Antimony Urine Test

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These results are from a real test done August 7, 2019. Patient was a 4 year old male.

Antimony Urine Test
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LAB #: #####-###-##
PATIENT:
 ##### #####
ID:
 ########-#####-##-8
SEX:
 Male
DOB:
 ##/##/2014

AGE: 4

CLIENT #: #####
DOCTOR:
 ##### #######

### #### ######
###### ####### ####### ###

Antimony Urine Test

TOXIC METALS

RESULT

REFERENCE

WITHIN 

#

g/g creat

INTERVAL

REFERENCE

  

OUTSIDE REFERENCE

Aluminum

(Al)

50

<     60

Antimony

(Sb)

1.5

<    0.3

Arsenic

(As)

13

<    120

Barium

(Ba)

24

<      7

Beryllium

(Be)

< dl

<      1

Bismuth

(Bi)

< dl

<      2

Cadmium

(Cd)

< dl

<    0.4

Cesium

(Cs)

33

<     12

Gadolinium

(Gd)

< dl

<    0.4

Lead

(Pb)

3.4

<      3

Mercury

(Hg)

0.6

<    4.5

Nickel

(Ni)

5.5

<     14

Palladium

(Pd)

< dl

<    0.3

Platinum

(Pt)

< dl

<    0.1

Tellurium

(Te)

< dl

<    0.5

Thallium

(Tl)

0.9

<    0.8

Thorium

(Th)

< dl

<   0.05

Tin

(Sn)

4.2

<      9

Tungsten

(W)

0.2

<    0.6

Uranium

(U)

< dl

<   0.04

URINE CREATININE

RESULT

REFERENCE

mg/dL

INTERVAL

        -2SD      -1SD

MEAN

        +1SD   +2SD

Creatinine

40.3

    25-   180

SPECIMEN DATA

Comments:

    

Date Collected:

08/04/2019

pH upon receipt:

  

> 8.0

Collection Period:

timed: 12 hours

Date Received:

08/07/2019

<dl:

less than detection limit

Volume:

 

Date Reported:

08/12/2019

Provoking Agent:

 

DMSA 4 TABLETS/DA

Provocation:

 

POST PROVOCATIVE

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.

                                                                    ANTIMONY HIGH 
 
     This individual’s urine antimony is significantly higher than expected. 
Symptoms or toxic effects depend upon the amount and chemical form of absorbed 
antimony. Antimony (Sb) has two valences, SB+3 and Sb+5. Sb+3 is the more toxic 
but is mostly excreted in feces. Sb+5 is less toxic, binds less well to body 
tissues, and is mostly excreted in urine. Most orally ingested Sb+3 and Sb+5 is 
not absorbed from the gut with organic forms being most bioavailable, followed 
by soluble salts. Oxides are least absorbed. 
 
     Sb dusts may be inhaled as oxides or salts in industrial areas where 
smelting or alloying is done (usually with copper, silver, lead, tin). A rather 
toxic vapor form is stibine, SbH3, which occurs when Sb2O3 is reduced with 
hydrogen and can be formed by some species of mold.  Electrodes and batteries 
may contain antimony.  Ceramics, fireproofed textiles, solders, and pigments may 
also contain antimony.  Exposure to antimony can also occur with handling of gun 
powder and frequent use of firearms.
 
     Inhalation of antimony dust causes irritation of respiratory tissues, and 
chronic inhalation may cause pneumoconiosis. Dermal contact can cause ”antimony 
spots” or rashes which resemble chicken pox. Exposure to stibine causes 
hemolysis of erythrocytes. Less acute exposures or ingestion of bioavailable Sb 
can result in enzyme inhibition and impaired cellular metabolism. Sb inhibits 
phosphofructokinase (”PFK”), monoamine oxidase (”MAO”), and enzymes that bear 
sulfhydryl groups (-SH). Numerous symptoms of Sb ingestion are possible and 
include: nausea, GI distress, anorexia, metallic taste, fatigue and muscle 
weakness, and myopathy. Cardiovascular effects are possible in chronic Sb 
poisoning including: hypotension, cardiac pain (like angina pectoris), and 
faulty ventricular polarization. 
 
     Hair analysis is a corroborative test for Sb excess, which is common among 
patients with Autism Spectrum Disorder. Other confirmatory tests include fecal 

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metals analysis, and urinary antimony post-DMPS or DMSA.  Other clinical 
findings that would be consistent are: subnormal blood platelet MAO functional 
activity, erythrocyte fragility and hemolysis, gout and signs of PFK inhibition 
such as elevated ammonia and hypoxanthine in venous blood, and inverted
T-wave on EKG.

 BIBLIOGRAPHY FOR ANTIMONY 
 1. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, 
Lewis Publishers, Chelsea MI, pp 21-26, 1987. 
 2. Tsalev D.L. and Z.K. Zaprianov. Atomic Absorption Spectrometry in 
Occupational and Environmental Health Practice. CRC Press, Boca Raton FL, pp 85-
87, 1983. 
 3. Scriver C.A. et al The Metabolic Basis of Inherited Disease, 6th ed. McGraw-
Hill, New York NY, pp 2349-50 on PFK deficiency. 1989. 

                                                                     Barium High

     Barium (Ba) has not been established to be an essential element.  Elevated levels of 
Ba often are observed after exposure to Ba (a contrast agent) during diagnostic medical 
tests (e.g. ”barium swallow”, ”upper GI series”, ”barium enema”, etc.).  Elevated levels of 
Ba may interfere with calcium metabolism and potassium retention.  Acutely high intake 
of soluble Ba-salts (nitrates, sulfides, chlorides) can be toxic.  Chronic exposure to Ba 
may be manifested by muscular and myocardial stimulation, tingling in the extremities, 
and loss of tendon reflexes.  

     Brazil nuts and peanuts/peanut butter are very high in Ba so urine Ba may be elevated
shortly after consumption of these foods; toxic effects would not be anticipated under such
conditions. Although Ba is poorly absorbed orally (<5%) it can be very high in peanuts and 
peanut butter (about 3,000 nanograms/gram), frozen and fast foods such as burgers, fries, 
and hot dogs (400-500 nanograms/gram). It is noteworthy that Ba intake is much higher in
children than adults (Health Canada 2005, www.atsdr.cdc.gov/toxprofiles/tp24-c6.pdf).

     Ba is surprisingly abundant in the Earth’s crust, being the 14th most abundant element. 
High amounts of Ba may be found in soils and in food, such as nuts (e.g. brazil nuts), 
seaweed, fish and certain plants. Because of the extensive use of barium in industry, human 
activitiesadd greatly to the release of barium in the environment. As a result barium concen-
trations in air, water and soil may be higher than naturally occurring concentrations in many 
locations. It can also enter the air during coal and oil combustion. Barium compounds are used 
by the oil and gas industries to make drilling mud. Drilling mud simplifies drilling through rocks 
by lubricating the drill. Barium compounds are also used to make paint, brics, tiles, glass, and
rubber. Soluble Ba compounds are highly toxic and may be used as insecticides. Ba-aluminates
are utilized for water purification, acceleration of concrete solidification, production of synthetic
zeolites, and in the paper and enamel industries.

     Ba levels (and the levels of 16 other elements) in water can be assessed with water testing 
as provided by DDI.  A possible confirmatory test for excessive  Ba is measurement of blood
electrolytes as hypokalemia may be associated with excessive Ba in the body. Hair elements
analysis may provide further evidence of exosure to Ba.

                                                                     Cesium High

 19992019  Doctor’s Data, Inc.


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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.

Commonly used chelating agents are not effective binders of Cs.

Resources:
Agency for Toxic Substances & Disease Registry (2015) Toxicological Profile for Cesium.  

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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

                                                                      LEAD HIGH

     This individual’s urine lead (Pb) is higher than expected which means that Pb exposure 
is higher than that of the general population. A percentage of assimilated Pb is excreted in 
urine. Therefore the urine Pb level reflects recent or ongoing exposure to Pb and the degree 
of excretion or endogenous detoxification processes.

     Sources of Pb  include: old lead-based paints, batteries, industrial smelting and alloying, 
some types of solders, Ayruvedic herbs, some toys and products from China and Mexico, 
glazes on(foreign) ceramics, leaded (anti-knock compound) fuels, bullets and fishing sinkers, 
artist paints with Pb pigments, and leaded joints in municipal water systems. Most Pb 
contamination occurs via oral ingestion of contaminated food or water or by children mouthing or 
eating Pb-containing substances. The degree of absorption of oral Pb depends upon stomach 
contents (empty stomach increases uptake) and upon the essential element intake and Pb 
status. Deficiency of zinc, calcium or iron increases Pb uptake. Transdermal exposure is 
significant for Pb-acetate (hair blackening products). Inhalation has decreased significantly with 
almost universal use of non-leaded automobile fuel.

     Lead accumulates in extensively in bone and can inhibit formation of heme and hemoglobin in 
erythroid precursor cells. Bone Pb is released to soft tissues with bone remodeling that can be 
accelerated with growth, menopausal hormonal changes, osteoporosis, or skeletal injury. Low 

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levels of Pb may cause impaired vitamin D metabolism, decreased nerve conduction,and 
developmental problems for children including: decreased IQ, hearing impairment, delayed growth, 
behavior disorders, and decreased glomerular function. Transplacental transfer of Pb to the fetus 
can occur at very low Pb concentrations in the body. At relatively low levels, Pb can participate in 
synergistic toxicity with other toxic elements (e.g. cadmium, mercury).

     Excessive Pb exposure can be assessed by comparing urine Pb levels before and after 
provocation with Ca-EDTA (iv) or oral DMSA. Urine Pb is higher post-provocation to some extent in 
almost everyone.  Whole blood analysis reflects only recent ongoing exposure and does not correlate 
well with total body retention of Pb. However, elevated blood Pb is the standard of care for diagnosis 
of Pb poisoning (toxicity).

BIBLIOGRAPHY FOR LEAD

1.ATSDR Toxicological Profile for Lead (2007 update) www.atsdr.cdc.gov/toxprofile 
2.  Centers for Disease Control and Prevention. Third National Report on Human Exposure to 
Environmental Chemicals. Atlanta, GA: CDC; 2005.
http://www.cdc.gov/exposure report/report.htm [Accessed 02/01/2009]
3. Lead Tech ’92, ”Proceedings and Papers from the Lead Tech ’92: Solutions for a Nation at Risk” 
Conference, Sept 30-Oct 2, 1992. Bethesda, MD, IAQ Publications, 4520 East-West Highway, Ste 610, 
Bethesda, MD, 20814.
4. ”Preventing Lead Poisoning in Young Children”, US Centers for Disease Control, Atlanta, GA, Oct. 1991 
Statement, US Dept. of Health and Human Services.
5. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers, Inc., 
Chelsea, MI, p. 128-135, 1986.
6. Tsalev D.L. et al. Atomic Absorption Spectrometry in Occupational and Environmental Health Practice 
Vol 1, CRC Press, Boca Raton, FL 1983.
7. Piomelli S. et al. ”Management of Childhood Lead Poisoning”, J. Pediatr 105 (1990) p. 523-32.
8. Shubert J. et al. ”Combined Effects in Toxicology – a Rapid 
Systematic Testing Procedure: Cadmium, Mercury and Lead” - J. Toxicology and Environmental Health,
4:763-776, 1978.
9.  Mayo Clinic. Mayo Medical Laboratories. http://www.mayomedicallaboratories.com/test-catalog/
clinical+and+Interpretive/60246 [Accessed 10/25/2011]
10. Saper RB et al. ”Lead, mercury and arsenic in U.S. and Indian manufactured ayrevedic medicines
sold via the internet.”  JAMA (2008) 300(8): 915-23.

                                                                    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. 
 

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     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
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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 19992019  Doctor’s Data, Inc.

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