
energy loss→poor cardiac output (fatigue).

©2012 MFMER | slide-43


Arsenic Toxicity

• Nervous System: Destruction of myelin


• Renal: Acute tubular necrosis
• Liver: jaundice-indicative of chronic exposure can progress to
cirrhosis.
• Cardiovascular effects: Decreased contractility (arrhythmias)
• Hematopoietic effects: Anemia and leukopenia, occur a few days
following exposure and are reversible.
• Cellular effects: Impairs mitochondrial enzymes and tissue
respiration.
• Carcinogen: Lung cancer, and skin cancer-hyperpigmentation and
hyperkeratosis.
• Death (70–180 mg)

©2012 MFMER | slide-44


Arsenic Toxicity: Signs & Symptoms

• Skin/Nails: Hyperpigmentation, Mee’s lines


• Neurologic: Bilateral peripheral neuropathy (most common)
• Renal: Acute nephropathy with proteinuria of unexplained etiology
• Cardiovascular: Acute cardiovascular collapse of unexplained
etiology, arrhythmia
• GI: Nausea, vomiting, diarrhea, weight loss
• Hematologic: Anemia, leukopenia, thrombocytopenia

©2012 MFMER | slide-45


Laboratory Assessment
Specimen Reference Range Fatal
Whole Blood 0-12 ng/mL 100-600 ng/mL
Urine 0-35 µg/L 100-400 µg/L
Hair 0-0.9 µg/g
Nails 0-0.9 µg/g

Note: Urine is the best screening test to detect arsenic exposure. However, the
total arsenic determination is only partially useful and fractionation testing must
be done to distinguish between the toxic inorganic and nontoxic organic forms

Treatment
• BAL used to treat chronic arsenic poisoning, acute dermatitis
and the pulmonary symptoms of excess arsenic exposure.

©2012 MFMER | slide-46


©2012 MFMER | slide-47
Case #1 Continued
• Laboratory results:
• Arsenic:
• Urine: 980 µg/L (0-35 µg/L)
• Arsenic Fractionation:
• Urine:
• Inorganic: 905 µg/L
• Organic: 75 µg/L

• Patient expired before chelation therapy was


begun

©2012 MFMER | slide-48


Heavy Metal Summary
• Symptoms of heavy metal poisoning may be absent or
vague:
– Nausea
– Vomiting
– Sudden, unexplained weight loss
– Peripheral neuropathy
• Elevated total heavy metal results should be interpreted
with caution
– Are symptoms present?
– Speciation can be done to determine the presence of toxic or nontoxic
species
– Rule-out contamination (venous vs capillary)
– Other sources (seafood consumption) of heavy metal
• Treatment
– Identify and remove the source
– Chelation therapy if necessary

©2012 MFMER | slide-49


Questions & Discussion

©2012 MFMER | slide-50


Self-Assessment Questions
• A 3 year-old child is brought to the Emergency department because
of a week-long history of abdominal discomfort, irritability, and
weakness. A complete blood count and blood smear demonstrate
microcytic, hypochromic anemia with basophilic stippling of the red
blood cells. Further history reveals that the family lives in a very old
apartment complex with pealing paint. The most likely cause of the
hematologic findings is:

A. Binding of carbon monoxide to hemoglobin


B. Inhibition of cytochrome oxidase
C. Inhibition of hemoglobin production caused by lead
D. Zinc deficiency
E. Iron intoxication

©2012 MFMER | slide-51


Self-Assessment Questions
• A 48 year-old woman with a diet rich in fish/shellfish was admitted
to the hospital. Her clinical history in the previous 5 days included
progressive deterioration in balance, gait, and speech. She had lost
15 pounds during the prior 2 months and had periods of nausea,
diarrhea, and abdominal discomfort. She complained of a metallic
taste and had a blue line along her gums.

• These findings/history are most consistent with exposure to what


heavy metal?
A. Chromium
B. Lead
C. Mercury
D. Copper
E. Cadmium

©2012 MFMER | slide-52


Self-Assessment Questions
• To screen for lead toxicity in a child, what is the preferred sample
type?

A. Hair
B. Capillary EDTA whole blood
C. Venous EDTA whole blood
D. Sodium citrate plasma
E. Random urine

©2012 MFMER | slide-53

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