Here are the results of my toxic metals urine test (and hair test here) which involved a challenge agent and six-hour timed urine collection (please excuse the typos introduced by OCR):
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. Due to its high density, Ba is utilized to absorb radiation and is utilized in concrete shields around nuclear reactors and in plaster used to line x-ray rooms. 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,
The main use of Sa in medicine is as a contrast medium. Long-term retention of Ba can occur – granuloma of the traverse colon has been reported after diagnostic use of Ba sulfate, Crystalline Ba-titanate is a ceramic compound which is used in capacitors and transducers. Ba is also used to produce pigments in paints and decorative glass. Soluble Ba compounds are highly toxic and may be used as lnsecticides. Ba-aluminates are utilized for water purification, acceleration of concrete solidification, production of synthetic zeolites, and in the paper and enamel industries.
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).
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 Sa retention is measurernent 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.
This individual’s urine lead (Pb) is higher than expected which means that Pb exposure is higher than that of the general popu’atlon, 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, Ayurvedic 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 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. ATSOR 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 Ohemicals, Atlanta, GA: CDC; 2005.
http://www.cdc.gov/exposurereporVreport.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 30-0ct 2,1992. Bethesda, MD, lAO Publicatlons, 4520 East-West Highway. Ste 610,
Bethe$d~, 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, CRG Press, Boca Raton, Fl1983.
7. Piomelli S. et al. “Management of Childhood Lead Poisoning”, J. Pediatr 105 (1990) p, 523-32.
8. Shubert J. et at. “Combined Effects in Toxicology• a Rapid
Systematic Testing Procedure: Cadmium, Mercury and LeadH – J. Toxicology and Environmental Health,
9. Mayo Clinic. Mayo Medical Laboratories. http://www.mayomedicallaboratories.comftest-catalog/
clinical+and+lnterpretive/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.” JAM A (2008) 300(8): 915-23.
This individual’s urine nickel (Ni) is elevated which mayor may not be of significance. Urinary excretion of nickel bound to cysteine or other thiol compounds (such as glutathione) or to amino acids (histidine, aspartic acid, arginine) is the predominant mode of excretion. With the exception of specific occupational exposures, most absorbed Ni comes from food or drink, and intakes can vary by factors exceeding 100 depending upon geographical location, diet, and water supply. Depending upon chemical form and physiological factors, from 1 to 10% of dietary Ni may be absorbed from the gastrointestinal tract. Urine Ni only reflects recent exposure to Ni and May vary widely from day to day.
Sources of nickel are numerous and include the following.
• Cigarettes (2 to 6 mcg Ni per average cigarette)
• Diesel exhaust (particulates may contain up to 10 mg/gram)
• Foods, especially: cocoa, chocolate, soya products, nuts, hydrogenated oils, and coffee
• Nickel-cadmium batteries (Ni-Cd)
• Nonprecious, semiprecious dental materials
• Nickel-containing prostheses
• Electroplating, metal plated objects, costume jewelry
• Pigments (usually for ceramics or glass)
• Catalyst materials (for hydrogenation processes in the food, petroleum and petrochemical industries)
• Arc welding
• Nickel refining and metallurgical processes
Most clinically relevant Ni exposures are manifested as dermatoses – contact dermatitis and atopic dermatitis. However, Ni hyper-sensitizes the immune system anti may cause hyperallergenic responses to many different substances, because Ni can displace zinc from binding sites on enzymes it can affect abnormal enzymatic activity. Nickel sensitivity is observed to be three to five times more prevalent in females than in males.
Other laboratory tests or possible clinical findings that may be associated with Ni exposure are; hair elements analysis, presentation of multiple allergic sensitivities, dermatitis, positive patch test for “Ni allergy”, proteinuria, hyperaminoaciduria (by 24-hour urine amino acid analysis). Administration of EDTA or sulfhydryl agents (DMPS, DMSA, D-penicillamine) may increase urine Ni levels; ~I,JCh chelator-induced elevations mayor may not be associated with adverse health effects.
BIBLIOGRAPHY FOR NICKEL
1. Tsalev D.L. and ZK Zaprienov Atomic Absorption Spectrometry in Occupational and
Environmental Health Practice, CRC Press, Boca Raton FL, pp 173-78,1983.
2. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers,
Chelsea MI, pp 162-67,1986.
3. Nial$QnF.H. in Modem Nutrition in Hoalth and Di:)¢Q~ccd. by Chila et .,1,Lea 8; rebiger,
Philadelphia, PA, pp 279-81,1994.
4. Medical and Biological Effects of Environmental Pollutants: Nickel, Nat. Acad. Sci,
5. Ambient Water Quality Criteria for Nickel, US EPA NTIS, Springfield, VA, Publ No. PB81-
This individual’s urine thallium (TI) is higher than expected, but associated symptoms or toxic effects mayor may not be presented. Pl’eSer’1tationof symptoms can depend upon several factors including: chemical form Of the TI mode of assimilation. severity and duration of exposure. and organ levels of metabolites and nutrients that effect the action of TI in the body.
Thallium can be assimilated transdermally, by inhalation, or by oral ingestion. Both valence states can have harmful effects: TI+1 may displace potassium from binding sites and influences enzyme activities; TI+3 affects RNA and protein synthesis. TI 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 TI exposure.
Symptoms that may be associated with excessive TI exposure are often delayed. Early signs of cnronic, low-level TI exposure and retention may include: mental confusion, fatigue, and peripheral neurological signs: parestnesias. 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 TI 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 TI exposure. Although urine is the primary natural route for excretion of thallium, the biliarylfecal route also contributes. Therefore. fecal metals analysis provides a confirmatory test for chronic ongoing exposure to TI, Clinical findings that might be associated with excessive TI are: albuminuria.
EEG with diffuse abnormalities. hypertension. and elevated urine creatinine phosphokinase (CPK). No provocation agents are currently available to estimate TI retention by means of urinalysis.
BIBLIOGRAPHY FOR THALLIUM
1. Centers for Disease C antral and Prevention. Third National Report on Human Exposure to Environmental Chemicals. Atlanta, GA: CDC 2005. http;lIwww.cdc.gov/exposurereport.htm [Accessed 2101/2009)
2. Graef J.W. “Thallium” in Harrison’s Principles of Intemal Medicine, 13th ed., isseioacner et al
3. Tsalav 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.
The level of tungsten (W) in this urine sample is higher than expected. After exposure and absorption via inhalation. ingestion or injection, most W is rapidly eliminated via urine and feces, W has no known biological role. Long-term chronic exposures have been associated with lung disease (pneumoconiosis or “hard metal lung disease”) and lung cancer. Skin contact with W may produce contact eczema, pruritis. folliculitis and neurodermatitis. Tungsten has an antagonistic relationship with molybdenum (Mo) decreasing hepatic Mo concentration and reducing the effectiveness of sulfite and xanthine oxidases.
Tungsten is a silvery-white lustrous element usually obtained as a grey powder and is mainly utilized as tungsten carbide in metal-working, mining and petroleum Industries. Calcium and magnesium tungstates are widely used in filaments for electric lamps, electron tubes and television tubes, Since W has the highest melting point of all metals it is used for high-speed and hot-worked steels, Other sources include catalysts and reagents in biological analysis, fire and waterproofing materials, and industrial lubricants.
For people exposed to hard-metal dust, W levies can reach .014 jJg/g in urine. Intestinal absorption of tungsten is rapid and seemingly significant. W is rapidly transported to the blood
and then to the kidneys for filtration and eventual excretion from the body, In a rat study, elimination of W via feces was slower than that of urine but reached 52% after three days. PUlmonary absorption of W-tungstic oxide has been studied in dogs, 60% of W is rapidly deposited in the respiratory tract and 33% of that fraction reaches systemic circulation. Tungsten is also easily transferred from mother to fetus usually later in gestation.
Urinary W levels may be elevated after administration of OMPS or DMSA; comparison of urine W before and after provocation provides and estimate of net retention of W over time.
BIBLIOGRAPHY FOR TUNGSTEN. HIGH
1. Marquet, P’I Francois, B.•Lotti, H” Turcant, A., Debord, J., Nedelec, G.•Lachatre, G. Tungsten aetermination in biological fluids, hair and nails by plasma emission spectrometry in a case of severe acute intoxication in man. J ForensiC Sci 42(3):527-30, 1997.
2. Seiler, H’I Sigel, A., Sigel, H. Handbook on Metals in Clinical and Analytical Chemistry.
New York. Marcel Dekker, lnc., 1994.