Actual test done February 22, 2020 by 48 year old female.
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Lead Urine Test
pH upon receipt:
timed: 6 hours
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.
©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
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
1999–2020 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 bismuth is higher than expected. Urine is the principal mode for
excretion of absorbed bismuth. This element is considered to be only slightly toxic with ingestion
of gram quantities necessary before signs of toxicity occur. Only between 5 and 10% of orally
ingested, soluble bismuth salts are absorbed into the blood.
Bismuth is a byproduct of lead and copper ore refining. Bismuth has therapeutic uses with
antimicrobial, anti-secretory and anti-inflammatory actions. Bismuth subsalicylate (”Pepto-Bismol”)
hydrolyzes in the stomach to salicylic acid and insoluble bismuth; it can be effective in halting
traveler’s diarrhea. Historically, bismuth was used to treat syphilis. Bismuth is used commercially
in low-melting-point alloys and solders and is commonly in ”automatic” sprinkler heads for in-
building fire protection. Bismuth often is a component of: pigments, paints, glazes for ceramics,
glass, and some semiconductor materials. Some cosmetics including lipstick may contain bismuth
oxides as a pigment (pearlescent white). Dry cell battery electrodes (cathode) may contain
At sub-gram quantities, no toxic effects are documented for bismuth. Also, the existence of
health problems due to environmental pollution by bismuth is not documented (Tsalev p. 101,
1983). Early physiological signs of bismuth excess may include: constipation or bowel irregularity,
foul breath, skin pigmentation changes, and gum pigmentation (blue-black) with stomatitis.
Laboratory tests that help to assess bismuth status are whole blood and hair element
analyses. Some increase in urine bismuth may follow administration of dithiol chelators (DMPS,
DMSA). Bismuth has a very high affinity for sulfhydryl groups.
BIBLIOGRAPHY FOR BISMUTH
1. Harrison’s Principles of Internal Medicine, 13th ed, McGraw Hill, New York, NY pp. 282, 534,
2. Tsalev D.L. and Z.K. Zaprianov Atomic Absorption Spectrometry in Occupational and
Environmental Health Practice CRC Press, Boca Raton FL, pp 101-103, 1983.
3. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans Lewis Publishers,
1999–2020 Doctor’s Data, Inc.
Chelsea MI pp 44-7, 1987.
This individual’s urine lead exceeds three times the upper expected limit per the
reference population. Because a percentage of absorbed or assimilated lead is excreted
in urine, the urine lead level reflects recent or ongoing exposure to lead and the degree
of excretion or detoxification.
Sources of lead include: old lead-pigment paints, batteries, industrial smelting and
alloying, some types of solders, ayruvedic herbs, some toys and products from China,
glazes on (foreign) ceramics, leaded (antiknock compound) fuels, bullets and fishing
sinkers, artist paints with lead pigments, and leaded joints in some municipal water
systems. Most lead contamination occurs via oral ingestion of contaminated food or water
or by children mouthing or eating lead-containing substances. The degree of absorption of
oral lead depends upon stomach contents (empty stomach increases uptake) and upon
the body’s mineral status. Deficiency of zinc, calcium or iron may increase lead uptake.
Transdermal exposure is slight. Inhalation has decreased significantly with almost universal
use of non-leaded automobile fuel.
Lead accumulates extensively in bone and inhibits formation of heme and hemoglobin in
erythroid precursor cells. Bone lead is released to soft tissues with bone remodeling that can
be accelerated with growth, menopausal hormonal changes and osteoporosis. Lead has
physiological and pathological effects on body tissues that may be manifested from relatively low
lead levels up to acutely toxic levels. In children, developmental disorders and behavior problems
may occur at relatively low levels: loss of IQ, hearing loss, poor growth. In order of occurrence
with increasing lead concentration, the following can occur: impaired vitamin D metabolism,
initial effects on erythrocyte and erythroid precursor cell enzymology, increased erythrocyte
protoporphyrin, headache, decreased nerve conduction velocity, metallic taste, loss of appetite,
constipation, poor hemoglobin synthesis, colic, frank anemia, tremors, nephrotoxic effects with
impaired renal excretion of uric acid, neuropathy and encephalopathy. At relatively low levels,
lead can participate in synergistic toxicity with other toxic elements (e.g. cadmium, mercury).
Excessive retention of lead can be assessed by urinalysis after provocation with Ca-EDTA (iv)
or oral DMSA. Whole blood analysis can be expected to reflect onlyrecent exposures and does
not correlate well with total body burden of lead.
BIBLIOGRAPHY FOR LEAD
1.ATSDR Toxicological Profile for Lead( 2007 update) www.atsdr.cdc.gov/toxprofile
2. 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.
3. ”Preventing Lead Poisoning in Young Children”, US Centers for Disease Control, Atlanta, GA,
Oct. 1991 Statement, US Dept. of Health and Human Services.
4. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers,
Inc., Chelsea, MI, p. 128-135, 1986.
1999–2020 Doctor’s Data, Inc.
5. Tsalev D.L. et al. Atomic Absorption Spectrometry in Occupational and Environmental Health
Practice Vol 1, CRC Press, BocaRaton, FL 1983.
6. Piomelli S. et al. ”Management of Childhood Lead Poisoning”, J. Pediatr 105 (1990) p. 523-32.
7. 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.
1999–2020 Doctor’s Data, Inc.