Below is a summary of the most common heavy metals, their sources and the burden they add to the human body as provided by Doctor’s Data Inc. Doctor’s Data Inc (DDI) is a premier clinical laboratory with over 30 years experience that specializes in essential and toxic elemental testing. Their tests are utilized to detect, asses, prevent and treat heavy metal burden in humans, as well as nutritional deficiencies, gastrointestinal function, hepatic detoxification, metabolic abnormalities, and diseases of environmental origin.
Common heavy metals:
Common sources of bioavailable Aluminum include: aluminum cookware, flatware and especially coffee pots; aluminum hydroxide anti-acid formulations; some types of cosmetics, especially deodorants; 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 Al203 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 aluminum that has poor bio-availability. Aluminum food containers are manufactured with polymer or plastic coatings that prevent direct food-aluminum contact provided such coatings are not damaged. In the GI tract, phosphates react with aluminum ions forming insoluble aluminum phosphates. If this phosphate-blocking were 100% efficient, then virtually no aluminum would be absorbed. Evidently, this phosphate-forming process is incomplete because body tissue levels (such as hair) usually contain measurable amounts of aluminum. In the body aluminum 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. Aluminum is considered neurotoxic and is implicated as a stabilizing agent (via aluminum phosphate bonds) in neurofibrillary tangles in Alzheimer’s disease (Science, 267, pp 793-4, 1995). In cells, Aluminum inhibits the citric acid cycle enzyme isocitrate dehydrogenase which catalyzes formation of alpha-ketoglutaric acid. An effect of this inhibition could be hyperammonemia. Aluminum also inhibits hexokinase, a magnesium dependent phosphorylating enzyme. Without intervention, Aluminum accumulates continually in the body with the highest concentration occurring at old age or death. Fatigue, hypophosphatemia, increased prothrombin time, and porphyria are consistent with Aluminum excess. A hair element test can be used to corroborate increased body burden of Aluminum. An oral provocation with the amino acid glycine, 80 mg/Kg body weight (in divided doses) 24 hours before a diagnostic EDTA chelation with subsequent urine collection can be done to confirm Aluminum excess.(Eliminate food/beverage sources of Aluminum during this procedure.)
1. Ganrot P.O. “Metabolism and Possible Health Effects of Aluminum”, Environ. Health Perspectives, 65, pp. 363-441 1986.
2. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis PubI, Chelsea Ml pp 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. “Aluminum from a Coffee Pot”; 3 letters all on pages 781-82 of Lancet,April 8, 1989.
4. Fulton B. and E.H. Jeffery, “Absorption and Retention from Drinking Water”, Fund. & AppI. 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.
In certain cases when the Antimony levels are higher than expected, the associated symptoms and toxic effects may not be presented. This is because Antimony (chemical symbol Sb) has two valences: Sb+3 and Sb+5. Sb+3 is the more toxic but is mostly excreted in feces. Sb+5, less toxic, binds less well to body tissues and is excreted mostly in urine. Antimony can be assimilated by inhalation of Sb salt or oxide dust, ingested with (contaminated) foods or fluids, or absorbed transdermally. Inhalation may occur in industrial areas where smelting or alloying is done (usually with copper, silver, lead, tin). Sb is present in tobacco at about 0.01% by weight; about 20% of this is typically inhaled by cigarette smoking (Carson et al., Toxicology and Biological Monitoring of Metals in Humans, Lewis Pub. p. 21, 1987). Antimony compounds are used for fireproofing textiles and plastics, and this element may be found in battery electrodes, ceramics and pigments. Antimony can be absorbed with the handling of gun powder or the frequent use of firearms. Recent studies indicate high levels of Antimony in sheepskin bedding produced in New Zealand. Symptoms of mild Antimony contamination may be insidious and multiple including: fatigue, muscle weakness, myopathy, and metallic taste. Chlorides and oxides of both valences of Antimony can be mutagenic and may affect leukocyte function. Antimony can bond to sulfhydryl (-SH) sites on enzymes and interfere with cellular metabolism. Acute symptoms of Antimony contamination include: respiratory tissue irritation and pneumoconiosis with (chronic) inhalation of Antimony dusts, RBC hemolysis with inhalation of stibine (SbH3) vapor, and GI distress if orally ingested. Skin exposure can produce “antimony spots” or rashes which resemble chicken pox. Certain molds can produce the highlyneurotoxic stibine gas from Antimony; stibine inhibits acetylcholinestelase activity. A hair element analysis may be used as a corroborative test for increased body burden of Antimony. Fecal metal analysis can be used to confirm exposure/retention of toxic Sb+3. Antimony may be elevated in urine following administration of DMPS or DMSA.
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. CRCPress, 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.
Arsenic is a complex metal, that forms a variety of compounds, either inorganic or organic. Organic Arsenic compounds like Arsenobetaine, Arsenocholine, Arsenosugars and Tetramethylarsonium salts contain carbon and are mainly found in sea-living organisms, however occasionally they can be found in species living on land. Inorganic forms of Arsenic, such as Arsenite and Arsenate are generally known to be more toxic and are mainly of geological origin. These can be found in agricultural soil and groundwater used for drinking or irrigation. When the water comes into contact with Arsenic containing minerals or deposits it causes exposure to humans and other life forms mainly through daily ingestion of contaminated food or water. Other ways of Arsenic absorption are through lungs and skin.
Industrially, Arsenic and its compounds are mainly used in the production of pesticides, herbicides and insecticides as well as in semiconductor manufacturing to strengthen copper and lead alloys during batteries manufacturing process. Due to its toxicity to insects, bacteria and fungi, Arsenic is still added to animal food (mainly in US grown industrial poultry and swine production) as a method of growth stimulation and disease prevention. In addition, an estimated of 70% of the world’s Arsenic production is being utilized every year in the preservation of timber used for outdoor products such as residential decks, play structures, fence enclosures or picnic tables. If these products were built before 2004 and have a greenish tinge, there are great changes that they were treated with Arsenic to prevent decay or insect damage. Research has shown that when raining, this Arsenic-based wood preservative leaches from wood and it can be rubbed off from the treated surfaces when in contact with the skin. Children who play on structures or other treated surfaces pick up Arsenic on their hands and later on ingest it when they put their hands in their mouth, rub their eyes or eat. According to Environmental Working Group (EWG) the amount of Arsenic in treated wood can be quite large. For example, a standard 12 foot long 2×6 contains as much as 1 oz. of pure Arsenic that could kill 250 adults. It has been estimated that children ingest 630 µg of Arsenic per playground visit and only 5 minutes hand contact with Arsenic treated wood can add up to 1,260 µg to the current Arsenic load. Even though the US Environmental Protection Agency (EPA) has recently lowered the Arsenic standard in drinking water from 50 ppm (50 µg/liter) to 10 ppm (10 µg/liter), there is still a risk of cancer or other illnesses as the total levels of previous, current and future exposure compound when it comes to one’s body burden.
When the concentration of inorganic Arsenic is measured in urine it shows the absorbed dose of Arsenic on an individual level which typically ranges from 5 to 20 µg Arsenic/liter, but in many instances may even exceed 1000 µg/liter. After entering the body, most toxins do not affect all the organs the same way. Usually, a specific molecular target or organ receives the primary toxic effect and when it comes to Arsenic, the peripheral nervous system is the main target. Early signs of Arsenic exposure are excessive perspiration, muscle tenderness or weakness and changes in the skin pigmentation. According to William A. Croft, medical pathologist and former professor at the University of Wisconsin School of Medicine people with acute exposure to Arsenic could develop associated symptoms and toxic side effects such as intestinal pain, burning eyes and throat, diarrhea, dizziness and/or nausea, sensory loss, cardiovascular failure and even death. Chronic long term exposure or survival of acute exposure can cause loss of peripheral sensory function and loss of central nervous system function, skin pigmentation changes (hyperkeratosis), cancer of the skin and lungs and/or blackfoot disease (BFD), a severe form of peripheral vascular disease (PVD) which leads to gangrenous changes.
Since no levels of Arsenic are considered safe when it comes to exposure to children, signs of Arsenic poisoning for them can be even more severe: loss of speech, seizures, rashes, brain damage, even cancer of the lung, skin or bladder.
Blood, hair, nails and urine biomarker analysis may be used to test for increased body burden of Arsenic. Most of the Arsenic in the blood is bound to red blood cells. When ingested, Arsenic is transformed by the liver to a methylated form of Arsenic and excreted in the urine with a half-life of 3 – 5 days. Since Arsenic is rapidly cleared from blood, this biomarker can only be used in cases of acute Arsenic poisoning or high level exposure. Arsenic is excreted through outer layer of skin and sweat. Arsenic binds to sulfhydryl-containing proteins and concentrates in the hair and fingernails which can be seen as white transversal bands called Mees’ lines.
1. Gilbert Stephen G., A Small Dose of Toxicology: The Health Effects of Common Chemicals, 1st ed, CRC Press LLC, 2004
Elevated levels Barium are often observed after exposure to Barium (a contrast agent) during diagnostic medical tests (e.g. “barium swallow”, “upper GI series”, “barium enema”, etc.). Elevated levels of Barium may interfere with calcium metabolism and potassium retention. Acutely high intake of soluble Ba-salts (nitrates, sulfides, chlorides) can be toxic. Chronic exposure to Barium may be manifested by muscular and myocardial stimulation, tingling in the extremities, and loss of tendon reflexes. Due to its high density, Barium is utilized to absorb radiation and is utilized in concrete shields around nuclear reactors and in plaster used to line x-ray rooms. The main use of Barium in medicine is as a contrast medium. Long-term retention of Barium can occur – granuloma of the traverse colon has been reported after diagnostic use of Barium sulfate. Crystalline Barium-titanate is a ceramic compound which is used in capacitors and transducers. Barium is also used to produce pigments in paints and decorative glass. Soluble Barium compounds are highly toxic and may be used as insecticides. Barium-aluminates are utilized for water purification, acceleration of concrete solidification, production of synthetic zeolites, and in the paper and enamel industries. Although Barium is poorly absorbed orally (less than 5%) it can be very high in peanuts and peanut butters (about 3,000 nanograms/gram) as compared to egg, frozen and fast foods such as burgers, fries and hot dogs (400-500 nanograms/gram). It is noteworthy that Barium intake is much higher in children than adults.
Barium levels (as well as the levels other elements) in water can be assessed with water testing as provided by DDI. A conformatory test for elevated Barium is measurement of blood electrolytes as hypokalemia may be associated with elevated Barium.
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 bismuth. 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.
1. Harrison’s Principles of Internal Medicine, 13th ed, McGraw Hill, New York, NY pp. 282, 534, 1994.
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, Chelsea Ml pp 44-7, 1987.
This element is insidiously toxic with chronic accumulations affecting renal function, pulmonary and cardiovascular tissues, bone, and the peripheral nervous system. Without intervention, the biological half-life of Cadmium in humans exceeds 20 years (Harrison’s Principles of Internal Medicine, 13th ed, pp 2463-64). Chronic manifestations associated with this degree of Cadmium excess include: hypertension, weight loss, microcytic-hypochromic anemia, lymphocytosis, proteinuria with wasting of beta2 microglobulin, emphysema and pulmonary fibrosis (if inhalation was a route of contamination), atherosclerosis, steomalacia and lumbar pain, and peripheral neuropathy. Acute inhalation of Cadmium dusts, fumes or soluble salts may produce cough, pneumonitis and fatigue. Manifestations of Cadmium toxicity may be lessened or delayed by an individual’s protective and detoxication capacities. Zinc and vitamin E are protective; metallothionein and glutathione bind Cadmium and help detoxify itinitially. Smoking can be a source for as much as 0.1 mcg Cadmium per cigarette (HEW Pub. No. NIOSH 76-1 92, US Govt. Printing Ofc., 1976). Some medical authorities consider Cadmium to be a carcinogen for lung cancer (Harrison’s Principles, 13th ed, op. cit. pp 2463). Other occupational or environmental sources include: mining and smelting activities, pigments and paints, electroplating, electroplated parts (e.g., nuts and bolts), batteries (Ni-Cd), plastics and synthetic rubber, photographic and engraving processes, old drums from some copy machines, photoconductors and photovoltaic cells, and some alloys used in soldering and brazing. “Cadmium Red” as used in dental acrylics (dentures) could be a significant source of exposure for those making dentures or dentists/dental techs making fine- tune adjustments (grinding) to dentures chair side. Cadmium- free acrylic dentures are now available. Depending upon the extent of net retention of Cadmium elevated urine Cadmium may occur after administration of EDTA, and to a much lesser extent DMPS, DMSA, or D-penicillamine. Blood Cadmium measurement may not be indicative (Harrison’s Principles of Internal Medicine, 13th ed., pp 2463).
1. Graef J.W. “Cadmium” in Harrison’s Principles of Internal Medicine, 13th ed, Isselbacher et al. eds,McGraw Hill, NY, NY pp 2462-63, 1994.
2. Nat. Inst. Occup. Safety and Health (NIOSH), “Criteria for a Recommended Standard…Occupational Exposure to Cadmium”, H.E.W. Publication No. (NIOSH) 76- 192, 1976.
3. Carson, B.L. et al, Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers,Chelsea Ml, pp 51-58, 1987.
4. Werbach M.R. Nutritional Influences on Illness 2nd ed., Third Line Press, Tarzana, CA, pp 102,348-49, 643, 679, 1993.
5. Lauwerys R.R. et al. “Cadmium: Exposure Markers as predictors of Nephrotoxic Effects” Clinical Chem. 40 no 7, pp 1391-94, 1994.
6. Whittemere A.S. et al. “Urinary Cadmium and Blood Pressure: Results from the NHANES Il Survey” Environ. Health Persp. 9, pp 133-40, 1991.
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 only recent exposures and does not correlate well with total body burden of Lead.
1. ATSDR Toxicological Profile for Lead( 2007 update) http://www.atsdr.cdc.gov/substances/toxsubstance.asp?toxid=22
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, Ml, p. 128-135, 1986.
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.
Symptomatology depends on many factors: the chemical form of absorbed Hg and its transport in body tissues, presence of other synergistic toxics (lead, cadmium have such effects), presence of disease that depletes or inactivates lymphocytes or is immunosuppressive, organ levels of xenobiotic chemicals and sulfhydryl-bearing metabolites (e.g. glutathione), and the concentration of protective nutrients, (e.g. zinc, selenium, vitamin E). Early signs of Mercury contamination 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, possibly immune dysregulation. Advanced disease processes from Mercury toxicity include: tremors and incoordination, anemia, psychoses, manic behaviors, possibly autoimmune disorders, renal dysfunction or failure. Note that in Mercury contamination of long duration, renal excretion of Mercury (and normal metabolites) may become impaired, and the urine level of Mercury might be only mildly elevated or not elevated at all due to renal failure. Mercury is used in: dental amalgams (50% by weight), explosive detonators; some vaccines in pure liquid form for thermometers, barometers, and laboratory equipment; batteries and electrodes (“calomel”); and in fungicides and pesticides and in the paper industry. The fungicide/pesticide use of Mercury has declined due to environmental concerns, but Mercury residues persist from past use. Emissions from coal fired power plants and hospital/municipal incinerators are significant sources of Mercury pollution. Methylmercury, the common, poisonous form, occurs by methylation 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. A daily diet of fish can cause 1 to 10 micrograms of mercury/day to be ingested; the majority of which is organic, methylmercury. Depending upon body burden and upon type, duration and dosage of detoxifying agents, elevated urine Mercury may occur after administration of: DMPS, DMSA, or D-penicillamine. Mercury accumulation can also be assessed by comparing pre- and post-l.V. vitamin C fecal mercury levels (DDI observations). Blood and especially blood cell analyses are only useful for diagnosing very recent or ongoing organic (methyl) Mercury exposure.
1. Suzuki T. et al eds, Advances in Mercury Toxicology, Plenum Press, New York, 1991.
2. World Health Organization: “Methylmercury” Environ. Health Criteria 101 (1990); “Inorganic Mercury” Environ. Health Criteria 118 (1991) WHO, Geneva, Switzerland.
3. Tsalev D.L. and Z.K. Zaprianov, Atomic Absorption Spectrometry in Occupational and Environmental Health Practice, CRC Press, Boca Raton FL, pp 158-69, 1983.
4. Birke G. et al “Studies on Humans Exposed to Methyl Mercury Through Fish Consumption”, Arch Environ Health 25, 1972 pp 77-91.
5. Pelletier L. “Autoreactive T Cells in Mercury-Induced Autoimmunity”, J. Immunology, 140 no.3 (1988) pp 750-54.
6. Werbach M.R. Nutritional Influences on Illness, 2nd ed, Third Line Press, Tarzana CA, pp 249, 647, 679, 1993.
With the exception of specific occupational exposures, most absorbed Nickel comes from food or drink, and intakes can vary by factors exceeding 100 depending upon geographical location, food type, and water supply. Depending upon chemical form and physiological factors, from 1 to 10% of dietary Nickel may be absorbed from the gastrointestinal tract into the blood. Urine reflects recent exposure to nickel and may vary widely in Nickel content from day to day due to the above factors. 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/grams
- Foods, especially: cocoa, chocolate, soya products, nuts, and hydrogenated oils
- Nickel-cadmium batteries
- Non precious, semiprecious dental materials
- Nickel-containing prostheses
- Electroplating, 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 observed Nickel contaminations are manifested as dermatoses – contact dermatitis and atopic dermatitis. However, Nickel hypersensitizes the immune system causing hyperallergenic responses to many different substances. Because Nickel can displace zinc from binding sites on enzymes, it can have inhibiting or activating effects on such enzymes. Nickel sensitivity is observed to be three to five times more frequent in women than in men. Other laboratory tests or clinical findings that would be indicative of nickel excess are; hair element analysis, presentation of multiple allergic sensitivities, dermatitis, positive patch test for “Nickel allergy”, proteinuria, hyperaminoaciduria (by 24-hour urine amino acid analysis). Detoxification treatments with administration of EDTA or sulfhydryl agents (DMPS, DMSA, D-penicillamine) may increase urine Nickel levels depending upon: body burden and mobility in tissues, duration of treatment, dosage and other factors.
1. Tsalev D.L. and Z.K. Zaprianov 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 Ml, pp 162-67, 1986.
3. Nielsen F.H. in Modern Nutrition in Health and Disease ed. by Shils et al, Lea & Febiger, Philadelphia, PA, pp 279-81, 1994.
4. Medical and Biological Effects of Environmental Pollutants: Nickel, Nat. Acad. Sci, Washington DC, 1975.
5. Ambient Water Quality Criteria for Nickel, US EPA NTIS, Springfield, VA. PubI No. PB81- 117715,1980.
Ingested tin is not significantly absorbed if it is an inorganic form. Oxide coatings readily form on metallic tin, and salts can quickly oxidize making them insoluble. Organic tin, however, is bioavailable and more readily absorbed. Some organic tin compounds such as short-chain alkyltins can be absorbed transdermally and can cause degeneration of myelin. Food and drink usually provide small daily intakes of (nontoxic) tin, with amounts depending upon type of food, packaging, quality of drinking water and water piping materials. Total daily intake is expected to vary from about 0.1 to 15 milligrams. Tin is present in many metal alloys and solders; bronze, brass and pewter contain the element. Dyes, pigments and bleaching agents often contain tin. Anticorrosion plating of steel and electrical components may also use tin. “Tin cans” are tin-plated steel with a thin outer oxide layer allowing the surface to be shiny but inert. Modern food-containing cans usually haveS polymer coatings that prevent food-metal contact. In the past some toothpastes contained stannous fluoride, a soluble fluoride source for strengthening tooth enamel. Currently most brands of fluoridated toothpastes contain sodium fluoride. Organic tins, the usually toxic forms, are: biocides (triphenyltin and alkyltins) used against rodents, fungi, insects and mites; curing agents for rubbers and silicones (dialkyltin); and methyltin formed bacteriologically (similar to methylmercury). Mildly elevated levels of tin in urine may reflect sporadic dietary intake and excretion; there may be no associated symptoms. A two- or three-fold increase in urine tin levels is not uncommon following administration of EDTA or with sulfhydryl agents (DMSA, D-penicillamine, DMPS). Early signs of chronic organic tin excess can be: reduced sense of smell, headaches, fatigue and muscle aches, ataxia and vertigo. Hyperglycemia and glucosuria are reported. Also, for organic tin exposure, there can be irritation of contacted tissues (eyes, skin, bronchial tubes, or GI tract). Later, immune dysfunction may occur with reduced lymphocytes and leukocytes; mild anemia may occur. A hair element analysis can be used to corroborate tin excess. Tin is commonly elevated in urine from autistic patients following administration of DMSA or DMPS.
1. Winship K.A. “Toxicity of Tin and Its Compounds”, Adverse Drug Reactions and Acute Poisoning Reviews, 7 no.1, pp 19-38, 1988.
2. Gray B.H. et al. “Inhibition of Tributyltin Mediated Hemolysis by Mercapto Compounds” J. Applied Toxicology 6 no.5 pp 363-70, 1986. Discussed BAL, DMSA, DMPS relative effectiveness in inhibiting a toxic effect of tin.
3. Ganguly B.B. et al “Cytotoxicity of Tin in Human Peripheral Lymphocytes in Vitro” Mutation Research, 282 no.2, pp 61-67, 1992.
4. Tsalev D.L. and Z.K. Zaprianov, Atomic Absorption Spectrometry in Occupational and Environmental Health Practice, vol. 2, CRC Press, Boca Raton, FL, pp 199-204, 1983.
5. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis Publ., Chelsea Ml, pp 260-63, 1987.
Uranium is a radioactive element having 10 isotopes with half lives that exceed one hour. U238 constitutes about 99% of the naturally-occurring uranium. U238 has a half life of 4.5 X 10 to the ninth years. It decays by alpha emission to produce thorium, Th234, the initial step in a decay chain that eventually leads to lead. Alpha, beta and gamma emissions occur during this decay process. Because of the very long half life, the radioactivity danger is only slight. However, exposure to enriched or nuclear fuel grade uranium (high in U235) does pose a health hazard. The major concern for (natural) uranium excess is toxochemical rather than radiochemical. Uranium is a chemically-reactive element, has four valences (3,4,5 or 6), and may combine with: carbonate, phosphate, citrate, pyruvate, matate, lactate, etc. in body tissues. When not excreted in urine, it may accumulate in the kidneys, spleen, liver, and in bone (substituting for calcium in hydroxyapatite). Uranium is nephrotoxic, causing damage to the glomeruli and proximal tubules. An early sign of uranium excess is general fatigue. Renal damage is reflected by proteinuria, hyperaminoaciduria and glucosuria. Albuminuria and urinary catalase are findings consistent with uranium excess. Elevated hair uranium is a confirmatory finding; whole blood and fecal analyses may corroborate recent or ongoing exposures. Uranium is more common than mercury, silver or cadmium in the earth’s rock strata, and may be present, at low levels, in ground (drinking) water. Most commercial use of uranium is for nuclear fuel, but it may be present in ceramics or colored glass, especially ancient or antique, yellow-colored glass.
1. Carson B.L. et al Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers, Chelsea Ml. pp. 272-75, 1986.
2. Handbook of Chemistry and Physics, 49th ed., CRC, Cleveland, OH, pp B-143-44, 1968.
3. Leggett R.W., “The Behavior and Chemical Assessment of U in the Kidney: a Reassessment”, Health Physics, 57 no.3, pp 365-83, 1989.
4. Byrne A.R. and L. Benedik, “Uranium Content of Blood, Urine and Hair of Exposed and Non Exposed Persons Determined by Radiochemical Neutron Activation Analysis The Science of the Total Environment, 107, pp 143-57 1991.
5. Bentley K.W. and J.H. Wyatt, “Quantitative Determination of Fissionable materials in Human Hair” Environ. Res. 21 pp 407-15, 1980.