Beryllium disease

Beryllium, on the other hand, is toxic. Beryllium disease, originally called berylliosis, was first noted in the 1930s in German and Russian plants set up to extract the metal from beryllium ores such as beryl. As the use of this metal has increased, so also has the incidence of this disease. It occurs in both acute and chronic forms. 

The acute form, which develops immediately after exposure, often shows up as a severe inflammation of the upper respiratory tract. Patients have severe difficulty in breathing, develop a disabling cough, and have a buildup of fluids in the lungs. If the beryllium is lodged in a crack in the skin, an ulcer develops, which heals only after the metal is removed. Most patients afflicted with the acute form recover, but some develop the chronic form. 

Both forms of beryllium disease are most likely related to the ability of the beryllium to bond covalently with the nitrogen and oxygen atoms in proteins. Beryllium replaces magnesium in Mg-activated enzymes and therefore interferes with the 

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Beryllium-containing materials can be potentially harm fill if mishandled. Care must be taken in the fabrication and processing of beryUium products to avoid inhalation of airborne beryllium particulate matter such as dusts, mists, or fumes in excess of prescribed workplace limits. Inhalation of fine airborne beryllium may cause chronic beryllium disease, a serious lung disorder, in certain sensitive individuals. However, most people, perhaps as many as 99%, do not react to beryUium exposure at any level (see Beryllium and beryllium alloys). 

Similarly, data already available indicate that SNPs will be quite relevant in immunotoxicology and immunopharmacology. Findings that SNPs of immune-related proteins have an impact on the development of beryllium disease and silicosis suggest that SNPs may explain much of the daunting diversity of human responses to environmental and pharmaceutical agents. 

Maier, L. A., et al., High beryllium-stimulated TNF-alpha is associated with the -308 TNF-alpha promoter polymorphism and with clinical severity in chronic beryllium disease, Am. J. Respir. Crit. Care Med., 164, 1192, 2001. 

An immunologic basis for chronic beryllium disease has been postulated and a hypersensitivity phenomenon demonstrated. Consistent with the concept of chronic berylliosis as a hypersensitivity pulmonary reaction are the following Persons with berylliosis also show delayed cutaneous hypersensitivity reactions to beryllium compounds their peripheral blood lymphocytes undergo blast transformation and release of macrophage inhibition factor after exposure to beryllium in vitro helper/suppressor T-cell ratios are depressed and there is lack of a dose-response relationship in chronic beryllium cases. Hypersensitization may lead to berylliosis in people with relatively low exposures, whereas nonsensitized individuals with higher exposures may have no effects. 

Steenland K, Ward E Lung cancer incidence among patients with beryllium disease a cohort mortality study. J Natl Cancer Inst 83 1380-1385, 1991... 

The current permissible exposure levels for beryllium of 0.01 mcg/m3 averaged over a 30-day period or 2 mcg/m3 over an 8-hour period are insufficiently protective to prevent chronic beryllium disease. Both NIOSH and the ACGIH have recommended that the PEL and TLV be reduced to 0.05 mcg/m3. These recommendations have not yet been implemented. 

Because of the increasing use of beryllium in a growing diversity of end products, a new study of beryllium disease was undertaken by the U.S. Department of Defense and the U.S. Department of Energy, as of December 1991. This study was precipitated by finding that nuclear-related weapons... 

H.C. Williams, Beryllium workers sarcoidosis or chronic beryllium disease sarcoidosis, 6(supp.) 34-35, 1989. 

LB = Lewis base bht = 2,6-di(f-butyl)-4-methylphenoxide bo = l-metalla-2,6-dioxo-3-aza-4,5-diphenylcyclohex-3-ene CBD = Chronic beryllium disease dbp = 2,6-di(t-butyl)phenoxide dfhd = 1,1,1,2,2,3,3,7,7,7-decafluorohept-ane-4,6-dionato dmmhd = 2,6-dimethyl-2-methoxyheptane-... 

Beryllium metal has properties that make it technologically attractive (Alderighi et al, 2000), but these advantages are counterbalanced by the toxicity of inhaled beryllium dust, which can cause chronic beryllium disease (Sauer et a/., 2002). The etiology of this immune hyper-response disease (Eontenot et a/., 2001) is poorly understood, but the final disease state is characterized by lung failure. 

Sauer, N. N., McCleskey, T. M., Taylor, T. P., et al, Ligand associated dissolution of beryllium toward an understanding of chronic beryllium disease. Technical report LA-UR-02-1986, Los Alamos National Laboratory (2002). 

Skin lesions are the most common industrial exposure symptom. Three distinct skin lesions have been noted following exposure to beryllium dermatitis, ulceration, and granulomas. There appears to be an immunological component to chronic beryllium disease, including the dermal responses. 

Williams WJ (1988) Beryllium disease. Postgraduate Medical Journal 64 511-516. 

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