Acute beryllium disease

A major restraint concerning the utility of the clinical determination of beryllium in biological samples is the lack of correlation between beryllium levels and disease (Dutra et al. 1949). However, measuring the mass of alveolar-deposited beryllium may make this possible (Kent etal. 2001). Acute beryllium disease is a toxic tracheo-bronchitis/pneumonitis, and a correlation... 

In contrast to acute beryllium disease, chronic beryllium disease still occurs but is due to an immune response to beryllium that occurs in a minority of exposed vorkers (Eisenbud and Lisson 1983). Therefore, in this condition the determination of an immune response to beryllium has more important clinical utility than the determination of beryllium levels (US Department of Energy 1999). 

In 1949, the Atomic Energy Commission adopted limits for beryllium exposure in the workplace of 25 pg m as a peak value and 2 pg m averaged over an 8-h day. These standards have essentially eliminated acute beryllium disease, and the last reported case occurred during the 1960s in the United States (Eisenbud and Lisson 1983). However, chronic beryllium disease has continued to occur, and recently the... 

Exposure to elevated concentrations of beryllium, usually in the 25 pg/m range or greater, (120) can result in inflammation of the upper and lower respiratory tract and airways, tracheitis, bronchiolitis, pulmonary edema, and a lymphocyte-predominant chemical pneumonitis (12,121-123). Although significantly less common than CBD, acute beryllium disease stiU occurs globally. In 2004, nine cases were reported from a South Korean liquid metal factory where measured beryllium exposures ranged from 3.13 to 112.3 pg/m (12). The manifestations... 

Rom WN, Lockey JE, Bang KM. Reversible beryllium sensitization in a prospective study of beryllium workers. Arch Environ Health 1983 38 302-307. Kim Y. Acute beryllium disease in metal workers. Eur Respir J 2004 24 149S. Henneberger PK, Cumro D, Deubner DD, et al. BerylUum sensitization and disease among long-term and short-term workers in a herylUum ceramics plant. Int Arch Occup Environ Health 2001 74(3) 167-176. 

Acute pulmonary disease is due exclusively to inhalation of soluble beryllium salts and is not caused by exposure to the oxide, the metal, or its alloys. The exact forms of beryllium causing the chronic pulmonary disease and the degree of exposure necessary to induce it are not precisely known. It is known that under the completely uncontrolled conditions existing in bery llium extraction plants before the establishment of air-count standards in 1949, when beiyllium air-counts were in milligrams per cubic meter of air rather than micrograms, only about 1% of the exposed workers became ill This would indicate a sensitivity of a limited number of individuals to beryllium. 

Exposure is usually by inhalation. It s compounds can cause dermatitis, acute pnemnonitis, acute lung disease and a specific disease (beryllium disease), that erodes the limgs leading to lung cancer, making it hard to walk, causing severe pain and exhaustion, and usually resulting in a slow, painful death by suffocation. 

Examples Silicosis, asbestosis, pneumonitis, pharyngitis, rhinitis or acute congestion farmer s lung, beryllium disease, tuberculosis, occupational asthma, reactive airways dysfunction S5mdrome (RADS), chronic obstructive pulmonary disease (COPD), hypersensitivity pneumonitis, toxic inhalation injury, such as metal fume fever, chronic obstructive bronchitis, and other pneumoconioses. 

Beryllium-related pulmonary manifestations exist on a continuum from acute inhalational injury to acute pneumonitis, beryllium sensitization, and the chronic form, that has been called berylliosis, chronic berylliosis, and which is now known as chronic beryllium disease (CBD). 

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. 

Beryllium disease occurs in acute and chronic forms. Acute berylliosis is a form of adult respiratory distress syndrome and for all practical purposes is no longer seen, since it only occurs with high exposure. 

Beryllium exposure occurs in a wide variety of occupations. It may cause acute berylliosis (currently very rare), beryllium sensitization, chronic beryllium disease, or lung cancer. Imaging manifestations of chronic beryllium disease are generally similar to those of sarcoidosis, with nodules, ground glass abnormality, septal thickening, conglomerate masses, and mediastinal or hilar lymphadenopathy. 

Elemental Be and its compounds are very poisonous by inhalation or intravenous route. Chronic inhalation of beryUium dusts or fumes can cause a serious lung disease, beryUiosis, after a latent period ranging from several months to many years. Inhalation of airborne dusts can also cause an acute disease manifested as dyspnea, pneumonitis and tracheobronchitis with a short latency period of a few days. Skin contact with soluble salts of the metal can cause dermatitis. Beryllium also is a carcinogen. There is sufficient evidence of its inducing cancer in animals and humans. 

Beryllium is a very toxic metal. It is especially dangerous in powder form. The effects of inhaling beryllium powder can be acute or chronic. Acute effects are those that occur very quickly as the result of large exposures. Chronic effects are those that occur over very long periods of time as the result of much smaller exposures. Acute effects of inhaling beryllium powder include pneumonia-like symptoms that can result in death in a short time. Chronic effects include diseases of the respiratory system (throat and lungs), such as bronchitis and lung cancer. 

Treatment of the acute disease includes bed rest, oxygen therapy, mechanical ventilation when needed, and corticosteroids. Chelation has been used to treat beryllium toxicity however, no one agent is recommended over another. Aurin tricarboxylic acid has been used to protect primates from beryllium overdose, but human trials have not been conducted. 

Beryllium Metallic Chemical cartridge, clean work clothes daily, gloves and eye protection. Acute disease may require hospitalization with administration of oxygen, chest x-ray should be taken immediately. Flush with water followed by washing with soap and water. All cuts, scratches, and injuries should get medical attention. 

Caution Death may result from short exposure to very low concns of the element and its salts. Contact dermatitis, chemical conjunctivitis, corneal burns, non-healing ulceration at site of injury, subcutaneous nodules may occur following exposure. Acute Pneumonitis may result from single exposure to beryllium and occasionally is fatal. Chronic Pulmonary granulomatous disease may appear in 3 months tn 15 years, often after short exposure to low concn. Uncertainty as to complete recovery. Death rate about 25%. See I. Schubert. Beryllium and Barylliosis in Set. Am. 199, no. 2, pp 27-33 (1938). This substance and certain beryllium compounds may reasonably be anticipated to be carcinogens Fourth Annual Report on Carcinogens (NTP... 

Chronic fibrotic occupational lung diseases include asbestosis (see p 121), silicosis, coal workers pneumoconiosis, and a few other less common fibrotic lung diseases associated with occupational exposures to such substances as beryllium and hard metal (cobalt-tungsten carbide). These conditions occur after years of exposure and with long latency, although patients may present for evaluation after an acute exposure. Referral for follow-up surveillance is appropriate if exposure is anticipated to be long term. 

Beryllium (CAS 7440-41-7) Very high acute exposure to dusts and fumes cause eye, skin, and respiratory tract irritation. However, more importantiy, chronic iow-ievei exposures to beryiiium oxide dusts can produce interstitiai iung disease caiied beryiiiosis, which is a sarcoidlike condition that can have extrapulmonary manifestations. A carcinogen in test animals. There is limited evidence of carcinogenicity in humans (lARC 1). 

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