Hair is a site of excretion for essential, nonessential and potentially toxic elements. In general, the amount of an element that is irreversibly incorporated into growing hair is proportional to the level of the element in other body tissues. Therefore, hair analysis may provide an indirect screening test for physiological excess, deficiency or maldistribution of elements in the body. Clinical research indicates that hair levels of specific elements, particularly potentially toxic elements such as cadmium, mercury, lead and arsenic, are highly correlated with pathological disorders. For such elements, levels in hair may be more indicative of body stores than the levels in blood and urine.

 

All screening tests have limitations that must be taken into consideration. Scalp hair is vulnerable to external contamination by water, hair treatments and products. Likewise, some hair treatments (e.g. permanent solutions, dyes, and bleach) can strip hair of minerals resulting in falsely low values. There are differences in the results among laboratory facilities. In a JAMA article in January 2001, hair samples were sent to several labs with widely variable results. The results depend on the technique used, the preparation of the hair sample but the lab, and good quality controls. Careful consideration of the limitations must be made in the interpretation of results of hair analysis. The data that hair analysis do provide should be considered in conjunction with symptoms, diet analysis, occupation and lifestyle, physical examination and the results of other laboratory tests. There is virtually no situation that hair analysis alone is diagnostic. Using the hair analysis for treatment based solely on the results of this screening test is not prudent. However, accepting these limitations, hair analysis may provide useful insights into the biochemical and hormonal condition of the body.

 

Aluminum (Al) hair levels reflect past or chronic exposure to this element. The level in hair is a reliable indicator of assimilation of this element, provided that hair preparations or scissors have not added aluminum to the hair. Aluminum is a nonessential element that can be toxic if excessively assimilated into cells. Hair is easily contaminated with aluminum from hair treatment and possibly by wash water if it is high in Al content.

 

Aluminum can impair cellular energy transfer processes by interfering with phosphate and ATP metabolism. Excess aluminum can inhibit the formation of alpha-keto glutarate and result in toxic levels of ammonia in tissues. Aluminum can bond to phosphorylated bases on DNA and disrupt protein synthesis and catabolism. Neuronal cells are susceptible to long term accumulation of aluminum, and Al bonding to phosphate can inhibit normal catabolism of neuronal filaments in the CNS. Correlation of elevated Al with degenerative dementia and Alzheimer’s disease has been documented. Excessive dietary aluminum can also form insoluble aluminum phosphates in the GI tract and may lead to hypophosphatemia.

 

Symptoms of elevated Al may include fatigue, headache and signs of phosphate depletion. However, low level Al exposures may not provoke any immediate symptoms. Aluminum excess should be considered when symptoms of presenile dementia or Alzheimer’s disease are observed. Hair aluminum is commonly elevated in children and adults with low zinc and behavioral/learning disorders such as ADD, ADHD and autism. Individuals with renal problems or on renal dialysis may have elevated aluminum. Al has neurotoxic effects at high levels, but low levels of accumulation may not illicit immediate symptoms.

 

Possible sources of Al include some antacid medications, Al cookware, baking powder, processed cheese, drinking water, and antiperspirant components that may be absorbed. Many colloidal mineral products have very high levels of aluminum according to analyses performed at DDI laboratories. In fact, an independent lab tested five major brands of colloidal minerals and each showed a substantial level of aluminum. In two of the five samples, aluminum or a toxic metal was the highest concentration of any of the minerals found!

 

Al has been reported to be effectively complexed and excreted with silicon, a complex of malic acid and magnesium, and (DDI clients), and acetoacetic acid (Deitrich Klinghardt, M.D.). No other nutrients beside magnesium and silicon have protective effects against aluminum toxicity.

 

A urine test can be used to corroborate aluminum exposure.

 

Antimony (Sb) hair levels reflect past or chronic skin exposure, inhalation or ingestion of this element. Hair is a preferred tissue for analysis of antimony exposure and body burden. Elevated hair antimony levels have been noted as long as a year after exposure.

 

Antimony is a nonessential element considered by some to be more toxic than arsenic, but others say it is less toxic. Like arsenic, Antimony has a high affinity for sulfhydryl groups on many enzymes. Antimony is conjugated with glutathione and excreted in urine and feces. Therefore, excessive exposure to antimony has the potential to deplete intracellular glutathione pools. Antimony’s deposition in body tissues and its detrimental effects depend upon the oxidation state of the element. Antimony+3 affects liver functions, impairs enzymes, and may interfere with sulfur chemistry. If antimony impairs phosphofructokinase (PFK), then purine metabolism may be disrupted, resulting in elevated blood and/or urine levels of hypoxanthine, uric acid and possibly ammonia. Antimony+5 deposits in bone, kidney, and in organs of the endocrine system. “Antimony spots” may result from skin contact with antimony salts and vapors. Symptoms can be variable, including fatigue, myopathy (muscle aches and inflammation), hypotension, angina and immune dysregulation.

 

Early signs of Antimony excess include: fatigue, muscle weakness, myopathy, nausea, low back pain, headache, and metallic taste. Later symptoms include hemolytic anemia, myoglobinuria, hematuria and renal failure. Trans-dermal absorption can lead to “antimony spots” which resemble chicken pox. Respiratory tissue irritation may result from inhalation of antimony particles or dust.

 

Food and smoking are the usual sources of antimony. Thus cigarette smoke can externally contaminate hair, as well as contribute to uptake via inhalation. Gunpowder (ammunition) often contains antimony. Firearm enthusiasts often have elevated levels of antimony in hair. Other possible sources are textile industry, metal alloys, and some anti-helminthic and anti-protozoal drugs. Antimony is also used in the manufacture of paints, glass, ceramics, solder, batteries, bearing metals and semiconductors.

 

A confirmatory test for recent or current exposure is the measurement of Antimony in the urine.

 

Arsenic (As) hair levels correlate with past or chronic exposure or ingestion. Excessive arsenic in cells can inhibit mitochondrial processes, especially those related to cofactor activity of lipoic acid. Typical early symptoms of As excess include fatigue, dermatitis, increased salivation and possibly peripheral paresthesias with tingling or numbness. More advanced symptoms or chronic exposures can lead to muscular weakness, hair loss, hypopigmentation of skin, anemia with hemolysis and neuronal degeneration. Even at low levels, arsenic may cause digestive problems, fatigue and skin rashes. See our web page on arsenic for more information.

 

Bismuth (Bi) hair levels has not correlated bismuth exposure with hair bismuth levels, therefore, hair bismuth levels are measured primarily for investigational purposes. Bismuth is a non-essential element of low toxicity. However, excessive intake of insoluble, inorganic bismuth containing compounds can cause nephrotoxicity and encephalopathy. Absorption is dependent upon solubility of the bismuth compound, with insoluble bismuth excreted in the feces while soluble forms are excreted in the urine. Sources of Bismuth include: cosmetics (lipstick), Bismuth containing medications such as ranitidine Bismuth-citrate, antacids (Pepto Bismol), pigments used in colored glass and ceramics, dental cement, and dry cell battery electrodes.

 

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

 

Urine elements analysis can be used to corroborate bismuth absorption for a period of days or a few weeks after the exposure.

 

Dithiol chelating/complexing agents (DMPS, DMSA) markedly reduced bismuth levels in liver and kidneys, and increased Bismuth in urine in animal studies (J. Lab. Clin. Med.; 119:529-537,1992). In the same study, EDTA increased brain bismuth levels.

 

Cadmium (Cd) hair levels correlate with body burden and with past or chronic ingestion of this element. Cadmium is considered a toxic heavy metal with no known metabolic function in the body. Cadmium exerts toxic effects by inhibiting sulfur-bearing enzymes and by displacing enzyme bound zinc or copper. In cells, cadmium can inhibit gluconeogenesis and phosphorylation processes. Cadmium’s deleterious effects may be slow and not recognized for years before manifestations are apparent. Excessive body burden of cadmium is associated with high blood pressure (hypertension) and impaired renal transport with proteinuria and urinary wasting of beta 2-microglobulin. Chronic Cd excess can lead to microcytic, hypochromic anemia. Cadmium can also adversely affect heart, arterial walls, bone and testes. Cadmium excess is also commonly associated with fatigue, weight loss, osteomalacia, and lumbar pain. Inhalation of cadmium salts or vapors may produce emphysema. In children, elevated Cd has been correlated with lowered IQ.

 

According to Science News, trace amounts of cadmium can mimic estrogen’s effects on cells and alter the reproductive system of females (Nature Medicine 08/03). The implications for hormone related malignancy such as breast cancer are even more concerning because cadmium has been shown to disrupt DNA repair (Nature Genetics 07/03).

 

Smoking and high sugar diets appear to increase Cd levels. Cadmium is found in varying amounts in foods, from .04 pg/g for some fruits to 3-5 pg/g in some oysters and anchovies. Cigarette smoking significantly increases Cd intake. Refined carbohydrates have very little zinc in relation to the Cadmium. Cadmium absorption is reduced by zinc, calcium, and selenium.

 

If hair zinc is not abnormal, external contamination from permanent solutions, dyes, bleach, and some hair sprays may have caused the elevated hair cadmium level. A confirming test for elevated body burden of cadmium is urine analysis following administration of an appropriate chelating agent such as EDTA or sulfhydryl agents (DMSA, D-Penicillamine, DMPS).

 

Lead (Pb) hair levels correlate with body tissue deposition levels (bone, aorta, liver, kidney) and also correlate with blood levels if the exposure is periodic or chronic. At the cellular level, lead interferes with membrane transport processes and with enzyme functions because it is able to bond to many chemically active sites. The interaction of lead with sulfhydryl (SH) sites causes most of the toxic effects which include impaired heme synthesis, inhibition of erythrocyte Na/K ATPase, diminished RBC glutathione, shortened RBC life span, impaired synthesis of RNA, DNA and protein and impaired metabolism of vitamin D. Lead may also affect the body’s ability to utilize the essential elements calcium, magnesium, and zinc. Lead is toxic to nerves and at moderate levels of body burden; lead may have adverse effects on memory, cognitive function, and nerve conduction. Children with hair Pb levels greater than 1 pg/g have been reported to have a higher incidence of hyperactivity than those with less than 1 pg/g. Children with hair Pb levels above 3 pg/g have been reported to have more learning problems than those with less than 3 pg/g. Lead is also toxic to kidneys resulting in disordered renal transport with uricemia (possibly gout), hyperaminoaciduria, glycosuria and phosphaturia. Excess body burden of lead is often associated with fatigue, headaches, loss of appetite, insomnia, nervousness, anemia, weight loss, decreased nerve conduction and possibly motor neuron disorders.

 

Hair is sensitive to external contamination with certain hair preparations, especially dyes and darkening agents, e.g. “Grecian Formula.” Although these agents can cause contamination, some of the lead is absorbed into body burden. Hair levels of iron, boron, calcium, and zinc are often concomitantly elevated with lead burden.

 

Lead exposure includes welding, old leaded paint (chips/dust), drinking water, some fertilizers, industrial pollution, lead-glazed pottery, and newsprint.

 

Detoxification therapy by means of chelation results in transient increases in hair lead. Eventually, the hair Pb level will normalize after detoxification is complete.

 

Confirmatory tests for lead excess are urine elements analysis following provocation with intravenous EDTA, DMPS, or oral DMSA. Whole blood analysis for lead only reflects recent or ongoing exposures and may not correlate with total body burden. Increased blood or urine protoporphyrins is a finding consistent with Pb excess, but may occur with other toxic elements as well.

 

Zinc, iron, calcium, vitamin C, vitamin E, and sulfur amino acids have protective effects.

 

Nickel (Ni) hair levels correlate with chronic exposures and ingestion. Hair is sensitive to external contamination with Ni. Some shampoos and many hair perm dye bleach products place Ni into the hair. In blood, Ni binds to albumin, globulins and amino acids, and is deposited in leukocytes. In cells, it binds to mitochondrial and cytosolic proteins. In so doing, it can displace zinc and copper, thereby activating, inhibiting, or dysregulating enzymes. A nickel exposure may hypersensitize the immune system, resulting in inflammatory responses to many environmental substances to which there was formerly little or no response. Possible symptoms of nickel excess include panallergy with rhinitis, sinusitis, conjunctivitis and asthma. Other symptoms may include vertigo, weakness and fatigue, nausea and headache. Nickel contact allergy (“nickel itch”) or contact dermatitis is not necessarily reflected by elevated hair Ni.

 

Tin hair levels correlate with past or chronic exposure. Inorganic tin is mildly toxic and may impair liver function by inhibition of the P-450 mixed function oxidase enzyme system. Hence, tin can have a synergistic effect of rendering organic chemical xenobiotics or drugs more difficult to detoxify.

 

Organic tin compounds – dimethyl tin, dialkyl tin, triphenyl tin – are biocidal and can be severely toxic. Exposure to organic tin compounds may produce headache, muscle ataxia, general fatigue, vertigo and reduced sense of smell. Kidney damage may also result. Erythrocyte hemolysis, anemia and subnormal lymphocytes may occur, causing immune dysfunction. Other conditions include hyperglycemia, lesions in testes and ovaries, and inflammation or congestion of binary ducts.

 

Uranium (U) hair levels reflect past or chronic ingestion. Most exposure comes from natural uranium in ground and drinking water. The U238 isotope of uranium is more than 99% of naturally occurring uranium. Radioactivity danger from trace quantities of natural uranium is slight because of its very long half life (billions of years). The finding of elevated U238 in this test does not imply nor does it rule out exposure to enriched uranium fuel (U235) or to other radioactive isotopes that may be radiation hazards. The major toxicological concern of U238 excess is biochemical rather than radiochemical. Uranyl cations bind tenaciously to protein, nucleotides, and bone, where it substitutes for calcium. Uranium is a reactive element that is able to combine with and affect the metabolisms of: lactate, citrate, pyruvate, carbonate and phosphate. Kidney and bone are the primary sites of uranium accumulation, but it also deposits in the liver and spleen. The primary symptom of low level chronic uranium excess (hair levels >0.5 ppm) is chronic fatigue. Possible conditions from more severe uranium contamination include damage to kidney glomeruli with disordered renal transport (proteinuria, albuminuria, and hyperaminoaciduria) and hematopoiesis in bone marrow. Published data are sparse, but there appears to be a correlation between U exposure, kidney damage and all forms of cancer.

 

Although hair is sensitive to external contamination with Uranium by shampoos or hair products, the levels of Uranium in hair usually reflect levels of uranium in other tissues.

 

Uranium is a nonessential element that is very abundant in rock, particularly granite. It is present at widely varying levels in ground (drinking) water, root vegetables, and present in high phosphate fertilizers. Other sources of include ceramics, some colored glass, many household products (uranyl acetate) and tailings from uranium mines.

 

Because uranium is rapidly cleared from blood and deposited in tissues, urine analysis rather than blood analysis may need to be performed to confirm excess exposure to uranium.

 

Calcium (Ca) hair levels correlate with long term dietary intake, absorption from the GI tract and retention. The hair calcium level does not necessarily reflect current serum calcium or calcium ion concentrations and may not have a linear or direct relationship with tissue deposition or bone density. The reported level of hair Ca may reflect external contamination from hair preparations, which contribute to the measured level. Hair is not particularly valuable for assessing calcium in my opinion. It may be useful as part of ratios, however.

 

Copper (Cu) hair levels may be indicative of excess copper in the body. Medical conditions that may be associated with excess copper include: biliary obstruction (reduced ability to excrete Cu), liver disease (hepatitis or cirrhosis), and renal dysfunction. Symptoms associated with excess Cu accumulation are muscle and joint pain, depression, irritability, tremor, hemolytic anemia, learning disabilities, and behavioral disorders. See my webpage on copper-zinc imbalances.

 

However, it is important first to rule out contamination from permanent solutions, dyes, bleaches, swimming pool/hot tub water, and washing hair in acidic water carried through copper pipes. In the case of contamination from hair preparations, other elements (aluminum, silver, nickel, titanium) are usually also elevated.

 

Sources of excessive copper include contaminated food or drinking water, excessive Cu supplementation, and occupational or environmental exposures. Insufficient intake of competitively absorbed elements such as zinc or molybdenum can lead to, or worsen Cu excess.

 

Confirmatory tests for copper excess are a comparison of copper in pre vs. post provocation (D-Penicillamine, DMPS) urine elements tests and a whole blood elements analysis. Ceruloplasmin can also be useful in copper retention syndromes.

 

Zinc (Zn) hair levels when low correlate with low tissue levels and possible inadequate zinc function. Zinc is an essential element that is required in numerous biochemical processes including protein, nucleic acid and energy metabolism. Zinc is an obligatory co-factor for numerous enzymes including alcohol dehydrogenase, carbonic anhydrase, and superoxide dismutase. Low hair zinc may be the result of poor dietary intake, digestive dysfunction, malabsorption syndromes, chronic diarrhea, or excessive tissue levels of copper or iron.

 

Many possible dysfunctional conditions may be associated with zinc inadequacy. These include impaired taste or smell, poor night vision, fatigue, skin disease (dermatoses), sexual dysfunction, growth retardation in children and (partial) alopecia. Conditions which have been associated with low hair zinc include maldigestion, celiac disease, chronic hepatitis, sickle cell anemia, kidney dialysis, cancer, anorexia, obesity and Wilson’s disease. Low hair zinc has also been noted in premature birth babies and their mothers, as well as mothers of infants with spina bifida. Hair zinc is commonly low in diabetics, and in association with ADD/ADHD and autism (DDI observation). Reported symptoms of zinc deficiency include: fatigue, apathy, hypochlorhydria, decreased vision and dysgeusia, anorexia, anemia, dermatitis, weak/brittle nails and hair, white spots on nails, alopecia, impaired would healing, sexual dysfunction (males), and hypogonadism. See my webpages on zinc and pyroluria for more information.

 

Low hair zinc is very likely to be indicative of low zinc in whole blood, red blood cells, and other tissues. Hair analysis is a good screen for provided that the hair sample has not been chemically treated (permanent solutions, dyes, and bleaches); such hair treatments can significantly lower the level of zinc in hair.

 

Zinc competes for absorption with copper and iron. Cadmium, lead and mercury are potent zinc antagonists. Zinc deficiency can be caused by malabsorption, chelating agents, poor diet, excessive use of alcohol or diuretics, metabolic disorder of metallothionein metabolism, surgery, and burns. Hair levels of Zn (copper and selenium) were decreased in human subjects after switching from a mixed to a lactovegetarian diet (Am. J. Clin. Nutr.; 55:885-90,1992).

 

Other laboratory tests to confirm zinc status are whole blood or packed red blood cell elements analysis, and urine amino acid analysis (Zn dependent peptidase activity).

 

Manganese (Mn) hair levels may reflect external contamination from hair preparations that contribute to the measured level.

 

Chromium (Cr) hair levels have been reported to correspond to nutritional and physiological status. However, hair chromium occasionally reflects contamination from hair preparations, which contribute to the measured level.

 

Cobalt (Co) hair levels occasionally reflect external contamination from hair preparation products. Occupational or environmental exposures to cobalt dusts or chemicals may cause exogenous contamination.

 

Molybdenum (Mo) hair levels reflect ingestion and tissue levels, but may not reflect its function as an enzyme activator. Occupational or environmental exposures to molybdenum are an unusual occurrence, although copper deficiency can increase Mo uptake and retention. Molybdenum excess may result in anorexia, anemia and headache. Elevated Mo may cause arthritic symptoms if copper is deficient.

 

Boron (B) hair levels suggest long-term ingestion. Ingested B is well absorbed into the blood stream and rapidly deposited in tissues (brain, bone, heart, spleen, kidney, liver, testicles). Effects of excess boron depend strongly upon chemical form and mode of exposure. Elemental boron has low toxicity while borates and boranes can have cumulative neurotoxic effects. Boranes interfere with pyridoxal phosphate-dependent metabolic steps for amino acids. Symptoms may include dizziness, muscular tremors and incoordination.

 

Boron is sensitive to contamination from hair preparation products, which may contribute to the measured level of hair boron. Additionally, increased body burdens of toxic elements or organic chemicals are observed * to raise hair boron levels, without evidence of boron excess itself. Thus, elevated boron may be due to a combination of factors – endogenous excess, external contamination, and maldistribution secondary to toxic excesses.

 

Iodine (1) hair levels are indicative of past ingestion of iodine and of health conditions relating to deficiency or excess. The reported iodine level may include some external contamination by hair preparation products.

 

Selenium (Se) hair levels may reflect external contamination from Se-containing shampoos, which can contribute to the measured level.

 

Sulfur (S) hair levels can reflect the status of important sulfur bearing amino acids: cysteine, cystine, and taurine. However, hair sulfur is susceptible to external influences, particularly from hair straightener products, that may significantly lower sulfur content, or hair conditioning or permanent treatments, which raise it.

 

Other elements in hair do not correlate with blood or other tissue levels, but they can be markers for contamination or may have special meaning:

 

Hair sodium (Na) levels are very subject to external contamination by shampoos and hair treatment products, which may contribute to the measured levels. Sodium is an essential element that is classified as an extracellular electrolyte. High hair sodium may have no clinical significance or it may be the result of an electrolyte imbalance. A possible imbalance for which high hair Na is a consistent finding is adrenocortical hyperactivity. Blood testing for sodium and electrolyte levels is much more diagnostic and indicative of status.

 

Hair potassium (K) is less subject to external contamination. As with hair sodium, hair potassium varies with metabolic, homeostatic and stress conditions. High hair Potassium (K) is not necessarily reflective of dietary intake or nutrient status. However, elevated hair potassium may be reflective of metabolic disorders associated with exposure to potentially toxic elements. Potassium is an intracellular electrolyte. Hair is occasionally contaminated with potassium K from some shampoos. Appropriate tests for potassium include measurements of packed red blood cells and serum potassium, sodium/potassium ratios, measurement of urine K and sodium/K ratio; and an assessment of adrenocortical function.

 

Rubidium is a relatively benign element that typically parallels the potassium level. It varies according to levels found in water supplies. At extremely high levels, Rb may compete with potassium for activity in the cellular potassium pump; in practical terms this is rarely seen. Hair iron is not usually reflective of iron status but can be a marker for external contamination. Additionally, elevated hair iron may be found in smokers, x- ray technicians and individuals with certain forms of cancer. Notably low or high hair phosphorus is consistent with abnormal calcium and/or magnesium metabolism. Hair phosphorus also is typically elevated with kidney dialysis, and appears to be depressed in chronic hepatitis. Hair phosphorus is seldom altered by external influences. Hair is extremely susceptible to contamination with titanium from hair treatment products. Most common forms of titanium are inert, insoluble and nontoxic, especially titanium dioxide pigment. Titanium can be used as an indicator for external contamination of hair with various elements.

 

High levels of vanadium (V) in hair may be indicative of excess absorption of the element. It is well established that excess vanadium can have toxic effects in humans. Symptoms of vanadium toxicity vary with chemical form and route of absorption. Inhalation of excess VANADIUM may produce respiratory irritation and bronchitis. Excess ingestion of VANADIUM can result in decreased appetite, depressed growth, diarrhea/gastrointestinal disturbances, nephrotoxic and hematotoxic effects. Pallor, diarrhea, and green tongue are early signs of excess vanadium and have been reported in human subjects consuming about 20 mg V/day (Modern Nutrition in Health and Disease, 8th edition, eds. Shils, M., Olson, J., and Mosha, S., 1994). Although it appears that vanadium may have essential functions, over zealous supplementation is not warranted. Excess levels of vanadium in the body can result from chronic consumption of fish, shrimp, crabs, and oysters derived from water near offshore oil rigs (Metals in Clinical and Analytical Chemistry, 1994). Environmental sources of vanadium include: processing of mineral ores, phosphate fertilizers, combustion of oil and coal, production of steel, and chemicals used in the fixation of dyes and print.

 

Confirmatory tests for excess vanadium are red blood cell elements analysis, and urine vanadium which reflects recent intake.

 

Observations of Bob Smith, Vice President, Elemental Analysis, who has approximately 30 years experience working with hair analysis reports.