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Acute beryllium poisoning | |
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Specialty | Emergency medicine |
Beryllium poisoning is illness resulting from the toxic effect of beryllium in its elemental form or in various chemical compounds. The toxicity of beryllium depends upon the duration, intensity and frequency of exposure (features of dose), as well as the form of beryllium and the route of exposure (i.e. inhalation, dermal, ingestion). According to the International Agency for Research on Cancer (IARC), beryllium and beryllium compounds are Category 1 carcinogens; they are carcinogenic to both animals and humans.
Since its discovery in the 1920s, Beryllium has been used in electronics, ceramics, research and development labs, aircraft, and the atomic energy and defense industry. In the 1940s the United States first recorded respiratory and dermal reactions among residents of communities surrounding beryllium manufacturing facilities and workers within them. At that time most construction trades and industries were unaware of the potential risks associated with beryllium exposure.
Chronic berylliosis is a pulmonary and systemic granulomatous disease caused by exposure to beryllium. Acute beryllium disease in the form of chemical pneumonitis was first reported in Europe in 1933 and in the United States in 1943. Cases of chronic berylliosis were first described in 1946 among workers in plants manufacturing fluorescent lamps in Salem, Massachusetts. Chronic berylliosis resembles sarcoidosis in many respects, and the differential diagnosis is often difficult. It occasionally killed early workers in nuclear weapons design, such as Herbert L. Anderson.
Although the use of beryllium compounds in fluorescent lighting tubes was discontinued in 1949, potential for exposure to beryllium exists in the nuclear weapons production and aerospace industries and in the refining of beryllium metal and melting of beryllium-containing alloys, the manufacturing of electronic devices, and the handling of other beryllium-containing material.
Early researchers tasted beryllium and its various compounds for sweetness in order to verify its presence. Modern diagnostic equipment no longer necessitates this highly risky procedure. Beryllium and its compounds should be handled with great care and special precautions must be taken when carrying out any activity which could result in the release of beryllium dust (lung cancer is a possible result of prolonged exposure to beryllium laden dust).
Beryllium in air and on surfaces can be detected using dilute ammonium bifluoride for dissolution and fluorescence detection with beryllium bound to sulfonated hydroxybenzoquinoline, allowing detection up to 100 times lower than the recommended limit for beryllium concentration in the workplace.
Inhalation
Beryllium is harmful if inhaled and the effects depend on the duration, intensity, and frequency of exposure. When inhaled, beryllium becomes deposited into the lungs, from which the body has difficulty expelling it. If beryllium concentrations in air are high enough (greater than 100 µg/m), an acute condition can result, called acute beryllium disease, which resembles pneumonia. Occupational and community air standards are effective in preventing most acute lung damage. Long-term beryllium exposure can increase the risk of developing lung cancer.
The more common serious health problem from beryllium today is chronic beryllium disease (CBD). It continues to occur in industries as diverse as metal recycling, dental laboratories, alloy manufacturing, nuclear weapons production and metal machine shops that work with alloys containing small amounts of beryllium. CBD can occur even when levels of beryllium are lower than the legal limits for workers. A 2008 report from the United States National Research Council said that worker exposure to beryllium should be kept "at the lowest feasible level," as the agency's research could not establish any safe level of exposure.
Acute beryllium disease
Overexposure to beryllium can cause inflammation of the upper and/or lower respiratory tracts. The symptoms of acute beryllium disease are non-specific, resembling other inhalational injuries, viral infections, or pneumonia. Upper respiratory findings include nasopharyngitis and tracheobronchitis. Symptoms may include irritation of the nares and pharynx, epistaxis, cough, and a metallic taste. Nasopharyngitis can progress to formation of nasal fissures, ulcerations, or perforation.
Therapy is supportive and includes removal from further beryllium exposure. Acute beryllium pneumonitis produces severe cough (occasionally with blood-streaked sputum), chest pain or burning, and shortness of breath. The patient is usually ill-appearing, and presents with hypoxemia, cyanosis, tachycardia, and shallow rapid breathing. Systemic symptoms include fever (usually low-grade), malaise, and anorexia. The chest X-ray can reveal diffuse, bilateral alveolar infiltrates.
There is no specific diagnostic test for acute beryllium disease. Biopsy of the lungs reveals a nonspecific granulomatous inflammation. Treatment is supportive, including oxygen supplementation as needed, and removal from further beryllium exposure. Corticosteroids are sometimes tried, but no good controlled studies are reported. The signs and symptoms of acute beryllium pneumonitis usually resolve over several weeks to months, but it may be fatal, and about 15–20% of cases may progress to CBD.
Chronic beryllium disease (CBD)
Main article: BerylliosisSensitization is not an illness, but some exposed individuals, after inhaling sufficient quantities of beryllium dust in the micrometer-size range, may have an inflammatory reaction that principally targets the respiratory system and skin. This condition is called chronic beryllium disease (CBD), and can occur within a few months or many years (average 10 years in some series) after exposure to higher-than-normal levels of beryllium (greater than 0.2 µg/m). This disease causes fatigue, weakness, night sweats and can cause difficulty in breathing and a persistent dry cough. It can result in anorexia, weight loss, and may also lead to right-side heart enlargement and heart disease in advanced cases.
Typically, CBD has an insidious onset and runs an indolent course. Some people who are sensitized to beryllium may not have symptoms, and just being sensitized is not a recognized health effect. CBD occurs when the body's immune system recognizes beryllium particles as foreign material and mounts an immune system attack against the particles. Because these particles are typically inhaled into the lungs, the lungs become the major site where the immune system responds. The lung sacs become inflamed and fill with large numbers of white blood cells that accumulate wherever beryllium particles are found. These cells form balls around the beryllium particles called "granulomas." When enough of these develop, they interfere with the normal function of the organ. Over time, the lungs become stiff and lose their ability to transfer oxygen from the air into the bloodstream. Early on in the disease, there may be a mild obstructive ventilatory defect. In advanced cases, there is a restrictive defect and reduced diffusion capacity. Patients with CBD develop difficulty inhaling and exhaling sufficient amounts of air, and the amount of oxygen in their bloodstreams falls.
Most of the clinical features of CBD are indistinguishable from thoracic involvement with sarcoidosis. The chest radiograph usually reveals bilateral, mid- and upper-lobe predominant reticulonodular infiltrates, as well as hilar and mediastinal adenopathy. For suspected cases of CBD, fiber-optic bronchoscopy with bronchoalveolar lavage (BAL) is indicated. Beryllium lymphocyte proliferation testing (BAL BeLPT) of the lavage fluid is the gold standard for diagnosis, detecting approximately 70-90% of cases. The measurement of beryllium in urine or tissue is not sufficient to diagnose CBD.
CBD is treatable, but not curable with traditional drugs and medicine. Removal from further beryllium exposure is advisable. Treatment includes supplemental oxygen and corticosteroids (such as prednisone) to lower the body's overreaction to beryllium. If corticosteroid therapy is successful, treatment is usually continued for the rest of the affected person's life due to potential relapse after steroid cessation. In general, CBD worsens without treatment. Prognosis is best for those diagnosed at an earlier stage. Overall mortality rates are 5-38%.
The general population is unlikely to develop acute or chronic beryllium disease because ambient air levels of beryllium are normally very low (<0.03 ng/m).
Ingestion
Swallowing beryllium has not been reported to cause effects in humans because very little beryllium is absorbed from the stomach and intestines. Harmful effects have sometimes been seen in animals ingesting beryllium.
Dermatological effects
Beryllium can cause local irritation and contact dermatitis. Beryllium contact with skin that has been scraped or cut may cause rashes, ulcers, or bumps under the skin called granulomas. Beryllium dust or powder can irritate the eyes, producing itching, burning, or conjunctivitis.
Effects on children
There are no studies on the health effects of children exposed to beryllium, although individual cases of CBD have been reported in children of beryllium workers from the 1940s. It is unknown whether children differ from adults in their susceptibility to beryllium. It is unclear whether beryllium is teratogenic.
Detection in the body
Beryllium can be measured in the urine and blood. The amount of beryllium in blood or urine may not indicate time or quantity of exposure. Beryllium levels can also be measured in lung and skin samples. While such measurements may help establish that exposure has occurred, other tests are used to determine if that exposure has resulted in health effects.
Beryllium sensitivity testing was first performed as a cutaneous beryllium patch test in the early 1950s but was discontinued due to the test stimulating sensitization or aggravating existing chronic beryllium disease.
A blood test, the blood beryllium lymphocyte proliferation test (BeLPT), identifies beryllium sensitization by measuring immune cell response, and has predictive value for CBD. It is detected immunologically in peripheral blood cells. Although there is a variability of results between laboratories, the BeLPT has become the standard test for detecting beryllium sensitization and CBD in individuals who are suspected of having CBD. The test can help distinguish it from similar conditions such as sarcoidosis. The test can detect disease that is at an early stage, or can detect disease at more advanced stages of illness as well. The BeLPT can also be performed using cells obtained from a person's lung by bronchoscopy.
BeLPT is also the main test used in industry health programs to monitor whether disease is occurring among current and former workers who have been exposed to beryllium on the job. Using the BeLPT as a surveillance test gives companies information needed to take preventative measures against beryllium exposure.
Industrial release and occupational exposure limits
Typical levels of beryllium that industries may release into the air are of the order of 0.01 µg/m, averaged over a 30-day period, or 2 µg/m of workroom air for an 8-hour work shift. Compliance with the current U.S. Occupational Safety and Health Administration (OSHA) permissible exposure limit for beryllium of 2 µg/m has been determined to be inadequate to protect workers from developing beryllium sensitization and CBD. The American Conference of Governmental Industrial Hygienists (ACGIH), which is an independent organization of experts in the field of occupational health, has proposed a threshold limit value (TLV) of 0.05 µg/m in a 2006 Notice of Intended Change (NIC). This TLV is 40 times lower than the current OSHA permissible exposure limit, reflecting the ACGIH analysis of best available peer-reviewed research data concerning how little airborne beryllium is required to cause sensitization and CBD.
Because it can be difficult to control industrial exposures to beryllium, it is advisable to use any methods possible to reduce airborne and surface contamination by beryllium, to minimize the use of beryllium and beryllium-containing alloys whenever possible, and to educate people about the potential hazards if they are likely to encounter beryllium dust or fumes.
On 29 January 2009, the Los Alamos National Laboratory announced it was notifying nearly 2,000 current and former employees and visitors that they may have been exposed to beryllium in the lab and may be at risk of disease. Concern over possible exposure to the material was first raised in November 2008, when a box containing beryllium was received at the laboratory's short-term storage facility.
Researchers from the National Institute for Occupational Safety and Health (NIOSH) estimate that as many as 134,000 workers in the government and private industry are potentially exposed to beryllium in the United States.
References
- "IARC Monograph, Volume 58". International Agency for Research on Cancer. 1993. Retrieved 18 September 2008.
- Dobis, D.R (2008). "Modulation of lymphocyte proliferation by antioxidants in chronic beryllium disease". Am J Respir Crit Care Med. 9: 1002–1011. doi:10.1164/rccm.200707-1021oc.
- Klein, R (2004). "Diagnostic Revelance of the Lymphocyte Transformation Test for Sensitization to Beryllium and Other Metals". Pure and Applied Chemistry. 76: 12169-1281. doi:10.1351/pac200476061269.
- Lang, L (1994). "Beryllium: A Chronic Problem". Environ Health Perspect. 102 (6–7): 526–531. doi:10.1289/ehp.94102526. PMC 1569745. PMID 9679108.
- Middleton, D (2006). "The BeLPT: algorithms and implications". Am J Ind Med. 49 (1): 36–44. doi:10.1002/ajim.20241.
- ^ Rossman, M (1996). "Chronic beryllium disease: diagnosis and management". Environ Health Perspect. 104 Suppl 5: 945–947. doi:10.1289/ehp.96104s5945.
- Maier, L (2008). "Recent chronic beryllium disease in residents surrounding a beryllium facility". Am J Respir Crit Care Med. 177 (9): 1012–1017. doi:10.1164/rccm.200607-1042oc.
- Welch, L (2013). "Beryllium Disease Among Construction Trade Workers at Department of Energy Nuclear Sites". American Journal of Industrial Medicine. 56: 1125–1136. doi:10.1002/ajim.22202.
- ^ Lang, Leslie (June–July 1994). "Beryllium: A Chronic Problem". Environmental Health Perspectives. 102 (6–7): 526–31. doi:10.1289/ehp.94102526. PMC 1569745. PMID 9679108.
- "Photograph of Chicago Pile One Scientists 1946". Office of Public Affairs, Argonne National Laboratory. 19 June 2006. Retrieved 18 September 2008.
- "ASTM D7458 – 08". American Society for Testing and Materials. Retrieved 8 August 2009.
- Minogue, EM; Ehler, DS; Burrell, AK; McCleskey, TM; Taylor, TP (2005). "Development of a New Fluorescence Method for the Detection of Beryllium on Surfaces". Journal of ASTM International. 2 (9): 13168. doi:10.1520/JAI13168.
- Rosenman, Kenneth; et al. (October 2005). "Chronic Beryllium Disease and Sensitization at a Beryllium Processing Facility". Environmental Health Perspectives. 113 (10). National Institute of Environmental Health Sciences: 1366–72. doi:10.1289/ehp.7845. PMC 1281281. PMID 16203248. Retrieved 3 June 2011.
- "NRC urges minimal Beryllium Exposure". Chemical & Engineering News. 86 (33): 26. 18 August 2008.
- ^ Tepper LB, Hardy HL, Chamberlain RI. Toxicity of beryllium compounds. In: Browning E, Ed. Elsevier monographs on toxic agents. Amsterdam: Elsevier Publishing Co.; 1961. pp1-190.
- Hardy, HL (1965). "Beryllium poisoning--lessons in control of man-made disease". The New England Journal of Medicine. 273 (22): 1188–99. doi:10.1056/NEJM196511252732205. PMID 5847559.
- Yoshida, T; Shima, S; Nagaoka, K; Taniwaki, H; Wada, A; Kurita, H; Morita, K (1997). "A study on the beryllium lymphocyte transformation test and the beryllium levels in working environment". Industrial health. 35 (3): 374–9. doi:10.2486/indhealth.35.374. PMID 9248221.
- Bartell, S (2000). "Risk estimation and value-of-information analysis for three proposed genetic screening programs for chronic beryllium disease prevention". Risk Anal. 20 (1): 87–99. doi:10.1111/0272-4332.00009.
- Kriebel, D; Brain, JD; Sprince, NL; Kazemi, H (1988). "The pulmonary toxicity of beryllium". The American review of respiratory disease. 137 (2): 464–73. doi:10.1164/ajrccm/137.2.464. PMID 3277503.
- "The Beryllium Lymphocyte Proliferation Test". Retrieved 10 September 2013.
- ^ Stange, A (1996). "Possible health risks from low level exposure to beryllium". Toxicology. 111 (1–3): 213–224. doi:10.1016/0300-483x(96)03378-1.
- Newman, LS; Lloyd, J; Daniloff, E (1996). "The natural history of beryllium sensitization and chronic beryllium disease". Environmental Health Perspectives. 104 Suppl 5 (Suppl 5): 937–43. doi:10.2307/3433014. PMC 1469683. PMID 8933038.
- National Research Council (U.S.). Committee on Beryllium Alloy Exposures, National Research Council (U.S.). Committee on Toxicology (2007). Health effects of beryllium exposure. National Academies Press. p. 11. ISBN 0-309-11167-6.
- Duncan, C. W.; Miller, E. J. (1935). "Results of feeding various levels of soil containing beryllium to chickens, dogs and rats" (PDF). 11 (4): 371.
{{cite journal}}
: Cite journal requires|journal=
(help)CS1 maint: multiple names: authors list (link) - Robert L. Rietschel, Joseph F. Fowler, Alexander A. Fisher (2008). Fisher's Contact Dermatitis. PMPH-USA. p. 651. ISBN 1-55009-378-9.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - Tinkle, S (2003). "Skin as a route of exposure and sensitization in chronic beryllium disease". Environ Health Perspect. 111 (9): 1202–1208. doi:10.1289/ehp.5999.
- John Burke Sullivan, Gary R. Krieger (2001). Clinical environmental health and toxic exposures. Lippincott Williams & Wilkins. p. 333. ISBN 0-683-08027-X.
- Barna, B (2003). "Clinical application of beryllium lymphocyte proliferation testing". Clin Diagn Lab Immunol. 10 (6): 990–994. doi:10.1128/cdli.10.6.990-994.2003.
- Donovan, E (2007). "Performance of the beryllium blood lymphocyte proliferation test based on a long-term occupational surveillance program". Int Arch Occup Environ Health. 81 (2): 165–178. doi:10.1007/s00420-007-0202-3.
- Henneberger, P (2001). "Beryllium sensitization and disease among long-term and short-term workers in a beryllium ceramics plant". International Archives of Occupational and Envirnmental Health. 74: 167–176. doi:10.1007/s004200100237.
- Witorsch, Philip and Spagnolo, Samuel V. (1994). Air pollution and lung disease in adults. CRC Press. p. 257. ISBN 0-8493-0181-5.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - Muller, C (2010). "Beryllium contamination and exposure monitoring in an inhalation laboratory setting". Toxicol Ind Health. 26 (1): 39–45. doi:10.1177/0748233709359276.
- Marshall, E (1999). "Beryllium screening raises ethical issues". Science. 285 (5425): 178–179. doi:10.1126/science.285.5425.178b.
- Kolanz, M (2006). "Evaluating beryllium exposure data". Environ Health Perspect. 114 (4): A213-A215. doi:10.1289/ehp.114-a213a.
- "Beryllium exposure". CNN. 29 January 2009.
- Henneberger, PK; Goe, SK; Miller, WE; Doney, B; Groce, DW (2004). "Industries in the United States with airborne beryllium exposure and estimates of the number of current workers potentially exposed". Journal of Occupational and Environmental Hygiene. 1 (10): 648–59. doi:10.1080/15459620490502233. PMID 15631056.
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