Cadmium (Cd) was discovered by Friedrich Strohmeyer, a German chemist, in 1817 while studying samples of calamine (ZnCO3). When heated, Strohmeyer noticed that some samples of calamine glowed with a yellow color while other samples did not. After further examination, he determined that the calamine that changed color when heated contained trace amounts of a new element – cadmium. 

 

Like zinc, Cd can be electroplated to other materials to protect them from corrosion. In the last 30 years, the use of Cd for electroplating has dropped by about 70% due to environmental concerns. Discarded electroplated steel puts Cd into the environment. Another important use of Cd is in the production of nicad (nickel-cadmium), or rechargeable batteries. Cd easily absorbs neutrons and is used to make control rods for nuclear reactors. Cd is alloyed with silver to form solder, a metal with a relatively low melting point used to join electrical components, pipes and other metallic items. Cd-based solders must be handled with care to prevent Cd poisoning. Cd compounds are used as coloring agents - cadmium sulfide and cadmium selenide. The sulfide is yellow, orange, or brown, while the selenide is red. These compounds are used to color paints and plastics. There is concern about possible environmental effects of using cadmium for this purpose. Despite Cd being ranked 8th in the Top 20 Hazardous Substances Priority List, human activity has markedly increased the distribution of Cd in the global environment. 

Cd

Cadmium

48

Atomic mass: 112.41

Sources of Exposure

The major sources of Cd in humans are cigarette smoking, certain foods grown in cadmium-laden soil, seafood (crab, flounder, mussels, oysters, scallops), liver and kidney meats, coal burning, and contaminated water.

 

Other sources of cadmium are: paints colored with Cd, bone meal, fungicides, highway dusts, and nickel-cadmium batteries. Phosphate fertilizers also show a big Cd load. 

 

Although some cadmium-containing products can be recycled, a large share of the general Cd pollution is caused by dumping and incinerating cadmium-polluted waste. Cd can escape from landfills (where trash is buried) and get into the ground and groundwater. From there, it can become part of the food and water that humans and animals ingest.

 

Smelting plants and welding fumes are also a source. Regular cigarette smoking doubles the daily intake of Cd, as compared to the normal intake that results mostly from exposure through ingestion of foods with trace levels of Cd.

Biochemistry

Basically, there are three possible ways of Cd resorption: gastrointestinal, pulmonary and dermal. Once taken up by the blood, most Cd is transported bound to proteins, such as albumin and metallothionein. The first organ reached after uptake into the GI-blood is the liver. Here cadmium induces the production of metallothionein. After consecutive hepatocyte necrosis and apoptosis, Cd-Metallothionein (Cd-MT) complexes are washed into sinusoidal blood. From here, parts of the absorbed cadmium enter the entero-hepatical cycle via secretion into the biliary tract in form of cadmium-glutathione conjugates. Enzymatically degraded to cadmium-cysteine complexes in the biliary tree, cadmium re-enters the small intestines.

 

The main organ for long-term Cd accumulation is the kidney. Here the half-life period for cadmium is approx. 10 years. A life-long intake can therefore lead to a Cd accumulation in the kidney, consequently resulting in tubulus cell necrosis. An increasing cadmium load in the kidney may also result in a higher calcium excretion, thus leading to a higher risk of kidney stones. Excretion of Cd takes place via feces and urine.

 

Numerous other target organs are likely for Cd accumulation, as experimental poisonings with cadmium have also been shown to have cardiovascular effects such as increased blood pressure, anemia, and cardiomyopathy, effects on the reproductive system in both sexes, and skeletal effects. 

 

Cd and mercury, along with zinc, are Group II transition metals. Not surprisingly, both Cd and mercury antagonize processes that require zinc, although cadmium does this much more readily than mercury due to its smaller molecular weight. Zinc participates in about 18 metalloenzymes and about 15 Zn2+ ion-protonated enzymes.

 

Listed below are a few such zinc dependent enzymes: 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

While Cd has been shown to inhibit these enzymes/proteins in a test tube, it is not as clear the extent to which cadmium readily inhibits these enzymes in vivo, and whether this occurs through direct displacement of zinc from the apo-enzyme. Nevertheless, this list should serve to illustrate the vast number of potential molecular targets that cadmium can affect. Aside from zinc, Cd can inhibit the metabolism and transport of other divalent cations, such as calcium and copper. 

 

Because Cd has an outer shell filled with electrons, it tends to form tight covalent bonds with positively charged molecules, such as proteins and DNA. It readily binds to proteins with sulfhydryl groups and may inactivate enzymes in this way. It may also directly damage DNA through direct binding, or indirectly through production of reactive oxygen species. It decreases the cytochrome P450 mixed oxidase system, and therefore, impends detoxification of other metals and xenobiotics. It may also modify catecholamine activity. 

Target Tissues

The main site of accumulation of Cd is the proximal tubules of the kidneys, but Cd also accumulates in the brain (appetite and pain centers), heart and blood vessels (changes in arterial endothelium seen), liver and lungs.

The effects of extensive Cd exposure are not known, but are thought to include heart and kidney disease, high blood pressure, and cancer.


A Cd poisoning disease called itai-itai, Japanese for “ouch-ouch", causes aches and pains in the bones and joints. Itai-Itai disease manifests a wide range of symptoms such as: low grade of bone mineralization, high rate of fractures, increased rate of osteoporosis, and intense bone-associated pain. An epidemic of the Itai-Itai disease was observed in the Jinzu river basin (Japan) in the 1940s. In a study on this occasion, patients were found to show the characteristic symptoms after having eaten rice, grown on fields irrigated with highly cadmium-polluted water. Pseudo-fractures characteristic of osteomalacia and severe skeletal decalcification were also observed. This study, however, came under criticism because most of the patients observed were post-menopausal women. (Underlying osteoporosis, possibly enhanced by cadmium intoxication, was suggested to be the actual reason for the observed symptoms.) The Belgian CadmiBel study – conducted between 1985 and 1989 – came to similar conclusions: Even minimal environmental exposure to cadmium may cause skeletal demineralization. Lead and cadmium interact with renal mitochondrial hydroxylases of the vitamin D3 endocrine complex. Hence, a likely explanation for demineralization is the disturbance in vitamin-D metabolism.

 

There is evidence that Cd can cause cancer. Studies have shown that a subcutaneous injection of Cd chloride can induce prostate cancer in Wistar rats. Some studies have suggested an association of Cd and renal cancer in humans. This assumption was confirmed in 2005 by a systematic review of seven epidemiological and eleven clinical studies. Consequently, the IARC (International Agency for Research on Cancer) decided to classify cadmium as a human carcinogen group I. More recent data, however, supports the assumption that only an uptake of cadmium via the respiratory system has carcinogenic potential

Signs & Symptoms

Zinc, calcium, magnesium and copper are all antagonistic for reuptake and retention of Cd. Zinc is probably the most important nutrient that protects the body against cadmium - as it helps to increase thionein and metallothionein and protects the prostate in males. Zinc can induce protective levels of metallothionein even before the body is exposed to Cd; to a lesser extent, copper can do this as well. Iron, ascorbic acid, and protein can also reduce the absorption of low levels of dietary Cd. Calcium and thiols like cysteine reduce the toxicity of oral Cd. 

 

Selenium also protects against Cd toxicity, probably by a unique mechanism:  in male Wistar rats, selenium co-treatment with cadmium increased survival, increased distribution of cadmium to the liver and testes, and reduced kidney distribution compared to Cd treatment alone. As no enhancement of liver metallothionein was observed when rats were pre-treated with selenium, the authors speculate that other mechanisms of protection must be involved, including the formation of direct complexes with selenium, or the antioxidant effects of selenium. 

Nutrients Known to be Protective Against Cadmium

Testing for Cadmium Toxicity

Blood Testing: Commercial blood tests are available for many metals including cadmium. However, blood levels of cadmium are usually indicative of recent exposures and may not reflect whole body burdens. 

 

Urine: Because of differences in the rates of excretion of toxic metals, urine tests are indicative of cumulative exposure/total body burden for some metals (e.g., cadmium) and recent exposure for others (e.g., mercury). Post-challenge or post-provocation urine tests, which involve the measurement of urine metal concentrations following administration of a chelator, may reveal sources of stored toxic metals. However, since there are no broadly accepted reference ranges for urine metals determined by this technique, these tests are likely of limited diagnostic value and are not completely validated. Reference ranges for individual tests depend on the laboratory performing the analysis.

 

Hair toxic element analysis is an excellent test for cadmium exposure. Toxic elements may be 200 to 300 times more highly concentrated in hair than in blood or urine. Therefore, hair is an excellent tissue for detection of recent exposure to elements such as arsenic, aluminum, cadmium, lead and antimony. 

Protocols for Cadmium Detoxification

The following may serve as a basic guideline for detoxification of excess Cd from chronic exposure. After 60 days, laboratory screening should be used to reassess the protocol. Before initiating a detoxification program, a CBC with chemistry, including a thyroid panel with lipids should be performed. In addition, whole blood elements to assess the mineral status and a urine creatinine clearance should be performed every 60 days when using synthetic detoxifying agents (EDTA). Administration of synthetic agents may cause a depletion of essential elements such as zinc, iron, calcium, magnesium, copper and other trace minerals. Of greatest concern is potential kidney toxicity that can occur when the body releases its Cd stores for excretion through the kidneys. Those with underlying kidney disease may not be able to undergo aggressive cadmium detoxification therapy.

 

  1. First, identify the source(s) of cadmium in the individual’s environment and remove them - or remove the individual from the source(s).
  2. Assess whole blood cell element analysis to determine mineral nutrient deficiency and supplement appropriately.

  3. Supplement with vitamin C (corn free source) to reduce oxidative stress caused by excess cadmium. May administer gram quantities to bowel tolerance. 

  4. Supplement with oral zinc 50 mg daily for 50 days.

  5. Supplement 200 mcg of selenium daily.

  6. Algal cells have a remarkable ability to take up and accumulate heavy metals from their external environment. The primary ones used for toxic metal excess are Chlorella vulgaris, a green microalga, and Laminaria japonica, a brown alga. Chlorella and Laminaria japonica are both chelators, moving toxic metals out of the body, and transporters, moving metals from deeper stores to more readily removable areas. Both work in unison with each other and can remove toxic metals from the body through urinary excretion. Administer 1000 to 2000 mg of Laminaria japonica concentrate (Modifilan) daily and 1000 to 2000 mg of chlorella. Adjust dosage to bowel tolerance; may be taken for long periods of time.

  7. Cilantro works well with alga to chelate, or bind up toxic metals. The issue with cilantro taken alone is that although it chelates metals, it does not remove them in the urine. This means they can recirculate to deposit elsewhere in the body. Hence, taken with algas, metals are more effectively eliminated in the urine.

  8. Shilajit is an ancient traditional medicine (Tibetan and Ayurvedic) and has been ascribed a number of pharmacological activities. It has been used for ages as a rejuvenator and for treating a number of disease conditions. It is an effective detoxifier of metals and contains over 60 minerals. Modern scientific research has systematically validated a number of properties of shilajit and proven that shilajit is truly a panacea. It is important to purchase the highest grade of shilajit.

  9. Administer vitamin D3 at 2000 - 5000 IU daily.

  10. Calcium and phosphorus supplementation may also be necessary.

  11. Instruct patient to drink adequate amounts of pure water (Adult’s urine volume should be about 2 liters per day).

  12. DMPS has not been found to be an effective chelator for cadmium.

  13. Diethylenetriaminepentaacetic acid (DPTA) / pentetic acid is an effective chelator for cadmium, as well as lead. In 2004 the FDA determined zinc-DTPA and calcium-DTPA to be safe and effective for treatment of those who have breathed in or otherwise been contaminated internally by plutonium, americium, or curium. However, DPTA should be considered experimental for cadmium detoxification.

  14. IV EDTA chelation (edetate calcium disodium (CaNa2EDTA) (Calcium Disodium Edetate®) may be used for aggressive cadmium detoxification. The calcium form of EDTA may be more effective with cadmium chelation than the magnesium form. Reduced glutathione given orally before EDTA chelation can increase the urinary yield of excreted cadmium. Oral dosing of 10 mg per Kg of body weight divided in doses during the 24-hour period before IV EDTA chelation treatment usually increases urinary Cd excretion. Check for renal clearance first. The protocol for IV EDTA chelation is available from the American College for the Advancement in Medicine (ACAM). If you are unfamiliar with EDTA chelation therapy, you may wish to refer the patient to a physician who is board certified by the American Board of Chelation Therapy (ABCT).

ATSDR. ToxGuide for Cadmium. 2012a:1–2. Available online at www.atsdr.cdc.gov/toxguides/toxguide-5.pdf.

Barbee JYJ, Prince TS: Acute respiratory distress syndrome in a welder exposed to metal fumes. South Med J 1999,92(5):510-512.

Cantilena Jr, Louis R., and Curtis D. Klaassen. Comparison of the effectiveness of several chelators after single administration on the toxicity, excretion, and distribution of cadmium. Toxicology and applied pharmacology 58.3 (1981): 452-460.

Chalkley SR, Richmond J, Barltrop D: Measurement of vitamin D3 metabolites in smelter workers exposed to lead and cadmium. Occup Environ Med 1998,55(7):446-452.

Chang LW. Toxico-neurology and neuropathology induced by metals. In: Chang LW ed. Toxicology of Metals. Boca Raton: CRC Press; 1996:511-535.

Chang LW. Toxicology of Metals. Boca Raton, FL: CRC Press; 1996.

Elinder CG, Lind B, Kjellstrom T, Linnman L, Friberg L: Cadmium in kidney cortex, liver, and pancreas from Swedish autopsies. Estimation of biological half time in kidney cortex, considering calorie intake and smoking habits. Arch Environ Health 1976,31(6):292-302.

Gil, Hyo-wook, et al. Effect of glutathione on the cadmium chelation of EDTA in a patient with cadmium intoxication. Human & experimental toxicology 30.1 (2011): 79-83.

Goyer RA, Liu J, Waalkes MP: Cadmium and cancer of prostate and testis. Biometals 2004,17(5):555-558. 

Hotz P, Buchet JP, Bernard A, Lison D, Lauwerys R: Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Lancet1999,354(9189):1508–1513. 10.1016/S0140-6736(99)91145-5.

 

Il'yasova D SGG: Cadmium and renal cancer. Toxicol Appl Pharmacol 2005,207(2):179-186. 10.1016/j.taap.2004.12.005.

Jarup L, Berglund M, Elinder CG, Nordberg G, Vahter M: Health effects of cadmium exposure - a review of the literature and a risk estimate. Scand J Work Environ Health 1998, 24 Suppl 1: 1-51. 

Jarup L, Alfven T, Persson B, Toss G, Elinder CG: Cadmium may be a risk factor for osteoporosis. Occup Environ Med 1998,55(7):435-439. 

 

Jin T, Nordberg M, Frech W, Dumont X, Bernard A, Ye TT, Kong Q, Wang Z, Li P, Lundstrom NG, Li Y, Nordberg GF: Cadmium biomonitoring and renal dysfunction among a population environmentally exposed to cadmium from smelting in China (ChinaCad). Biometals 2002,15(4):397-410. 

Johnson MD, Kenney N, Stoica A, Hilakivi-Clarke L, Singh B, Chepko G, Clarke R, Sholler PF, Lirio AA, Foss C, Reiter R, Trock B, Paik S, Martin MB: Cadmium mimics the in vivo effects of estrogen in the uterus and mammary gland. Nat Med 2003, 9 (8):1081–1084. 10.1038/nm902.

 

Kazantzis G: Renal tubular dysfunction and abnormalities of calcium metabolism in cadmium workers. Environ Health Perspect 1979, 28: 155-159. 

 

Kazantzis G: Cadmium, osteoporosis and calcium metabolism. Biometals 2004,17(5):493-498. 

 

Kendrick, M.J et al. Metals in Biological Systems. E. Horwood, New York, 1992.

 

Kolonel LN: Association of cadmium with renal cancer. Cancer 1976,37(4):1782–1787. 10.1002/1097-0142(197604)37:4<1782::AID-CNCR2820370424>3.0.CO;2-F.

 

Nordberg GF: Cadmium and health in the 21st century - historical remarks and trends for the future. Biometals 2004,17(5):485–489. 10.1023/B:BIOM.0000045726.75367.85.

 

Nogawa K, Kobayashi E, Okubo Y, Suwazono Y: Environmental cadmium exposure, adverse effects and preventive measures in Japan. Biometals 2004,17(5):581-587. 

 

Ren H, Jia H, Endo H, et al. Cadmium detoxification effect of Chinese parsley Coriandrum sativum in liver and kidney of rainbow trout Oncorhynchus mykiss. Fish Sci 2009;75:731-741.

 

Sahmoun AE, Case LD, Jackson SA, Schwartz GG: Cadmium and prostate cancer: a critical epidemiologic analysis. Cancer Invest 2005,23(3):256-263. 

 

Staessen JA, Roels HA, Emelianov D, Kuznetsova T, Thijs L, Vangronsveld J, Fagard R: Environmental exposure to cadmium, forearm bone density, and risk of fractures: prospective population study. Public Health and Environmental Exposure to Cadmium (PheeCad) Study Group. Lancet1999,353(9159):1140–1144. 

 

Svartengren M, Elinder CG, Friberg L, Lind B: Distribution and concentration of cadmium in human kidney. Environ Res 1986,39(1):1–7. 10.1016/S0013-9351(86)80002-0. 

 

Waalkes MP, Rehm S, Riggs CW, Bare RM, Devor DE, Poirier LA, Wenk ML, Henneman JR, Balaschak MS: Cadmium carcinogenesis in male Wistar [Crl:(WI)BR] rats: dose-response analysis of tumor induction in the prostate and testes and at the injection site. Cancer Res 1988,48(16):4656-4663. 

 

Wester RC, Maibach HI, Sedik L, Melendres J, DiZio S, Wade M: In vitro percutaneous absorption of cadmium from water and soil into human skin. Fundam Appl Toxicol 1992,19(1):1-5. 10.1016/0272-0590(92)90021-9. 

 

Xue H.B., W.Stumm, L.Sigg: The binding of Heavy Metals to Algal Surfaces, Water Res 1988;22, 917.

References

202 Spring Street | Marion, MA  02738 | info@brmi.online | Tel: 508.748.0816 | Fax: 508.748.1976

  • Facebook
  • LinkedIn
  • YouTube
  • Twitter

THE CONTENT ON THIS SITE IS PRESENTED IN SUMMARY FORM, IS GENERAL IN NATURE, AND IS PROVIDED FOR INFORMATIONAL PURPOSES ONLY; IT IS NOT ADVICE, NOR SHOULD IT BE TREATED AS SUCH. If you have any healthcare-related concerns, please call or see your physician or other qualified healthcare provider. This site is NOT intended to be a substitute for a healthcare provider’s consultation: NEVER DISREGARD MEDICAL ADVICE OR DELAY IN SEEKING IT BECAUSE OF SOMETHING YOU HAVE SEEN ON THIS SITE. We make no representations, nor any warranties, nor assume any liability for the content herein; nor do we endorse any particular product, provider, or service.

© 2017-2019 Dr. James Odell, ND, OMD, L.Ac.