Actual test done October 21, 2019 by 33 year old female.
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PATIENT: ##### ####
CLIENT #: #####
DOCTOR: ##### #####
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Mercury Urine Test
pH upon receipt:
less than detection limit
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.
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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
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
1999–2019 Doctor’s Data, Inc.
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.
This individual’s urine arsenic (As) markedly exceeds the expected level. Because urine is
the major mode of excretion for As, excretion at this level reflects a significant exposure to As.
Arsenobetaine and arsenocholine are rather non-toxic forms of As that are high in shellfish.
Markedly elevated levels of thos inorganic As species are commonly exhibied within 48 hours
of consumption of shellfish.
Sources of As include: contaminated foods (e.g. chicken), water or medications. Industrial
sources are: ore smelting/refining/processing plants, galvanizing, etching and plating processes.
Tailings from or river bottoms near gold mining areas (past or present) may contain As.
Insecticides, rodenticides and fungicides (Na-, K- arsenites, arsenates, also oxides are
commercially available). Commercial arsenic 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 Ayrvedic herbs.
Chronic exposure to or ingestion of too much 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. Enzymes
inhibited by As include: pyruvate dehydrogenase, a’-ketoglutarate dehydrogenase, and the ”alpha-keto
dehydrogenase” enzymes in the oxidative catabolism sequences of leucine, isoleucine and valine
(an effect similar to that of thiamin deficiency).
Early symptoms of excess As include: fatigue, malaise, eczema or allergic-like dermatitis,
increased salivation and garlic-like breath. Increased net retention of As can lead to further
manifestations: skin hypopigmentation, white striae on fingernails, hair loss, stomatitis, peripheral
neuropathy, myocardial damage, hemolysis, and anemia (aplastic with leukopenia).
Hair element analysis may provide further evidence of exposure to inorganic As. Blood As
levels are not dose-related and may or may not reflect arsenic exposure or body burden.
Following provocation testing with sulfhydryl agents (D-penicillamine, DMPS, DMSA), some
increase in urine As may be exhibited; the extent to which depends on cummulative exposure
1999–2019 Doctor’s Data, Inc.
BIBLIOGRAPHY FOR ARSENIC
1. Centers for Disease Control and Prevention. Third National Report on Human Exposure
to Environmental Chemicals. Atlanta, GA; CDC: 2005.
htp://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
5. Harrison’s Principles of Internal Medicine, 13th ed., McGraw Hill, New York, NY, pp 2461-62,
6. Heyman A. et al. ”Peripheral Neuropathy Caused by Arsenical Intoxication” New Eng. J. Med.,
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.
This individual’s urine mercury (Hg) far exceeds the expected level for the general population under
non-provoked condititons. Presentation of symptoms associated with excessive Hg exposure can depend
on many factors: the chemical form of Hg its accumulation in specific tissues, presence of other toxicants,
presence of disease that depletes glutathione or inactivates lymphocytes or is immunosuppressive, and the
concentration of protective nutrients, (e.g. zinc, selenium).
Early signs of excessive Hg exposure include: decreased senses of touch, hearing, vision and taste,
metallic taste in mouth, fatigue or lack of physical endurance, and increased salivation. Symptoms may
progress with moderate or chronic exposure to include: anorexia, numbness and paresthesias, headaches,
hypertension, irritability and excitability and immune suppression/dysregulation. Advanced disease processes
from excessive Hg assimilaion include: tremors and incoordination, anemia, psychoses, manic behaviors,
possibly autoimmune disorders and renal dysfunction or failure.
Mercury is commonly used in: dental amalgams (50% by weight), explosive detonators; in pure liquid form
for thermometers, barometers, and laboratory equipment; batteries and electrodes, some medications and
ayruvedic herbs, and Hg in fungicides and pesticides. The use of Hg in fungicides/pesticides has declined due to
environmental concerns, but mercury residues persist from past use.
Methylmercury, the most common, organic form, occurs by methylation of inorganic in aquatic biota or
sediments (both freshwater and ocean sediments). Methylmercury accumulates in aquatic animals and fish and
is concentrated up the food chain reaching high concentrations in large fish and predatory birds. Except for fish,
the human intake of dietary mercury is negligible unless the food is contaminated with one of the previously listed
forms/sources. Daily ingestion of fish can result in the assimilation 1 to 10 micrograms of mercury/day.
Depending upon the extend of cumulative Hg exposure, elevated urine mercury may occur after administration
of DMPS, DMSA, or D-penicillamine. Blood and especially red blood cell elemental analyses are only useful for
diagnosing very recent or ongoing organic (methyl) mercury exposure.
BIBLIOGRAPHY FOR MERCURY
1999–2019 Doctor’s Data, Inc.
1. 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 2/01/2009]
2. Suzuki T. et al eds, Advances in Mercury Toxicology, Plenum Press, New York,
3. World Health Organization: ”Methylmercury” Environ. Health Criteria 101
(1990); ”Inorganic Mercury” Environ. Health Criteria 118 (1991) WHO, Geneva,
4. Tsalev D.L. and Z.K. Zaprianov, Atomic Absorption Spectrometry in
Occupational and Environmental Health Practice, CRC Press, Boca Raton FL, pp
5. Birke G. et al ”Studies on Humans Exposed to Methyl Mercury Through Fish
Consumption”, Arch Environ Health 25, 1972 pp 77-91.
6. Pelletier L. ”Autoreactive T Cells in Mercury-Induced Autoimmunity”, J.
Immunology, 140 no.3 (1988) pp 750-54.
7. Werbach M.R. Nutritional Influences on Illness, 2nd ed, Third Line Press,
Tarzana CA, pp 249, 647, 679, 1993.
8. 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.
1999–2019 Doctor’s Data, Inc.