Sign in →

Test Code HMSU (HMU24) Heavy Metals Screen, with Reflex, 24 Hour, Urine

Specimen Required

1. High concentrations of gadolinium and iodine are known to interfere with most metals tests. If either gadolinium- or iodine-containing contrast media has been administered, a specimen should not be collected for 96 hours.

2. Patient should not eat seafood for a 48-hour period prior to start of, or during, collection.

Supplies: Urine Tubes, 10 mL (T068)

Collection Container/Tube: Clean, plastic aliquot container with no metal cap or glued insert

Submission Container/Tube: Plastic, 10-mL urine tube

Specimen Volume: 10 mL

Collection Instructions:

1. Collect urine for 24 hours.

2. Refrigerate specimen within 4 hours of completion of 24-hour collection.

3. See Trace Metals Analysis Specimen Collection and Transport in Special Instructions for complete instructions.

Additional Information: See Urine Preservatives-Collection and Transportation for 24-Hour Urine Specimens in Special Instructions for multiple collections.

Useful For

Detecting arsenic, cadmium, mercury, and lead exposure and toxicity in 24-hour urine specimen

Profile Information

Test ID Reporting Name Available Separately Always Performed
ASHU Arsenic, 24 Hr, U Yes, (order ASU24) Yes
CDHMU Cadmium, 24 Hr, U Yes, (order CDU) Yes
HGHU Mercury, 24 Hr, U Yes, (order HGU) Yes
PBHU Lead, 24 Hr, U Yes, (order PBU) Yes

Reflex Tests

Test ID Reporting Name Available Separately Always Performed
ASFR Arsenic Fractionation, 24 Hr, U Yes No

Testing Algorithm

If arsenic concentration is greater than or equal to 35 mcg/L, then fractionation will be performed at an additional charge.

Method Name

Inductively Coupled Plasma-Mass Spectrometry (ICP-MS)

Reporting Name

Heavy Metal Scrn w/Reflex, 24 Hr, U

Specimen Type


Specimen Minimum Volume

3 mL

Specimen Stability Information

Specimen Type Temperature Time
Urine Refrigerated (preferred) 7 days
  Frozen  7 days

Reject Due To









Clinical Information


Arsenic is perhaps the best known of the metal toxins, having gained notoriety from its extensive use by Renaissance nobility as an antisyphilitic agent and, paradoxically, as an antidote against acute arsenic poisoning. Even today, arsenic is still 1 of the more common toxicants found in insecticides, and leaches from bedrock to contaminate groundwater.


The toxicity of arsenic is due to 3 different mechanisms, 2 of them related to energy transfer. Arsenic covalently and avidly binds to dihydrolipoic acid, a necessary cofactor for pyruvate dehydrogenase. Absence of the cofactor inhibits the conversion of pyruvate to acetyl coenzyme A, the first step in gluconeogenesis. This results in loss of energy supply to anaerobic cells, the predominant mechanism of action of arsenic on neural cells that rely on anaerobic respiration for energy. Neuron cell destruction that occurs after long-term energy loss results in bilateral peripheral neuropathy.


Arsenic also competes with phosphate for binding to adenosine triphosphate during its synthesis by mitochondria via oxidative phosphorylation, causing formation of the lower energy adenosine diphosphate monoarsine. This results in loss of energy supply to aerobic cells. Cardiac cells are particularly sensitive to this form of energy loss; fatigue due to poor cardiac output is a common symptom of arsenic exposure.


Arsenic furthermore binds avidly with any hydrated sulfhydryl group on protein, distorting the 3-dimensional configuration of that protein, causing it to lose activity. Interaction of arsenic with epithelial cell protein at the sites of highest physiologic concentration, the small intestine and proximal tubule of the kidney, results in cellular degeneration. Epithelial cell erosion in the gastrointestinal tract and proximal tubule are characteristic of arsenic toxicity. Arsenic is also a known carcinogen, but the mechanism of this effect is not definitively known.


A wide range of signs and symptoms may be seen in acute arsenic poisoning including headache, nausea, vomiting, diarrhea, abdominal pain, hypotension, fever, hemolysis, seizures, and mental status changes. Symptoms of chronic poisoning, also called arseniasis, are mostly insidious and nonspecific. The gastrointestinal tract, skin, and central nervous system are usually involved. Nausea, epigastric pain, colic abdominal pain, diarrhea, and paresthesias of the hands and feet can occur.


Arsenic exists in a number of different forms; organic forms are nontoxic, inorganic forms are toxic. See ASFR / Arsenic Fractionation, 24 Hour, Urine for details about arsenic forms.


Because arsenic is excreted predominantly by glomerular filtration, analysis for arsenic in urine is the best screening test to detect arsenic exposure.



The toxicity of cadmium resembles the other heavy metals (arsenic, mercury, and lead) in that it attacks the kidney; renal dysfunction with proteinuria with slow onset (over a period of years) is the typical presentation. Measurable changes in proximal tubule function, such as decreased clearance of para-aminohippuric acid also occur over a period of years, and precede overt renal failure.


Breathing the fumes of cadmium vapors leads to nasal epithelial deterioration and pulmonary congestion resembling chronic emphysema.


The most common source of chronic exposure comes from spray painting of organic-based paints without use of a protective breathing apparatus; auto repair mechanics represent a susceptible group for cadmium toxicity. Another common source of cadmium exposure is tobacco smoke, which has been implicated as the primary source of the metal leading to reproductive toxicity in both males and females.


The concentration of cadmium in the kidneys and in the urine is elevated in some patients exposed to cadmium.



The correlation between the levels of mercury (Hg) excretion in the urine and the clinical symptoms is considered poor. However, urinary Hg is the most reliable way to assess exposure to inorganic Hg.


For additional information, see HG / Mercury, Blood



Increased urine lead excretion rate indicates significant lead exposure. Measurement of urine lead excretion rate before AND after chelation therapy has been used as an indicator of lead exposure. An increase in lead excretion rate in the post chelation specimen of up to 6 times the rate in the prechelation specimen is normal. Blood lead is the best clinical correlate of toxicity.


For additional information, see PBDB / Lead with Demographics, Blood.

Reference Values


0-17 years: not established

≥18 years: <18 mcg/24 hour



0-17 years: not established

≥18 years: <0.6 mcg/24 hour



0-17 years: not established

≥18 years: <2 mcg/24 hour

Toxic concentration: >50 mcg/24 hour


The concentration at which toxicity is expressed is widely variable between patients. 50 mcg/24 hour is the lowest concentration at which toxicity is usually apparent.



0-17 years: not established

≥18 years: <1 mcg/24 hour



Normally, humans consume 5 to 25 mcg of arsenic each day as part of their normal diet; therefore, normal urine arsenic output is less than 25 mcg/specimen. After a seafood meal (seafood contains a nontoxic, organic form of arsenic), the urine output of arsenic may increase to 300 mcg/specimen for 1 day, after which it will decline to less than 25 mcg/specimen.


Exposure to inorganic arsenic, the toxic form of arsenic, causes prolonged excretion of arsenic in the urine for many days.


Urine excretion rates greater than 1,000 mcg/specimen indicate significant exposure. The highest level observed at Mayo Clinic was 450,000 mcg/specimen in a patient with severe symptoms of gastrointestinal distress, shallow breathing with classic "garlic breath," intermittent seizure activity, cardiac arrhythmias, and later onset of peripheral neuropathy.



In chronic cadmium exposure, the kidneys are the primary target organ. Urine concentrations of cadmium can be useful to assess long-term exposure and determine cadmium body burden. Collection of urine over 24 hours minimizes fluctuations of observed cadmium concentrations in random urine samples.



Daily urine excretion of mercury above 50 mcg/day indicates significant exposure (per World Health Organization standard).



Urinary excretion of less than 125 mcg of lead per 24 hours is not associated with any significant lead exposure.


Urinary excretion of more than 125 mcg of lead per 24 hours is usually associated with pallor, anemia, and other evidence of lead toxicity.


Consumption of seafood before collection of a urine specimen for arsenic testing is likely to result in a report of an elevated concentration of arsenic found in the urine, which can be clinically misleading.


Collection of urine specimens through a catheter frequently results in elevated values because rubber contains trace amounts of cadmium that are extracted as urine passes through the catheter.


To avoid contamination by dust, specimen should be collected away from the site of suspected exposure.

Method Description

Arsenic (As), cadmium (Cd), mercury (Hg), and lead (Pb) in urine are analyzed by inductively coupled plasma-mass spectrometry (ICP-MS) in kinetic energy discrimination (KED) mode using gallium (Ga), rhodium (Rh), and iridium (Ir) as internal standards and a 5% nitric acid salt matrix calibration.(Unpublished Mayo method)

Day(s) and Time(s) Performed

Monday through Saturday; 7 p.m.

Analytic Time

1 day

Specimen Retention Time

14 days

Performing Laboratory

Mayo Clinic Laboratories in Rochester

Test Classification

See Individual Test IDs

CPT Code Information





LOINC Code Information

Test ID Test Order Name Order LOINC Value
HMU24 Heavy Metal Scrn w/Reflex, 24 Hr, U In Process


Result ID Test Result Name Result LOINC Value
8678 Cadmium, 24 Hr, U 5612-7
48539 Arsenic, 24 Hr, U 5587-1
92408 Mercury, 24 Hr, U 6693-6
92409 Lead, 24 Hr, U 5677-0
TIME4 Collection Duration 13362-9
92215 Arsenic Concentration w/Reflex 21074-0
VL16 Total Volume 3167-4

NY State Approved


Urine Preservative Collection Options

Note: The addition of preservative or application of temperature controls must occur within 4 hours of completion of the collection.







50% Acetic Acid


Boric Acid


Diazolidinyl Urea


6M Hydrochloric Acid


6M Nitric Acid


Sodium Carbonate






Clinical Reference

1. Fillol CC, Dor F, Labat L, et al: Urinary arsenic concentrations and speciation in residents living in an area with naturally contaminated soils. Sci Total Environ 2010 Feb 1;408(5):1190-1194

2. Caldwell K, Jones R, Verdon C, et al: Levels of urinary total and speciated arsenic in the US population: National Health and Nutrition Examination Survey 2003-2004. J Expo Sci Environ Epidemiol 2009 Jan;19(1):59-68

3. Lee R, Middleton D, Caldwell K, et al. A review of events that expose children to elemental mercury in the United States. Environ Health Perspect 2009 Jun;117(6):871-878

4. Kosnett MJ, Wedeen RP, Rotherberg SJ, et al: Recommendations for medical management of adult lead exposure. Environ Health Perspect 2007;115:463-471

5. De Burbane C, Buchet JP, Leroyer A, et al: Renal and neurologic effects of cadmium, lead, mercury, and arsenic in children: evidence of early effects and multiple interactions at environmental exposure levels. Environ Health Perspect 2006;114:584-590