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March 28, 2024

Toxic Heavy Metals Guide

Living in an industrialized society exposes all inhabitants to metals in the environment. Some minerals are toxic to life in all but the tiniest of amounts, including lead, mercury, arsenic, cadmium, nickel, and aluminum. The increasing rates of cancer, vascular disease, dementia, and other diseases are directly related to the increase of toxic heavy metals and other chemicals in our environment, as chronic, even low-grade, environmental exposures raise the body burden.

Aluminum   Antimony   Arsenic   Barium   Bismuth   Cadmium   Cesium   Gadolinium   Lead   Mercury   Nickel   Platinum   Thallium   Thorium   Tin   Tungsten   Uranium

With the industrialization of the world, the environmental amounts of toxic metals have markedly increased.  Lead, arsenic, mercury, cadmium and other toxic metals have been known to have adverse biological effects on humans since ancient times.  Over the years, the nervous system, vascular system, and the immune system have been shown to be adversely effected by heavy metal toxicity. The extent of the problem has just been brought into focus during the past decade.  The United Nations and the World Health Organization are very concerned about the effect of toxic metals.  A recent article in the NEJM concluded that there is an inverse association between blood lead levels and IQ scores.  The chief author, Richard L. Canfield, Ph.D., stated in a subsequent interview, “There is no safe level of lead”.

The USA National Science Foundation’s Institute of Medicine recently stated in a meeting in Washington, D.C. that children vaccinated with thimerosal (ethyl-mercury) containing vaccines had a 27 Times (2,700%) greater chance to develop autism than those vaccinated with vaccines not containing the thimerosal. The USA Environmental Protection Agency and the Food and Drug Administration have released guidelines for restricting fish consumption based on the mercury content.  Peer reviewed medical journals, such as the New England Journal of Medicine, the Journal of the American Medical Association and others, have published multiple recent articles about lead and mercury, even low levels, affecting the entire vascular system, leading to hypertension, stroke, heart attack,  cardiomyopathy and renal failure. Other journals have shown lead and other heavy metals as a partial causation of macular degeneration as well as decreased intelligence, reading disability, gout, thyroid diseases, and other physiologic problems.  Archives of Internal Medicine published a 2002 study demonstrating that morbidity and mortality at all ages is directly influenced by lead levels.

Mercury in both organic and inorganic forms is neurotoxic. Mercury has been shown to be related to autism, Alzheimer’s disease, and cancer. Metallic mercury is readily converted under physiological conditions to substantially more toxic biologically active forms (e.g. methylmercury, dimethylmercury, mercuric sulfides and other mercurial compounds, etc.) and constitutes is a major public health risk. Biologically active mercury is considered by Nriagu and colleagues to be the most toxic of all the toxic minerals. Primary non-occupational sources of mercury exposure in humans include: medications and devices (including amalgams and vaccines), metallic mercury, mercurial fungicides, water, and recreational exposures including from ceramic glazes. Dietary sources are important, especially due to bio-concentration in fish and fowl, in ruminants and game of toxic minerals the ‘higher’ up the food chain the dietary choices.

Some 300 tons annually are added to the American ecosystem from all industrial and consumer sources. An additional ~ one kiloton of mercury is derived from trans-Atlantic dust storms that contain enough mercury to qualify as ‘mine able ore’ if only this dust could be trapped before it reaches the Southern United States and Caribbean Basin. This last environmental burden was unknown until as recently as 1990. This illustrates how substantial sources of ‘high toxic effects compounds’ can greatly enrich an environment in a toxicant without general awareness of the influx of that toxicant. These largely invisible depositions remain, in aggregate, just as potent as toxicants. The addition of 1,300 tons of mercury to the ecosystem equals 1.18 x 1015 micrograms (µg). Given that toxicity of mercury is usually measured in micrograms, there are about a quadrillion toxic doses of mercury released into the environment each year. With a population of 300 million (or 3 x 108) in the United States, this equates to 3.93 x 107 µg (39,000,000 µg) per citizen per year.

Similar in toxic potential to mercury, arsenic is a potent metabolic, hormonal, immune and gene toxin. Primary sources of arsenic exposure in humans are water, food, arsenical biocides and therapeutics. In aggregate, exposures to total arsenicals pose a significant human health risk above levels at or below 1 part per billion (ppb). The EPA recommended, in 2001, a 10 ppb arsenic maximum acceptable level in drinking water. The Institute of Medicine of the United States National Academy of Sciences expert panel on arsenic, recommends a drinking water standard of less than 1 ppb because the cancer promoting effects of even this level of arsenic in the water are deemed to be too high.

Arsenic, at 1 ppb in the drinking water, increases the risk of cancer by 1 in 1,000 in a life-time. Toxicologists are used to thinking about risks in terms of excess cancers per million people. Thus 1 ppb arsenic in the drinking water over a lifetime increases the risk of cancer by 1,000 per 1,000,000 people. This is above the historically accepted, conservative EPA risk threshold of one (1) extra cancer per million population. To many physicians and scientists, even this level of risk is unacceptable given that cost effective solutions are available. (Examples of this approach are given in the book Natural Capitalism and the report of the Department of Consumer Affairs of the State of California, titled Clean Your Room.)

With regard to lead, the evidence base of pervasive sub-acute toxicities is stronger and reviewed elsewhere. Cadmium and nickel are also potent toxicants with similar mechanisms of action to arsenic, including cardiovascular risk. Cadmium has been accepted by the International Agency for Research on Cancer as a Category 1 human carcinogen. Determination of immunotoxicity from toxic minerals such as mercury and arsenic depends upon mechanisms that are still being elucidated. Excess iron impairs nitric oxide action, causes free radical damage, and contributes to endothelial dysfunction in cardiovascular disease.

The public health burden due to toxic minerals is an acquired and reversible health risk for at least 80 million Americans. The human cost is a reduction of 8.8 years of life for the average person due to the effects of these toxicants. The direct disease care cost induced by toxic minerals are calculated to be in excess of $100 Billion annually (HCFA, 2000; Princeton University, 2001).  The public health risk from toxic minerals is yet greater due to suspected but not extensively defined or replicated synergies of mineral toxicities.

ASSESSMENT OF THE TOTAL BODY BURDEN OF TOXIC METALS:

Blood levels of heavy metal toxicity are not representative of tissue levels and frequently fail to identify significantly toxic tissue levels, i.e. levels that are causing tissue damage.  Determination of blood metal levels does not accurately reflect total body retention, but rather is more useful for assessment of recent or ongoing exposure, per the Agency for Toxic Substances and Disease Registry (ATSDR).  For instance, the relationship between blood lead levels and the quantity of lead excreted after EDTA Chelation is nonlinear in that arithmetic increases in blood lead are associated with exponential increases in lead excretion, and in adults with past exposure, the correlation between blood lead and chelatable lead is poor. 

Determining the total body heavy metal toxicity of any given toxic metal is not a straightforward matter, as tissues levels vary significantly and many factors complicate the assessment of a given individual.  For example, the pituitary is known to significantly concentrate toxic metals; brain, kidney, liver, lung, thyroid, and thymus tissue tested far higher levels than blood; and the adverse effects may only be revealed by long-term morbidity and mortality studies, such as the one published in Archives of Internal Medicine. The assumption that serum levels correlate with body burden has been clearly recognized as erroneous. There is no single test that adequately determines the total body burden of toxic metals. Metals are detoxified via the skin, hair, finger and toenails, stool and urine.  However, all tests for mineral excesses and deficiencies have their limitations, including hair, random urine collection, blood (serum or intracellular-red cell), and fecal testing.

Perhaps the optimal test of tissue burden currently available may be tissue biopsies of heart muscle, quadriceps muscle, liver, kidney, brain, and other organs, examined using x-ray florescence guided by electronic microscope to assess intracellular levels, or x-ray fluorescence of bones such as the patella.  However, these tests are obviously impractical and not widely available.

Blood levels of toxic metals show only recent or ongoing exposure still remaining in the blood.  Thirty days after exposure there is little evidence of any remaining toxic metal in the serum as it has been deposited to other tissues and partially excreted.  Random urine tests for toxic metals show only what is being detoxified via the kidneys from serum.  Intracellular (red blood cell) mineral analysis is one form of a “tissue” analysis but is also most significant for recent exposure (four to six months about 63 days for Me-Hg). Hair analysis for toxic metals, while controversial, has been widely accepted and validated for epidemiological studies by the World Health Organization and the EPA as being extremely useful and cost effective for identifying toxic metal exposures (when performed by laboratories with the appropriate expertise and quality control). Any of these tests may be used for screening, with the awareness that false negatives are common, in that other tissues may contain toxic levels not present in the sample screened.  These samples should be carefully collected and processed according to the instructions provided by the laboratory running the test, especially urine specimens since the volatility of mercury, for instance, can lead to a false negative if not properly handled.

The most valid, readily available test to show the total body burden of toxic metals is the provoked urine test, where urine is collected and analyzed following administration of EDTA or other chelating agents.   However, even a properly performed provoked urine specimen can significantly under-estimate the adverse effects on various individual tissues and or organs in the body.  Measured levels may increase following several treatments with chelating agents, indicating mobilization of tissue stores of heavy metals. An unpublished study demonstrated an average 147-fold increase over baseline lead excretion in healthy individuals receiving 3 gm of Ca EDTA.  A hair sample is much more practical, as it does not require a provoking agent.  As long as hair dyes have been avoided for about two months,  can give an indication of long term heavy metals exposure.  As 

As demonstrated, heavy metal toxicity can cause cellular damage and disease even in very small amounts. Given the growing evidence of correlation between heavy metal burden and disease states, any test showing heavy metals deserves to be treated, if only for preventative purposes. Ideal level of heavy metals in human tissue is zero, if we are to prevent the development of chronic illness.  Arbitrary threshold values to define “toxic” level proposed by conventional occupational medicine are not useful and may be harmful if the patient is left untreated. For example, urinary levels of mercury up to 50 ug/gm creatinine are considered to be within the “normal” range, despite the fact that neurological impairment has been reported for occupationally exposed subjects who had urinary mercury levels well below the W.H.O. standard.

Over the years, the recommended “reportable” blood levels for lead have been reduced repeatedly. As recently as 1990, the Connecticut Department of Health Services considered 25 mcg/dl as the “reportable” level. While the CDC currently considers greater than 10 mcg/dl as a level of concern, it is commonly acknowledged that “lead can have neurological and other negative effects on health at much lower levels of exposure.”  However, the principle that there are no safe levels of environmental toxins such as heavy metals is becoming more widely accepted.  For instance, the NEJM study cited above, which examined the effects on IQ of low levels of lead, caused the chief investigator to come to the conclusion that there is NO SAFE LEVEL OF LEAD.  A manuscript published in The Archives of Internal Medicine concludes that patients with lower levels of lead live longer with less morbidity and mortality from ALL diseases.  Bruce Fowler, PhD commented in a recent lecture  that the average American has a serum lead level of 3 mcg/dl. Longer-term studies have demonstrated the persistence of lead in the body over many years and that “exposure to lead in childhood is associated with deficits in central nervous system functioning that persist into young adulthood.” Furthermore, synergistic effects of heavy metal combinations could be more damaging than a single toxin.

One of the basic principles of integrative and environmental medicine is that every patient is unique, biochemically, genetically, and physiologically.  Individual tolerance to a given level of a toxic metal varies considerably, based on presence of other antagonistic metals and chemicals, and genetically determined detoxification capabilities. Some individuals may be more susceptible to toxic effects of a heavy metal or other chemical than others, for example:  patients with autism, multiple chemical sensitivity, chronic fatigue syndrome, genetic deficiency of glutathione production, aberrant homocysteine metabolism, and other genomic variations. For example, impaired glutathione synthetase activity due to a DNA translational error would impair detoxification competence for toxic minerals like mercury and arsenic. Acquired susceptibility, for example, impaired glutathione synthetase activity due to a RNA transcriptional error from haptenic binding and distortion of the mRNA complex or due to impaired and disordered protein synthesis due to low ATP production in the cellular mitochondria would have similar adverse effects. When zinc, selenomethionine, and magnesium are marginal or deficient, metallothionein loses functionality. Such individuals are sensitive and/or at high risk of toxic metals’ effects. On the other hand, certain individuals are dramatically affected by the mercury from their amalgams, or they are seriously affected by a vaccine injection with thimerosal (which typically contains 50-75 µg of mercury).  These individuals are not protected and are at relatively high risk.  These individuals will most likely be symptomatic and require treatment at lower levels of toxic metals than a healthy individual.

Heavy Metal Sources, Occupational Exposures, and Symptoms
Listed below are common sources of exposure, both occupational and in everyday life of the most common and most toxic of the heavy metals. While some of these sources are historical, it is important to remember that heavy metals often accumulate in bone, brain, connective tissue, muscle (including heart muscle), fat, kidneys, and other tissues.  They are not efficiently excreted by the body. Therefore, even exposures from the distant past may be relevant as well as small daily doses over years of exposure.  The list of signs and symptoms is not intended to be exclusive as chronic toxicity may cause a variety of the symptoms listed and other diseases as well.

Aluminum (Al)

SOURCES: Common sources of Aluminum include: beverage containers, aluminum pots and pans, foil, flatware and especially coffee pots; aluminum hydroxide anti-acid formulations; buffered aspirin, food additives, injectables, dialysis, some types of cosmetics, especially deodorants; some colloidal minerals and some herbs or herbal products.  Aluminum cookware is particularly of concern if acid foods are cooked such as tomato paste (contains salicylates). Aluminum beverage containers are especially concerning if they contain acidic substances such as tomato juice, carbonated drinks, or coffee, or fat soluble substances such as milk, oils, etc.  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 Al2O3 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.

ACTION: 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. Without intervention, aluminum accumulates continually in the body with the highest concentration occurring at old age or death.  Aluminum can cause pulmonary disease, Osteomalacia, neurotoxicity, and is suspected as a cause of Alzheimer’s disease

TESTING: A hair element test can be used to corroborate increased body burden of aluminum. If you suspect that you have an elevated aluminum level, it is important for you to know that a simple blood test will determine recent exposure to aluminum, but does not show long term exposure or total tissue levels of aluminum.  Here at Health Always you can order a hair test to show body load of aluminum, as well as other heavy metals. . Just click here or give us a call.

Antimony (Sb)

SOURCES: Food and smoking are the usual sources of Antimony (Sb). Thus cigarette smoke can externally contaminate hair, as well as contribute to uptake via inhalation. Gunpowder (ammunition) often contains Sb. Firearm enthusiasts often have elevated levels of Sb in hair. Other possible sources are textile industry (fire resistant fabrics), metal alloys, and some antihelminthic and antiprotozoal drugs. Sb is also used in the manufacture of paints, glass, ceramics, solder, batteries, bearing metals and semiconductors, rubberized goods and plastic. Confirming a report from New Zealand, analysis performed at Doctor’s Data Laboratory (DDI) revealed high levels of Sb and arsenic in sheepskin bedding designed for an infants crib. In addition, studies performed at DDI identified elevated levels of Sb in the hair of HAZMAT fire fighters who were previously wearing outdated flame retardant under garments.

SYMPTOMS:  Early signs of Sb excess include: fatigue, muscle weakness, myopathy, nausea, low back pain, headache, and metallic taste. Cardiac tissue Sb levels have been reported to be extremely high in patients with idiopathic dilated cardiomyopathy. Later symptoms include hemolytic anemia, myoglobinuria, hematuria and renal failure. Transdermal absorption can lead to “antimony spots” which resemble chicken pox. Respiratory tissue irritation may result from inhalation of Sb particles or dust. Elevated levels of Sb in scalp hair are common in patients with ADD/ADHD and autism. The clinical significance or physiological mechanism for increased uptake/retention of Sb in ADD/ADHD and autism are not known at this time.

ACTION: Sb is a nonessential element that is chemically similar to arsenic, but Sb compounds are generally less toxic than arsenic. Like arsenic, Sb has a high affinity for sulfhydryl groups on many enzymes. Sb is conjugated with glutathione and excreted in urine and feces. Therefore, excessive exposure to Sb has the potential to deplete intracellular glutathione pools.

TESTING: The preferred tissue for analysis of Antimony (Sb) exposure and body burden is hair analysis. Elevated hair Sb levels have been noted as long as a year after exposure.  Sb burden can be confirmed by urine elements analysis. Comparison of Sb levels pre and post provocation (DMPS, DMSA) permit differentiation between recent uptake and body stores.

Arsenic (As)

SOURCES: Contaminated foods (especially seafood), water or medications. Industrial sources of arsenic are: ore smelting/refining/processing plants, galvanizing, etching plating processes. Tailing from ore river bottoms near gold mining areas (past or present) may contain arsenic. 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 (arsenic pressure treated wood).

SYMPTOMS: fatigue, malaise, eczema or allergic-like dermatitis, and garlic-like breath. Increased salivation may occur.

ACTION: Chronic exposure to or ingestion of arsenic causes tissue levels to gradually increase as arsenic binds to sulfur, phosphorus and selenium. An important detrimental effect of arsenic is inactivation of Lipoic acid, a vitamin cofactor needed for metabolism of Pyruvate and alpha-ketoglutarate.

TESTING If you suspect that you have an elevated Arsenic level, it is important for you to know that a simple blood test is limited only determining recent exposure to arsenic. It will not measure long term exposure or total tissue levels of arsenic. Click here to choose one of Health Always hair tests.

Barium (Ba)

SOURCES: Exposure to Barium (Ba) which is used as a contrast agent during diagnostic medical tests such as “barium swallow”, “upper GI series”, “barium enema”, etc. Acutely high intake of soluble Barium salts (nitrates, sulfides, chlorides) can be toxic. 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. 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 (<5%) it can be very high in peanuts and peanut butter (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 (Health Canada 2005, www.atsdr.cdc.gov/toxprofiles/tp24-c6.pdf).

SYMPTOMS: Chronic exposure to Ba may be manifested by skeletal muscle and cardiac muscle stimulation, tingling in the extremities, and loss of tendon reflexes. Long-term retention of Barium can occur – granuloma of the traverse colon has been reported after diagnostic use of Barium sulfate.

ACTION: Barium has not been established to be an essential nutritional element. Elevated levels of Barium may interfere with calcium metabolism and potassium levels.

TESTING: A confirmatory test for elevated Barium is measurement of urine levels of Barium after a chelation provocation, and blood electrolytes should be checked as hypokalemia (low potassium) may be associated with elevated Barium. Barium levels  in water can be assessed with water testing. If you suspect that you have an elevated Barium level, it is important to determine total body load, not just a blood level. Click here for a simple hair test from Trace Elements that will give long term information on Barium.

Bismuth (Bi)

SOURCES: Sources of Bismuth (Bi) include: cosmetics (lipstick), Bi containing medications such as rantidine Bi-citrate, antacids (Pepto Bismol), pigments used in colored glass and ceramics, dental cement, and dry cell battery electrodes.

SYMPTOMS: Symptoms of moderate Bi toxicity include: constipation or bowel irregularity, foul breath, blue/black gum line, and malaise. High levels of Bi accumulation can result in nephrotoxicity (nephrosis, proteinuria) and neurotoxicity (tremor, memory loss, monoclonic jerks, dysarthria, dementia).

ACTION: Bi is a non-essential element of low toxicity. However, excessive intake of insoluble, inorganic Bi containing compounds can cause nephrotoxicity and encephalopathy. Absorption is dependent upon solubility of the Bi compound, with insoluble Bi excreted in the feces while soluble forms are excreted in the urine.

TESTING: Bismuth (Bi) levels are measured primarily for investigational purposes. Bi levels can be measured with a hair test for long term exposure from Trace Elements, or a urine elements analysis and can be used to corroborate Bi absorption for a period of days or a few weeks after the exposure. Dithiol chelating/complexing agents (DMPS, DMSA) markedly reduced Bi levels in liver and kidneys, and increased Bi in urine in animal studies (J. Lab. Clin. Med.; 119:529-537,1992).

Cadmium (Cd)

SOURCES: Smoking can be a source for as much as 0.1 mcg Cadmium per cigarette (HEW Pub. No. NIOSH 76-192, US Govt. Printing Ofc., 1976). 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 and dental technicians making fine tune adjustments (grinding) to dentures chair side. Cadmium free acrylic dentures are now available.

SYMPTOMS: Chronic manifestations associated with this degree of Cadmium excess include: hypertension, weight loss, microcytic-hypochromic anemia, lymphocytosis (excess white blood cells), proteinuria (protein in the urine) with wasting of beta2 microglobulin, emphysema and pulmonary fibrosis (if inhalation was a route of contamination), atherosclerosis, osteomalacia, osteoporosis, lumbar (lower back) pain, and peripheral neuropathy. Acute inhalation of Cadmium dusts, fumes or soluble salts may produce cough, pneumonitis and fatigue.

ACTION: Without intervention, the biological half-life of Cadmium in humans exceeds 20 years (Harrison’s Principles of Internal Medicine, 13th ed, pp 2463-64). Cd is insidiously toxic with chronic accumulations affecting kidney function, lungs, cardiovascular tissues, bone, and the peripheral nervous system. Manifestations of Cadmium toxicity may be lessened or delayed by an individual’s protective and detoxification capacities. Zinc and vitamin E are protective; metallothionein and glutathione bind Cadmium and help detoxify initially. Some medical authorities consider Cadmium to be a carcinogen for lung cancer (Harrison’s Principles, 13th ed, op. cit. pp 2463).

TESTING: If you suspect that you have an elevated Cadmium level, it is important for you to know that a simple blood test is limited in only determining recent exposure to Cadmium.  It will not show long term exposure or total tissue levels of Cadmium.  Cadmium can be tested with a simple hair analysis here at Health Always. 

Cesium (Cs)

SOURCES: 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 133 Cesium (the radioactive isotopes 134 Cesium and 137 Cesium are usually not measured or reported). Cesium is not used extensively in industry but some uses are in the production of photoelectric cells, vacuum tubes, spectrographic instruments, scintillation counters and various optical and detecting devices. In biochemistry, cesium chloride is used to extract DNA from cells. The isotope 137 Cesium is used in radiation therapy for certain types of cancer. Other medical uses of Cesium are monitoring left ventricular function with 137 Cesium iodide probes and monitoring pulmonary (lung) endothelial permeability with 137 Cesium iodide crystal mini-detectors. Environmental contamination by 137 Cesium as a result of radioactive fallout could be a major concern, however, little data is available on this matter.

SYMPTOMS: Target organs of Cesium toxicity are the liver, intestine, heart, and kidneys. Cesium may cause epileptic seizures because it can share the same receptor as the inhibitory neurotransmitter amino acid glycine.

ACTION: 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 Cesium in humans ranges from 15 days in infants to 100-150 days in adults. Physiological effects of Cesium include ventricular arrhythmias and displacement of potassium from muscle and erythrocytes. Cesium can have significant effects on both the central and peripheral nervous systems. Cesium can interfere with active ion transport by blocking potassium channels and also can interfere with lipid metabolism. Cesium may modify plasma membrane integrity, alter cytoplasmic components and cause cell damage. It is unlikely that children or adults would be exposed to enough 133 Cesium to experience any health effects that could be related to the stable cesium itself. Animals given very large doses of cesium compounds have shown changes in behavior, such as increased activity or decreased activity, but it is highly unlikely that a human would be exposed to enough stable cesium to cause similar effects.

TESTING: Cesium can be measured with a Doctors Data hair Toxic Elements test here at Health Always or provoked urine analysis. It is emphasized that cesium measured is 133 Cesium, not 137 Cesium.  Blood testing is not an accurate indicators of tissue levels of Cesium. 

Gadolinium (Gd)

SOURCES: Gadolinium is one of the most abundant “rare-earth” elements but is never found as a free element in nature. Gadolinium has no known biological role in humans.  Gadolinium is often used in alloys, improving the workability and resistance of metals (e.g. chromium, iron). Other technical uses include the phosphors of color cathode-ray television tubes and in making magnets and electronic components such as recording heads for video recorders and in the manufacture of compact disks and computer memory.  In medicine Gadolinium, chelated with diethylenetriaminepentaacetic acid (DTPA), is used as a non-radioactive contrasting agent in magnetic resonance imaging (MRI) and has a half life in blood of about 90 minutes. It is also used in control rods for nuclear reactors and power plants, in making garnets for microwave applications.

SYMPTOMS: If exposure to high enough doses and/or if absorption does occur, symptoms of acute parenteral toxicity may develop, including abdominal cramps, diarrhea, lethargy, muscular spasms, and even eventual death due to respiratory collapse. Gadolinium salts can cause irritation of the skin and eyes and are suspected to be possible carcinogens.  As reported by Perazella (2009) Gadolinium-based contrast (GBC) agents have been linked on occasion with a rare systemic fibrosing condition called nephrogenic systemic fibrosis (NSF) and their use in patients with advanced kidney disease should be avoided.

ACTION: Toxicity due to Gadolinium is rare due to its poor gastrointestinal absorption (it is suspected that very little Gadolinium is absorbed from the gastrointestinal tract (<0.05%), similar to other rare earth metals) and there is no information on the tissue distribution of Gadolinium. Most likely Gadolinium is excreted slowly through the fecal and urinary routes.

TESTING: Gadolinium levels can be tested using the Doctors Data Hair Toxic Elements Test, a Doctors Data Stool Gadolinium Toxic Elements Test or a provocative Doctors Data Urine Toxic Elements Test.  In vitro evidence suggests that EDTA may effectively bind to Gadolinium therefore EDTA would be a good choice as a provocator/chelator for Gadolinium. Blood testing is not an accurate indicators of tissue levels of Gadolinium.  Here at Health Always we think a Doctors Data Stool Gadolinum is the best test. You can click here for the stool Gadolium test.

Lead (Pb)

SOURCES: Most common sources of Lead include old lead-pigment paints, lead acid 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, gunshot wounds, and leaded joints and/or pipes 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. Transdermal (skin) exposure is slight.  Inhalation has decreased significantly with almost universal use of non-leaded automobile fuel.

SYMPTOMS:  In children, developmental disorders and behavior problems may occur at relatively low levels such as: loss of IQ, hearing loss, and 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 blood hemoglobin synthesis, colic, frank anemia, tremors, nephrotoxic effects with impaired kidney excretion of uric acid, neuropathy and encephalopathy (altered brain function and structure. It is caused by diffuse brain disease.

ACTION: 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. Lead accumulates extensively in bone and inhibits formation of heme and hemoglobin in erythroid precursor cells (blood cells).  Bone lead can be stored in bones for many years and 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. At relatively low levels, lead can participate in synergistic toxicity with other toxic elements (e.g. cadmium, mercury).

TESTING: If you suspect that you have an elevated Lead level, it is important for you to know that whole blood analysis can reflect only recent exposures and does not correlate well with total body burden of lead. Lead can be measured at Health Always with a simple hair test by Trace Elements, Analytical Research, Doctors Data or can be done by a provoked Doctors Data Urine Toxic Elements Test

Mercury (Hg)

SOURCES: Mercury is commonly used in: dental amalgams, vaccines, explosive detonators; in pure liquid form for thermometers, barometers, and laboratory equipment; batteries and electrodes (“calomel”); and in fungicides and pesticides. The fungicide/pesticide use of mercury has declined due to environmental concerns, but mercury residues persist from past use. 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, with about three-quarters of this (typically) as Methylmercury.

SYMPTOMS: Symptoms associated with 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 system dysfunction.  Advanced disease processes from mercury toxicity include: tremors and incoordination, anemia, psychoses, manic behaviors, possibly autoimmune disorders, kidney dysfunction or failure.

ACTION: Effects of excessive mercury can depend on many factors: the chemical form of absorbed Hg and its transport in body tissues, presence of other synergistic toxics (lead and 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).

TESTING: If you suspect that you have elevated Mercury levels, it is important for you to know that blood analysis can reflect only recent exposures and does not correlate well with total body burden of Mercury. Mercury can be tested with a hair analysis or provoked urine test

Nickel (Ni)

SOURCES: Sources of nickel are numerous and include the following: Cigarettes (2 to 6 mcg Nickel per average cigarette), Diesel exhaust (particulates may contain up to 10 mg/gram Nickel), Foods, especially: cocoa, chocolate, soya products, nuts, and hydrogenated oils, Nickel-cadmium batteries, Nonprecious, 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. 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.

SYMPTOMS: Most clinically observed nickel contaminations are manifested as dermatosis – contact dermatitis, atopic dermatitis or multiple allergic sensitivities. However, Nickel hypersensitizes the immune system causing hyperallergenic responses to many different substances.  Nickel sensitivity is observed to be three to five times more frequent in women than in men.

ACTION: Urinary excretion of nickel bound to cysteinyl or thiol compounds (such as glutathione) or to amino acids (histidine, aspartic acid, arginine) is the predominant mode of excretion. Because Nickel can displace zinc from binding sites on enzymes, it can have inhibiting or activating effects on such enzymes.

TESTING: Ni can be measured with a hair analysis or a provocative urine collection.  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. If you suspect that you have an elevated Nickel level, it is important to determine total body load, not just a blood level.

Platinum (Pt)

SOURCES: Platinum exposure can come from chemotherapy treatments (cis-platinum).  Since it is a relatively rare element, most Platinum exposures are of occupational origin. Industrial workers exposed to Platinum showed higher concentrations in the blood and urine (> 2 μg Platinum/24 hours) in comparison to non-exposed workers. In recent years, there may have been a slight increase in environmental Platinum due to the use of Platinum as a catalyst in automobile exhaust converters. Platinum is a byproduct of copper refining and used as an alloy in dental and orthopedic materials.

SYMPTOMS: Symptoms of excess exposure to Platinum include: dermatitis, irritation of mucus membranes, shortness of breath and wheezing (for inhaled Platinum dusts or salts), development of chronic allergic reactions (“platinosis”), nephrosis, and immune system suppression (from Platinum diamine salts).Platinum containing drugs, such as cisplatin and carboplatin, are used as chemotherapeutic agents. Such drugs are extremely toxic and cause nephrotoxicity with associated magnesium wasting and hypomagnesaemia (low magnesium), myelosuppression, inner ear toxicity, and neurotoxicity. 

ACTION: Platinum is poorly absorbed in the gut but may be absorbed via inhalation. Platinum is a nonessential element that can be found at elevated concentrations in urine with excessive exposure.

TESTING: Platinum can be measured with a hair analysis or provoked urine collection.  Urinary Platinum can be significantly elevated for patients that have received the Platinum containing chemotherapeutic agents. If you suspect that you have an elevated Platinum level, it is important to determine total body load.

Thallium (Tl)

SOURCES: Environmental and occupational sources of thallium include: contaminated drinking water, airborne plumes or waste streams from lead and zinc smelters, 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.

SYMPTOMS: Symptoms of thallium contamination are often delayed. Early signs of chronic, low-level contamination may include: mental confusion, fatigue, and peripheral neurological signs: tingling sensations, muscle aches, tremors and ataxia (loss of voluntary muscle control, resulting in lack of balance and coordination ). After 3 to 4 weeks, diffuse hair loss with sparing of pubic and body hair and a decreased density of eye- brows usually occurs. Increased salivation occurs less commonly. Longer term or residual symptoms may include: hair loss, ataxia, tremor, memory loss, weight loss, protein in the urine, and possibly psychoses.  Ophthalmologic neuritis and strabismus may be presented. Other clinical findings that would be consistent are: albuminuria, EEG with diffuse abnormalities, hypertension, and elevated urine creatinine phosphokinase (CPK).

ACTION: Thallium can be assimilated trans dermally (through the skin), by inhalation, or by oral ingestion. Both valence states can have harmful effects: Thallium+1 may displace potassium from binding sites and influences enzyme activities; Thallium+3 affects RNA and protein synthesis. Thallium leaves blood plasma rapidly and is readily transported between body organs and tissues. It can be deposited in kidneys, pancreas, spleen, liver, lungs, muscles, neurons and brain.

TESTING: Blood is not a reliable indicator of thallium status. Hair (pubic or scalp) element analysis from Trace Elements is an excellent corroborative test for suspected thallium excess. If you suspect that you have an elevated Thallium level, it is important to determine long term total body load.

Thorium (Th)

SOURCES: Thorium has about the same abundance in the earth as does lead and is encountered in mining activities for titanium and rare earth elements. Commercially, thorium is used in incandescent gas lantern mantles, refractory materials (thorium melts at 3300 degrees C), and as a coating for tungsten in electronic applications. It is present in nuclear fuels (Uranium 235 decays to Thorium 231). Thorium may also be present in tungsten-inert-gas (“TIG”) welding electrodes.

SYMPTOMS: Leukemia, granulomas, and malignant liver tumors. There is a literature report for abnormal lymphocytes in animals following a thorium challenge.

ACTION: Thorium is considered mildly toxic for two reasons, low-level radioactivity and slight biochemical toxicity. Thorium is a radioactive element having 7 isotopes with half lives that exceed one hour. Thorium 232 constitutes 99% of the naturally occurring thorium and this is the isotope measured. Thorium 232 has a half-life of 1.4×10 to the tenth years. It decays by alpha emission to produce radon, Radon 228. In turn Radon 228 (half life 6.7 years) decays to other radioactive isotopes, eventually reaching lead. This radioactive decay process produces alpha, beta and gamma emissions. Several decades ago, a thoria (Thorium O2) suspension (“Thorotrast”) was used diagnostically as a radiopaque agent. After a long period of latency, an unusually high proportion of individuals who received this procedure have developed leukemia, granulomas, and malignant liver tumors. These are slowly-developed diseases often with 20-30 year periods before onset or definite diagnosis. The biochemical effects of thorium are mild. Reactive thorium salts at high levels may inhibit amylase and phosphatase enzymes. Most orally ingested thorium, if not excreted in urine, binds to bone tissue where it has a long biological half-life (years).

TESTING: Because most thorium salts are excreted via urine, a high urine thorium level indicates exposure and probably increased body burden of this element.  Thorium can also be measured here at Health Always with a hair analysis from Doctors Data. If you suspect that you have an elevated Thorium level, it is important to determine total body load.

Tin (Sn)

SOURCES: 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 have 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).

SYMPTOMS: Mildly elevated levels of Tin in urine may reflect sporadic dietary intake and excretion; there may be no associated symptoms.   Early signs of chronic organic Tin excess can be: reduced sense of smell, headaches, fatigue and muscle aches, ataxia and vertigo. Hyperglycemia and glycosuria 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.

ACTION: 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 trans dermally and can cause degeneration of myelin.

TESTING: Tin can be measured with a hair analysis by Trace Elements or a provoked urine collection by Doctors Data. 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). Tin is commonly elevated in urine from autistic patients following administration of EDTA, DMSA or DMPS. If you suspect that you have an elevated Tin level, it is important to determine total body load.

Tungsten (W)

SOURCES: Tungsten is a silvery-white lustrous element usually obtained as a grey powder and is mainly utilized as tungsten carbide in metallurgy, mining and petroleum industries. Calcium and magnesium tungstates are widely used as filaments for electric lamps, electron tubes and television tubes. Since Tungsten has the highest melting point of all metals it is used for high-speed and hot-worked steels. Other sources of W include catalysts and reagents in biological analysis, fire and waterproof materials, and industrial lubrifications.

ACTION: The relationship between the levels of Tungsten (W) in hair and exposure/body burden has yet to be established. 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 appears to have an antagonistic relationship to Molybdenum decreasing hepatic Molybdenum concentration and reducing the effectiveness of sulfite and xanthine oxidases.

TESTING: Tungsten can be measured with a hair analysis or a provoked urine collection. Acute environmental exposures have been detected in hair (4.26 μg/g) up to two months after ingestion of a tungsten containing beverage. Other limited data suggests mean values of .015 μg/g in pubic hair for non-exposed persons and 5.2 μg/g in pubic hair for exposed persons. 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. 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. Confirmatory tests for W accumulation and exposure, respectively, are (DMPS/DMSA) urine provocation or Fecal Elements testing.

If you suspect that you have an elevated tungsten level, it is important for you to know that a simple blood test will determine recent exposure to tungsten, but does not show long term exposure or total tissue levels through a hair analysis from Trace Elements.

Uranium (Ur)

SOURCES: 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.

SYMPTOMS: Uranium is nephrotoxic, causing damage to the glomeruli and proximal tubules of the kidneys. An early sign of Uranium excess is general fatigue. Kidney damage is reflected by excess protein, amino acids, or glucose in the urine. Albuminuria and urinary catalase are findings consistent with Uranium excess.

ACTION: Uranium is a radioactive element having 10 isotopes with half lives that exceed one hour. Uranium 238 constitutes about 99% of the naturally-occurring Uranium and this is the isotope measured. Uranium 238 has a half life of 4.5 X 10 to the ninth years. Uranium 238 decays by alpha emission to produce thorium, Thorium 234, 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 Uranium 235) does pose a health hazard. The measured result (Uranium 238) does not reflect or imply exposure to enriched Uranium. The major concern for (natural) Uranium excess is chemical toxicity rather than radiological. Uranium is a chemically-reactive element, has four valences (3,4,5 or 6), and may combine with: carbonate, phosphate, citrate, pyruvate, malate, lactate, etc. in body tissues. When not excreted in urine, Uranium may accumulate in the kidneys, spleen, liver, and in bone (substituting for calcium in hydroxyapatite).

TESTING: Elevated hair Uranium is a confirmatory finding by Trace Elements; whole blood and fecal analyses may corroborate recent or ongoing exposures. If you suspect that you have an elevated Uranium level, it is important to determine your body load.

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