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Beryllium (Be) was discovered in 1798 by the French chemist Louis Nicolas Vauquelin, who found it in the oxide form in beryl and a green-colored variety of beryl, emerald. The metal was isolated in 1828 by two chemists, Friedrich Wölhler from Germany and Antoine Bussy from France, who independently reduced beryllium chloride (BeCl2) with potassium in a platinum crucible. These days, Be is typically obtained from the minerals beryl and bertrandite in a chemical process - or through the electrolysis of a mixture of molten Be chloride and sodium chloride. 


Pure Be metal is used in the manufacture of aircraft disc brakes‚ nuclear weapons and reactors‚ missile parts‚ heat shields‚ X-ray machine parts‚ and mirrors. Soluble salts, such as beryllium fluoride, chloride, and sulfate, are used in nuclear reactors, in glass manufacture, and as catalysts for certain chemical reactions. Be oxide is used in ceramics for electronics and high-tech applications. Beryllium-copper (BeCu) alloys usually contain about 2% beryllium, but vary greatly in composition to meet different industrial and consumer needs. For example, BeCu springs "bounce back" to their original shape again and again. 


Among other uses for beryllium alloys are electrical connectors‚ precision instruments‚ aircraft engine parts‚ wheels and pinions, televisions‚ calculators‚ computers‚ special non-sparking tools, dental alloys and dental bridges, switches, relays, connectors in automobiles, radar and telecommunications equipment, molds or casts to make metal-glass-plastic items, sports equipment such as golf clubs and bicycle frames. 


Be used in industry begins as a silicate (BeSiO3) in beryl and bertrandite ores. Bertrandite is mined in Utah, but other ores and scrap are imported into the United States, which is the world's leading producer, processor, and consumer of Be products. According to the U.S Geological Survey reports, total U.S. use of all forms of Be in 1996 was about 234 metric tons. According to data collected by the Environmental Protection Agency (EPA), the average concentration of airborne beryllium in the United States is very small (0.03 nanogram/cubic meter - a nanogram is one-billionth of a gram).






Atomic mass: 9.01218

Sources of Exposure

Probably, the greatest exposures to beryllium occur in the workplace where it is mined, processed, or converted into alloys and chemicals. People living near these industries may also be exposed to higher than normal levels of Be in the air. People living near uncontrolled hazardous waste sites may be exposed to higher than normal levels of Be. Individuals may also be exposed by inhalation of beryllium dust or fumes from the burning of coal or fuel oil and in tobacco smoke, by the ingestion of many fruits and vegetables and water, or through natural occurrence in the soil. The average concentration of Be measured in the air in the United States during the 1980s was 0.03 nanograms per cubic meter (ng/m3). Ambient concentrations measured in 50 cities between 1977 and 1981 were 0.1-0.4 ng/m3.

Pure Beryllium metal is used in the manufacture of aircraft disc brakes‚ nuclear weapons and reactors‚ missile parts‚ heat shields‚ X-ray machine parts‚ and mirrors.

Beryllium is one of the lightest of all metals and has one of the highest melting points of any light metal.  Be metal is used principally in aerospace and defense applications because of its stiffness, light weight, and dimensional stability over a wide temperature range.  Beryllium-copper alloys are used in a wide variety of applications because of their electrical and thermal conductivity, high strength and hardness, good corrosion and fatigue resistance, and nonmagnetic properties. Beryllium oxide is an excellent heat conductor, with high strength and hardness, and acts as an electrical insulator in some applications.   


Beryllium's brittleness is the downside of its advantageous stiffness. Brittleness also increases the hazards associated with Be toxicity. Unless ventilation and other controls are used, small particles and chips of insoluble beryllium-containing materials break off during the machining processes and spread through the air in the work area. Inhalation of these tiny particles is the type of exposure that can lead to chronic beryllium disease (CBD).

Physical Characteristics

Target Tissues

Be accumulation occurs primarily in the lungs, heart, spleen, liver, mesenchyme, and skin.

Beryllium has no biological role in the human body. Although the molecular basis for its toxicity is not well understood, it is well established that micromolar concentrations of beryllium specifically inhibit certain enzymes. As such, Be causes disturbances of calcium and vitamin D metabolism that may eventually result in the manifestation of rickets and mineral depletion. Be disease primarily affects the lungs, which occurs when people inhale beryllium dust or fumes. Occupational exposure most often occurs in mining, extraction, and in the processing of alloy metals containing Be. The adverse health effects of beryllium exposure are caused by the body's immune system reacting with the metal, resulting in an allergic-type response. Dust control is the primary preventative measure.


Skin disease with poor wound healing and rash or wart-like bumps can also occur. A person can develop beryllium disease even after being away from the beryllium industry for many years. There are two forms of beryllium disease:


  • Acute Beryllium Disease usually has a quick onset and resembles pneumonia or bronchitis. Excess exposure may result in death; however, the effects may be delayed. It is now rare due to improved industrial protective measures designed to reduce beryllium exposure levels.

  • What eventually came to be known as Chronic Beryllium Disease (CBD) was first identified in the 1940s, when a cluster of cases was observed in workers from the fluorescent light industry. CBD has a very slow onset. It still occurs in 1 - 6% of exposed people. CBD is an inflammation in the lungs that can occur when a person is exposed to respirable Be fumes, dusts or powder, and subsequently demonstrates an allergic reaction to beryllium. CBD is an occupational disease that may occur in the manufacture of metallic beryllium, beryllium oxide ceramic, or alloys containing Be. It was first identified more than 50 years ago. Interestingly, some individuals who are diagnosed with CBD do not develop clinical symptoms at all. In others, the disease can lead to clinical symptoms that include scarring and damage of lung tissue, causing shortness of breath, wheezing and/or coughing. Extreme cases of CBD can cause disability or death. The course of the disease can range from a few years to decades.


Be has also been shown to cause cancer in several species of animals including humans. Workers in some Be producing facilities have had an increased rate of lung cancer, as have Be cases in the U.S. Beryllium Case Registry. Be has recently been classified as a human carcinogen by the International Agency for Research on Cancer (IARC).


The current Be exposure standard has been recently revised. OSHA's current general industry standard sets a permissible exposure limit for Be at two micrograms per cubic meter (2 ug/m3) of air for an 8-hour time-weighted average or five micrograms per cubic meter of air not to exceed 30 minutes at a time. OSHA says employees should never be exposed to more than 25 micrograms of the metal, regardless of how short the exposure.


Beryllium disease primarily affects the lungs, which occurs when people inhale beryllium dust or fumes.

Signs & Symptoms


  • Beryllium compounds may cause contact dermatitis.

  • Beryllium ulcers occur where a beryllium crystal penetrates the skin at a site of previous trauma.

  • Beryllium chloride, fluoride, nitrate or sulphates are acute eye irritants.



  • Gastrointestinal beryllium absorption is poor and systemic toxicity via this route does not occur.



    Mild inhalation

  • Metallic taste, cough, breathlessness.

    Substantial inhalation

  • Cough, chest pain, metallic taste, exertional breathlessness, nasopharyngitis, tracheobronchitis, conjunctivitis, pneumonitis, epistaxis and fever.

  • Additional features seen in chronic beryllium disease include fever, anorexia, arthralgia, nausea, vomiting, hemoptysis, palpitation, convulsions, renal calculi, corneal calcification, hepatosplenomegaly (secondary to corpulmonale) and systemic granulomas causing lymphadenopathy and parotid gland enlargement.

  • Chest X-ray may show upper zone nodules and fibrosis and there may be a restrictive ventilatory defect.


The average time from first beryllium exposure to the development of CBD symptoms (the latency period) can be a few months or as long as 40 years. Once a person has been exposed to beryllium‚ there is a lifelong risk of developing the disease.


There are no studies on the health effects of children exposed to Be. It is likely that the health effects seen in children exposed to Be will be like the effects seen in adults. It is undetermined whether children differ from adults in their susceptibility to Be. It is also undetermined if exposure to Be will result in birth defects or other developmental effects in people. The studies on developmental effects in animals are not conclusive.

As with other toxic metals, Be can be measured in the urine, blood and hair.


Blood Testing: Commercial blood tests are available for many metals; however, the amount of Be in blood may not indicate as to amount or how recent the exposure. Another blood test, the blood beryllium lymphocyte proliferation test (BeLPT), identifies beryllium sensitization and has predictive value for chronic beryllium disease. 


Urine: Because of differences in the rates of excretion for 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). Urine element analysis is an invaluable tool for the identification or confirmation of Be toxicity and most toxic element burdens, as well as for monitoring of detoxification therapy. 


It is very important to note the total time and volume of urine collections. Otherwise, one cannot calculate the actual mass or rate of excretion of elements (i.e., ug/24 hours). This can be especially problematic during detoxification therapy that is associated with markedly increased urine volume.


For increased convenience, urine elements can also be analyzed in specimens that are collected for less than 24 hours. For shorter collection periods, elements will be reported per mg creatinine.


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 analysis for beryllium reflects a more chronic long-term exposure pattern. Beryllium levels can also be measured in lung and skin samples, though this is rarely done. 

Testing for Beryllium Toxicity

Nutrients Known to be Protective Against Beryllium

Iron, magnesium, zinc, calcium, selenium, and vitamin C are antagonistic for Be uptake and retention. Mg, Na2EDTA has been clinically shown to be an effective IV chelating agent for Be.

Protocols for Beryllium Detoxification

Acute beryllium poisoning is a medical emergency. For acute exposure, seek immediate medical attention and call Poison Control Services.

As with all detoxification protocols, the type, dose and duration of detoxification agents should always be individually assessed, and administered by a licensed medical practitioner.

The following may serve as a basic guideline for detoxification of excess Be 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 or DMPS). 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 beryllium 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 Be 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. Assess ferritin levels and administer iron if needed.

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

  4. Supplement with magnesium glycinate 100 to 300 mg daily (watch for diarrhea and, if present, reduce dose of magnesium).

  5. Supplement with selenium 200 mcg daily.

  6. Supplement with zinc 50 mg daily.

  7. Supplement with alpha lipoic acid at 100 twice daily.

  8. 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.

  9. 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 algae, metals are more effectively eliminated in the urine.

  10. 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 has proven that shilajit is truly a panacea. It is important to purchase the highest grade of shilajit.

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


It has been suggested through animal studies that N-(2- hydroxyethyl) ethylene diamine triacetic acid (HEDTA) is more effective than calcium disodium ethylenediamine tetraacetic acid (CaNa 2EDTA) in reducing the Be concentration of the blood. More aggressive treatment for Be excess also involves the use of sodium 2,3-dimercaptopropane-1-sulfonate (DMPS) and selenium. In one study it was shown that D-penicillamine (DPA] in combination with antioxidant (sodium selenite) was the most effective therapeutic agent followed by DMPS + sodium selenite and glutathione (GSH). Check for renal clearance first. The protocol for IV HEDTA chelation is available from the American College for the Advancement in Medicine (ACAM). If you are unfamiliar with HEDTA or DMPS chelation therapy, you may wish to refer the patient to a physician who is board certified by the American Board of Chelation Therapy (ABCT).

Aposhian, H. Vasken. DMSA and DMPS-water soluble antidotes for heavy metal poisoning. Annual Review of Pharmacology and Toxicology 23.1 (1983): 193-215.

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.

Dudek W, Walusiak J, Wittczak T. [Beryllium - underestimated occupational health hazard in Poland]. Med Pr. 2001;52(6):471-8. Review. Polish.

Figgs LW, Holsinger H, Freitas SJ, Brion GM, Hornung RW, Rice CH, Tollerud D. Increased suicide risk among workers following toxic metal exposure at the Paducah gaseous diffusion plant from 1952 to 2003: a cohort study. Int J Occup Environ Med. 2011 Oct;2(4):199-214.

Flora, S. J. S., Seema Mathur, and R. Mathur. Effects of meso-2, 3-dimercaptosuccinic acid or 2, 3-dimercaptopropane 1-sulfonate on beryllium-induced biochemical alterations and metal concentration in male rats. Toxicology 95.1-3 (1995): 167-175.

Gazalieva MA. [Genotoxic effects caused in workers by beryllium compounds]. Med Tr Prom Ekol. 2009;(9):32-6. Russian.

Guan H, Piao FY, Li XW, Li QJ, Xu L, Yokoyama K. Maternal and fetal exposure to four carcinogenic environmental metals. Biomed Environ Sci. 2010 Dec;23(6):458-65. doi: 10.1016/S0895-3988(11)60008-1.

Hardy, Harriet L. Beryllium disease: a clinical perspective. Environ. Res.;(United States) 21.1 (1980).

Hyslop, Frances, et al. The Toxicology of Beryllium. The Toxicology of Beryllium. 181 (1943).

Johri, Sonia, Sangeeta Shukla, and Pragya Sharma. Role of chelating agents and antioxidants in beryllium induced toxicity. (2002).

Mathur, Seema, et al. Mobilization and distribution of beryllium over the course of chelation therapy with some polyaminocarboxylic acids in the rat. Human & experimental toxicology 12.1 (1993): 19-24.

Meo SA, Al-Khlaiwi T. Health hazards of welding fumes. Saudi Med J. 2003 Nov;24(11):1176-82. Review.

Newman LS. Metals that cause sarcoidosis. Semin Respir Infect. 1998 Sep;13(3):212-20. Review.

Newman LS, Kreiss K, King TE, Seay S, Campbell PA. 1989. Pathologic and immunologic alterations in early stages of beryllium disease. Re-examination of disease definition and natural history. Am Rev Respir Dis 139:1479-1486.

Sanderson WT, Henneberger PK, Martyny J, Ellis K, Mroz MM, Newman LS. Beryllium contamination inside vehicles of machine shop workers. Appl Occup Environ Hyg. 1999 Apr;14(4):223-30.

Taylor TP, Ding M, Ehler DS, Foreman TM, Kaszuba JP, Sauer NN. Beryllium in the environment: a review. J Environ Sci Health A Tox Hazard Subst Environ Eng. 2003 Feb;38(2):439-69. Review.

U.S. Department of Health and Human Services, Public Health Service. Toxicological profile for beryllium. Atlanta, GA:1992.

U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Beryllium (Draft). Public Health Service, Atlanta, GA. 1992.


U.S. Environmental Protection Agency. Toxicological Review of Beryllium and Compounds. In support of summary information on IRIS. National Center for Environmental Assessment, Washington, DC. 1998.


U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Beryllium. National Center for Environmental Assessment, Office of Research and Development, Washington, DC. 1999.


Wang Z, White PS, Petrovic M, Tatum OL, Newman LS, Maier LA, et al. 1999. Differential susceptibilities to chronic beryllium disease contributed by different Glu69 HLA-DPB1 and -DPA1 alleles. J Immunol 163:1647-1653.

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


beryllium bibliography
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