Preventing occupational disease and injury, second edition. Levy BS, Wagner GR, Rest KM, Weeks JL, eds. Washington, DC: American Public Health Association, 2005 Jan; :120-126
Inhalation of beryllium-containing dusts can cause a chronic interstitial lung disease (chronic beryllium disease, or berylliosis), characterized by noncaseating granulomas associated with cell-mediated immunity to beryllium. In addition to chronic beryllium disease, dermatitis can occur without sensitization in the beryllium extraction industry, and skin granulomas can occur when insoluble beryllium salts enter the skin. As a result of workplace medical surveillance with a blood test for beryllium sensitization, chronic beryllium disease is frequently diagnosed before symptoms appear. Beryllium sensitization is a cell-mediated immune reaction to beryllium identified through the beryllium-specific lymphocyte proliferation test, an in vitro assay on blood or bronchoalveolar lavage mononuclear cells that is currently available at six laboratories in the United States. Workers identified as sensitized undergo bronchoscopy with lavage and transbronchial biopsy to establish whether they have chronic beryllium disease. Chronic beryllium disease is diagnosed in sensitized workers when granulomas or mononuclear cell infiltrates are identified in biopsy samples. The clinical disease usually begins with slow onset of dyspnea on exertion, which may be accompanied by dry cough, weight loss, chest pain, and fatigue. Basilar rales may be present on physical exam. In more advanced disease, finger clubbing and signs of cor pulmonale can occur. Pulmonary function tests may show a decrease in diffusing capacity, an increase in alveolararterial oxygen gradient, airflow limitation, restrictive lung volumes, or a decrease in compliance. The chest x-ray may show irregular or rounded interstitial opacities and, in some cases, hilar adenopathy. These abnormalities are not diagnostic for chronic beryllium disease, which is differentiated from similar diseases, such as sarcoidosis, by the demonstration of a beryllium-specific cell-mediated immune response. Historically, a second lung disease, acute beryllium disease, was associated with beryllium exposure in parts of the industry dealing with beryllium extraction and soluble beryllium salts. Acute beryllium disease was thought to be a form of chemical pneumonitis caused by inhalation of high concentrations of beryllium (>100 ug/m3). The disease had rapid onset and was characterized by dyspnea, cough and sputum, chest pain, tachycardia, crackles, and cyanosis. Chest x-rays showed diffuse or localized infiltrates, which evolved over a few weeks. Pulmonary function tests showed decreased lung volumes and hypoxemia at rest. The hallmark of acute beryllium disease was its reversibility over a period of months, in contrast to chronic beryllium disease, although about one-third of cases were reported to eventually progress to chronic beryllium disease. It is possible that acute beryllium disease was a manifestation of reversible granulomatous disease which resolved when the soluble salts were excreted. Acute beryllium disease has not been diagnosed in the United States for decades. Present-day exposures in excess of 100 ug/m3 have not been recognized to cause acute beryllium disease, and the nature of acute beryllium disease remains unclear. A number of other entities, such as tracheobronchitis, were described historically, but these are not recognized today in the beryllium industry.