Aluminum Urine Test

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These results are from a real test done October 02, 2019. Patient was a 53 year old male.

Personal information removed to protect patients privacy.

Aluminum Urine Test
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LAB #: U1###02-2###-1
PATIENT:
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 Male
DOB:
 

AGE: 

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DOCTOR:
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24 Hour Urine Test

TOXIC METALS

RESULT

REFERENCE

WITHIN 

µµµµ

g/g creat

INTERVAL

REFERENCE

  

OUTSIDE REFERENCE

Aluminum

(Al)

35

<     25

Antimony

(Sb)

< dl

<    0.2

Arsenic

(As)

150

<     75

Barium

(Ba)

6.2

<      7

Beryllium

(Be)

< dl

<      1

Bismuth

(Bi)

< dl

<      2

Cadmium

(Cd)

< dl

<    0.8

Cesium

(Cs)

24

<      9

Gadolinium

(Gd)

< dl

<    0.5

Lead

(Pb)

0.9

<      2

Mercury

(Hg)

< dl

<      3

Nickel

(Ni)

4.1

<      8

Palladium

(Pd)

< dl

<    0.3

Platinum

(Pt)

< dl

<    0.1

Tellurium

(Te)

< dl

<    0.5

Thallium

(Tl)

0.6

<    0.5

Thorium

(Th)

< dl

<   0.03

Tin

(Sn)

0.5

<      4

Tungsten

(W)

< dl

<    0.4

Uranium

(U)

< dl

<   0.03

URINE CREATININE

RESULT

REFERENCE

mg/dL

INTERVAL

        -2SD      -1SD

MEAN

        +1SD   +2SD

Creatinine

16.5

    35-   240

SPECIMEN DATA

Comments:

    

Date Collected:

pH upon receipt:

  

Acceptable

Collection Period:

Random

Date Received:

10/02/2019

<dl:

less than detection limit

Volume:

 

Date Reported:

10/05/2019

Provoking Agent:

 

Provocation:

 

Method:

ICP-MS

Creatinine by Jaffe Method

Results are creatinine corrected to account for urine dilution variations. Reference intervals and corresponding graphs
are representative of a healthy population under non-provoked conditions.
 Chelation (provocation) agents can
increase urinary excretion of metals/elements. 

V13

©DOCTOR’S DATA, INC. y

yyy ADDRESS: 3755 Illinois Avenue, St. Charles, IL 60174-2420 yyyy LAB DIR: Erlo Roth, MD yyyy CLIA ID NO: 14D0646470

0001523


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                                                                     INTRODUCTION

This analysis of urinary elements was performed by ICP-Mass Spectroscopy following acid 
digestion of the specimen.  Urine element analysis is intended primarily for:  diagnostic 
assessment of toxic element status, monitoring detoxification therapy, and identifying or 
quantifying renal wasting conditions.  It is difficult and problematic to use urinary elements 
analysis to assess nutritional status or adequacy for essential elements.  Blood, cell, and 
other elemental assimilation and retention parameters are better indicators of nutritional 
status.

1)  24 Hour Collections
”Essential and other” elements are reported as mg/24 h; mg element/urine volume (L) is 
equivalent to ppm.  ”Potentially Toxic Elements” are reported as µg/24 h; µg element/urine 
volume (L) is equivalent to ppb.

2)  Timed Samples (< 24 hour collections)
All ”Potentially Toxic Elements” are reported as µg/g creatinine; all other elements are 
reported as µg/mg creatinine.  Normalization per creatinine reduces the potentially 
great margin of error which can be introduced by variation in the sample volume.  It 
should be noted, however, that creatinine excretion can vary significantly within an 
individual over the course of a day.

If one intends to utilize urinary elements analysis to assess nutritional status or renal 
wasting of essential elements, it is recommended that unprovoked urine samples be 
collected for a complete 24 hour period.  For provocation (challenge) tests for potentially 
toxic elements, shorter timed collections can be utilized, based upon the 
pharmacokinetics of the specific chelating agent.  When using EDTA, DMPS or DMSA, 
urine collections up to 12 hours are sufficient to recover greater than 90% of the 
mobilized metals.  Specifically, we recommend collection times of: 9 – 12 hours post 
intravenous EDTA, 6 hours post intravenous or oral DMPS and, 6 hours post oral 
bolus administration of DMSA.  What ever collection time is selected by the physician, it 
is important to maintain consistency for subsequent testing for a given patient.

If an essential element is sufficiently abnormal per urine measurement, a descriptive text 
is included with the report.  Because renal excretion is a minor route of excretion for 
some elements, (Cu, Fe, Mn Zn), urinary excretion may not influence or reflect body 
stores.  Also, renal excretion for many elements reflects homeostasis and the loss of 
quantities that may be at higher dietary levels than is needed temporarily.  For these 
reasons, descriptive texts are provided for specific elements when deviations are  
clinically significant.  For potentially toxic elements, a descriptive text is provided 
whenever levels are measured to be higher than expected.  If no descriptive texts follow 
this introduction, then all essential element levels are within acceptable range and all 
potentially toxic elements are within expected limits.

Reference intervals and corresponding graphs shown in this report are representative of a 
healthy population under non-provoked conditions. Descriptive texts appear in this report 
on the basis of measured results and correspond to non-challenge, non-provoked conditions.

Chelation (provocation) agents can increase urinary excretion of metals/elements.  Provoked 

 19992019  Doctor’s Data, Inc.


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reference intervals have not been established therefore non-provoked reference intervals shown 
are not recommended for comparison purposes with provoked test results. Provoked results can be 
compared with non-provoked results (not reference intervals) to assess body burden of metals 
and to distinguish between transient exposure and net retention of metals. Provoked results can 
also be compared to previous provoked results to monitor therapies implemented by the treating 
physician. Additionally, Ca-EDTA provoked results can be used to calculate the EDTA/Lead 
Excretion Ratio (LER) in patients with elevated blood levels.   

CAUTION:  Even the most sensitive instruments have some detection limit below which 
a measurement cannot be made reliably.  Any value below the method detection limit is 
simply reported as ”< dl.”  If an individual excretes an abnormally high volume of urine, 
urinary components are likely to be extremely dilute.  It is possible for an individual to 
excrete a relatively large amount of an element per day that is so diluted by the large 
urine volume that the value measured is near the dl.  This cannot automatically be 
assumed to be within the reference range.

                                                                   ALUMINUM HIGH  
 
     This individual’s urine aluminum (Al) is higher than expected; urine is the primary route of 
excretion for absorbed aluminum. 
 
     Common sources of bioavailable Al include: aluminum cookware, flatware and especially 
coffee pots; aluminum hydroxide anti-acid formulations; some types of cosmetics, especially 
deodorants; some colloidal minerals and some herbs or herbal products. Aluminum cookware 
is particularly of concern if acid foods are cooked such as tomato paste (contains salicylates). 
In cosmetics and deodorants, aluminum chloride may be present as an astringent. In water 
purification, alum (sodium aluminum sulfate) may be used to coagulate dispersed solids and
improve water clarity. Alumina or Al2O3 is very stable chemically and not bioavailable. Silica
limits the solubility of aluminum and aluminum silicate is not very bioavailable. Clays, bentonite 
for example, contain Al that has poor bio-availabilty. Aluminum food containers are manufactured 
with polymer or plastic coatings that prevent direct food-aluminum contact provided such coatings 
are not damaged.
 
     In the gastrointestinal tract, phosphates react with Al ions forming insoluble Al phosphates. If this 
phosphate-blocking were 100% efficient, then virtually no Al would be absorbed. Evidently, this 
phosphate-forming process is incomplete because body tissue levels (such as hair) usually contain 
measurable amounts of Al. In the body Al follows a path of increasing phosphate concentration: plasma, 
cytosol, cell nucleus. Once in the nucleus, it adversely affects protein formation. Long-lived cells such 
as neurons are susceptible to long-term accumulation. Al is potentially neurotoxic.  Al accumulates 
continually in the body with the highest concentration occurring at old age or death. 
 
     A hair element test may be used to further evaluate the extent of Al exposure. Comparison of urine 
Al levels before and after intravenous administration of EDTA provides an estimate of the net retention 
of Al over time. Urine Al is commonly increased to some extent after administration of EDTA.

 BIBLIOGRAPHY FOR ALUMINUM 
 1. Ganrot P.O. ”Metabolism and Possible Health Effects of Aluminum”, Environ. Health 
Perspectives, 5, pp. 363-441 1986. 

 19992019  Doctor’s Data, Inc.


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 2. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis Publ, 
Chelsea MI p 16-20 1986. 
 3. Lukiw W.J. ”Aluminum and the Nucleus of Nerve Cells”; Brenner S. ”Aluminum, Hot Water 
Tanks and Neurobiology”; Jackson J.A. ”Alumi- num from a Coffee Pot”; 3 letters all on pages 
781-82 of Lancet, pril 8, 1989. 
 4. Fulton B. and E.H. Jeffery, ”Absorption and Retention from    Drinking Water”, Fund. & Appl. 
Toxicology 14 pp 788-96 1980. 
 5. Tsalev D.L. et al. Atomic Absorption Spectrometry in Occupational and Environmental Health 
Practice vol 1, CRC Press, Boca Raton FL, pp 81-84, 1983. 

                                                                    ARSENIC HIGH 
 
     This inidividual’s urine arsenic (As) is higher than expected. Because urine is the major mode of 
excretion for arsenic, an elevated level reflects increased assimilation of As. Ingestion of organic 
species of As in seafood is not uncommon and may be associated with very elevated urine As. 
Arsenobetaine and arsinocholine, commonly found in shellfish are relatively non-toxic and 90% is 
excreted in the urine with a half-life of about 48 hours.
 
     Sources of As include:  contaminated foods (e.g. chicken), water or medications. Industrial 
sources are:  ore smelting/refining/processing plants, galvanizing, etching plating processes. Tailing 
from or river bottoms near gold mining areas (past or present) may contain arsenic.  Insecticides, 
rodenticides and fungicides (Na-, K- arsenites, arsenates, also oxides are commercially available).  
Commercial As-containing products include: sodium arsenite, calcium arsenate, lead arsenate and 
”Paris green” which is cupric acetoarsenite, a wood preservative (pressure treated wood). Undesirable
 levels of As have been found in many Ayruvedic herbs.
 
     Chronic exposure to or ingestion of inorganic As causes tissue levels to gradually increase as 
the element binds to sulfur, phosphorus and selenium.  An important detrimental effect is inactivation 
of lipoic acid,a vitamin cofactor needed for metabolism of pyruvate and alpha-ketoglutarate. 
 
     Symptoms consistent with mild or moderate As exposure include:  fatigue, malaise, eczema or 
allergic-like dermatitis, and garlic-like breath.  Increased salivation may occur.  Hair element analysis 
may provide further evidence of As exposure to inorganic As. Blood As levels are not dose related and 
may or may not reflect As exposure or net retention of As.  Levels of As may exceed the expected 
range after administration of DMPS or DMSA depending upon cumulative exposures.  This does not 
necessarily indicate As excess to the point of toxic effects or physiological impairment. 

 BIBLIOGRAPHY FOR ARSENIC
1. Centers for Disease Control and Prevention. Third National Report on Human Exposure
to Environmental Chemicals. Atlanta, GA; CDC: 2005.
http://www.cdc.gov/exposurereport/report.htm [Accessed 2/01/2009] 
2. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers, 
Chelsea, MI, pp 27-33, 1987. 
3. Tsalev D.L. and Z.K. Zaprianov Atomic Absorption Spectrometry in Occupational and 
Environmental Health Practice, vol. 1, CRC Press, Boca Raton, FL, pp. 87-93, 1983. 
4. Clarkson T.W. et al. eds. Biological Monitoring of Toxic Metals, Plenum Press, NY, NY, pp 
309-15, 1988. 
5. Harrison’s Principles of Internal Medicine, 13th ed., McGraw Hill, New York, NY, pp 2461-62, 
1994. 
6. Heyman A. et al. ”Peripheral Neuropathy Caused by Arsenical Intoxication” New Eng. J. Med., 

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254 no.9, pp 401-9 1956. 
7. Saper RB et al. ”lead, mercury and arsenic in U.S.- and Indian-manufactured ayruvedic medicines
sold via the internet.” JAMA(2008) 300(8):915-23.

                                                                     Cesium High

This individuals urine Cesium (Cs) level is higher than expected, reflecting exposure to Cs  but symptoms 
may not be evident. Very high levels of Cs in urine are often associated with the use of cesium chloride as 
a questionable anti-cancer treatment. Cesium is a naturally-occurring element found in rocks, soil and dust 
at low concentrations. It is present in the environment only in the stable form of Cs133; the radioactive isotopes 
134Cs and 137Cs are not measured or reported by Doctor’s Data. Natural deposits of Cs ores occur in Main, 
South Dakota and Manitoba (Bernic Lake), Canada. Cesium may bio-accumulate in aquatic food chains; higher 
levels of cesium have been found in Pacific deep-sea fish and local shellfish since the 2011 Fukoshima reactor 
accident.  Cesium may be used in high-density drilling fluids (oil and gas industry) and may contaminate local 
water and vegetation; Cs has been found in cow’s milk.  Cesium may occur naturally in mineral waters; one 
study analyzed the Cs concentration in 163 mineral and thermal waters and found the level ranged from 4.5 
to 148 µg per liter.

Cesium can be absorbed after oral ingestion, upon breathing contaminated air and through contact with the 
skin.  Cesium is readily absorbed across the brush border of the intestines in a manner similar to potassium 
and most is eventually excreted through the urine and feces.  The biological half-life of Cs in humans ranges 
from 15 days in infants to 100-150 days in adults.

The cesium-137 isotope is used in cancer treatments, for ventricular function and pulmonary imaging 
studies, industrial radiology, and for food and instrument sterilization; Cs137 agents may contain small 
amounts of Cs133. Non-radioactive cesium chloride may be advertised on the internet as ”high pH therapy.” 
Currently there is no support in the scientific literature for that purpose as advertised.  Radioactive Cs 
isotopes may contaminate soil at nuclear waste sites.  Cesium may be used in industry for the production of 
photoelectric cells, vacuum tubes, spectrographic instruments, scintillation counters, DNA biochemistry, in 
various optical or detecting devices. 

Target organs of potential toxic effects of Cs are the liver, intestine, heart, and kidneys. Physiological effects 
of excessive Cs include ventricular arrhythmias and displacement of potassium from muscle cells and 
erythrocytes. Cesium can have significant effects on both the central and peripheral nervous systems. 
Cesium may cause epileptic seizures because it can share the same receptor as the excitatory bioamine 
glycine.  Cesium can interfere with active ion transport by blocking potassium channels and also can 
interfere with lipid metabolism.  Excessive Cs may modify plasma membrane integrity, alter cytoplasmic 
components and cause cytogenetic damage.

It is unlikely that children or adults would be exposed to enough Cs133 to experience any health effects that 
could be related to the stable Cs itself.  Animals given very large doses of Cs compounds have shown 
changes in behavior, such as increased activity or decreased activity, but it is unlikely that a human would be 
exposed to enough stable Cs to cause similar effects.

The isotope Cs137 is used in radiation therapy for certain types of cancer.  Other medical uses of Cs are 
monitoring left ventricular function with Cs137 iodide probes and monitoring pulmonary endothelial 
permeability with Cs137 iodide crystal mini-detectors.  Again, it is emphasized that Cs measured at Doctor’s 
Datais Cs133, not Cs137.  Environmental contamination by Cs137 as a result of radioactive fallout could be 
a concern. Exposure to Cs may be assessed by hair elemental analysis.

 19992019  Doctor’s Data, Inc.


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Commonly used chelating agents are not effective binders of Cs.

Resources:
Agency for Toxic Substances & Disease Registry (2015) Toxicological Profile for Cesium.  
https://www.atsdr.cdc.gov/toxprofiles/TP.asp(c)id=578&tid=107  Accessed 21 February 2017

Bermejo-Barrera P, Beceiro-Gonzalez E, Bermejo-Barrera A, Martinez F (1989) Determination of cesium 
in mineral and thermal waters by electrothermal atomic absorption spectrophotometry.  
Microchemical Journal 1989 vol: 40 (1) pp: 103-108

Davis D, Murphy E, London R (1988) Uptake of cesium ions by human erythrocytes and perfused rat heart: 
a cesium-133 NMR study.  Biochemistry 1988 vol: 27 (10) pp: 3547-3551

Ikenoue T, Takata H, Kusakabe M, Kudo N, Hasegawa K, et. al. (2017) Temporal variation of cesium 
isotope concentrations and atom ratios in zooplankton in the Pacific off the east coast of Japan.  
Scientific Reports 2017 vol: 7 pp: 39874

Relman A (1956) The physiological behavior of rubidium and cesium in relation to that of potassium.  
The Yale Journal of Biology And Medicine 1956 vol: 29 (3) pp: 248-62

Samadani U, Marcotte P (2004) Zero Efficacy With Cesium Chloride Self-Treatment for Brain Cancer.  
Mayo Clinic Proceedings 2004 vol: 79 (12) pp: 1588

United States Geological Service (2006) Cesium.  
https://minerals.usgs.gov/minerals/pubs/commodity/cesium/cesiumcs06.pdf  Accessed 22 February 2017

Yamagata N, Iwashima K, Nagai T, Watari K, Iinuma T (1966) In Vivo Experiment on the Metabolism of 
Cesium in Human Blood with Reference to Rubidium and Potassium.  Journal of Radiation Research 
1966 vol: 7 (1) pp: 29-46

Yorita Christensen KL (2013) Metals in blood and urine, and thyroid function among adults in the United 
States 2007-2008.  International Journal of Hygiene and Environmental Health 2013 vol: 216 (6) pp: 624-632

                                                                    THALLIUM HIGH 
 
     This individual’s urine thallium (Tl) is higher than expected, but associated symptoms or toxic 
effects may or may not be presented. Presentation of symptoms can depend upon several factors 
including: chemical form of the Tl, mode of assimilation, severity and duration of exposure, and 
organ levels of metabolites and nutrients that effect the action of Tl in the body. 
 
     Thallium can be assimilated transdermally, by inhalation, or by oral ingestion. Both valence 
states can have harmful effects: Tl+1 may displace potassium from binding sites and influences 
enzyme activities; Tl+3 affects RNA and protein synthesis. Tl is rapidly cleared from blood and is 
readily taken up by tissues. It can be deposited in kidneys, pancreas, spleen, liver, lungs, muscles, 
neurons and the brain. Blood is not a reliable indicator of Tl exposure. 
 
     Symptoms that may be associated with excessive Tl exposure are often delayed. Early signs 
of chronic, low-level Tl exposure and retention may include: mental confusion, fatigue, and peripheral 
neurological signs: paresthesias, myalgias, tremor and ataxia. After 3 to 4 weeks, diffuse hair loss

 19992019  Doctor’s Data, Inc.


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with sparing of pubic and body hair and a lateral fraction of eye- brows usually occurs. Increased 
salivation occurs less commonly. Longer term or residual symptoms may include: alopecia, ataxia, 
tremor, memory loss, weight loss, proteinuria (albuminuria), and possibly psychoses. Ophthalmologic 
neuritis and strabismus may be presented. 
 
     Environmental and occupational sources of Tl include: contaminated drinking water, 
airborne plumes or waste streams from lead and zinc smelting, photoelectric, electrochemical and 
electronic components (photoelectric cells, semiconductors, infrared detectors, switches), 
pigments and paints, colored glass and synthetic gem manufacture, and industrial catalysts used 
in some polymer chemistry processes. Thallium is present in some ”weight loss” supplements 
(e.g. Active 8) at undisclosed levels (”trade secret”).
 
     Hair (pubic or scalp) element analysis may be used to test for suspected Tl exposure.
Although urine is the primary natural route for excretion of thallium, the biliary/fecal route also 
contributes.  Therefore, fecal metals analysis provides a confirmatory test for chronic ongoing 
exposure to Tl.  Clinical findings that might be associated with excessive Tl are:  albuminuria,
EEG with diffuse abnormalities, hypertension, and elevated urine creatinine phosphokinase (CPK).
No provocation agents are currently available to estimate Tl retention by means of urinalysis.

 BIBLIOGRAPHY FOR THALLIUM 
1. Centers for Disease C ontrol and Prevention. Third National Report on Human Exposure
to Environmental Chemicals. Atlanta, GA: CDC 2005. http;//www.cdc.gov/exposurereport.htm
[Accessed 2/01/2009]
2. Graef J.W. ”Thallium” in Harrison’s Principles of Internal Medicine, 13th ed., Isselbacher et al 
eds., McGraw Hill, pp 2465, 1994. 
3. Tsalev D.L. and Zaprianov Z.K. Atomic Absorption Spectrometry in Occupational and 
Environmental Health Practice CRC Press, Boca Raton FL, pp 196-199, 1983. 
4. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans Lewis Publishers, 
Chelsea, MI, pp 243-254, 1987. 

 19992019  Doctor’s Data, Inc.

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