Abstracts of professional articles on
beryllium and beryllium disease

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Nonoccupational Beryllium Disease Masquerading as Sarcoidosis: Identification by Blood Lymphocyte Proliferative Response to Beryllium, by Lee S. Newman and Kathleen Kreiss, American Review of Respiratory Diseases 1992; 145:1212-1214

Chronic granulomatous lung disease caused by industrial exposure to beryllium continues to occur, but no community cases have been reported in more than 30 years. With the advent of a blood screening test that detects beryllium sensitization, physicians can discriminate chronic beryllium disease from sarcoidosis. A 56-yr-old woman in whom sarcoidosis was diagnosed had an unremarkable occupational history, but her husband was a beryllium production worker. Blood and bronchoalveolar lavage lymphocyte transformation tests, measuring the beryllium-specific cellular immune response, were abnormal, confirming a diagnosis of chronic beryllium disease. Chronic beryllium disease continues to occur in the nonoccupational setting and among bystanders in industry, masquerading as sarcoidosis. Because even transient or possibly low levels of exposure may cause disease, this case has important implications for how clinicians, industry, and government agencies define the populations at risk of chronic beryllium disease.

Beryllium Disease, by Lisa A. Maier and Lee S Newman, Environmental and Occupational Medicine, Third Edition, 1998, pgs 1021-1035

Beryllium is an excellent material for high technologic applications, but it produces a number of insidious adverse health effects. It is the fought lightest element (atomic weight=9.02), has a low density (1.85 g/cm3), high melting point, high tensile strength, and is corrosion resistant. Found in over 45 minerals, including some gemstones, beryllium is present at very low levels in soil and air in most urban centers. Exposure to beryllium occurs during the extraction of the mineral from its ores, beryl and bertrandite, and processing of beryllium into metal alloys and ceramic products. As indicated in Table 1, further exposure occurs during secondary machining and processing of the beryllium alloys and ceramic products in other industries, including electronics, aerospace, tool and die, nuclear weapons manufacturing, and dental prosthesis manufacturing. Historically, beryllium was used in the fluorescent light industry, although this practice was discontinued in the 1950’s upon recognition of its health hazards. Exposure to beryllium can induce delayed-type hypersensitivity, and dermatologic, pulmonary, and systemic disease, including the granulomatous condition chronic beryllium disease (CBD) (Table 2). This chapter summarizes our present state of knowledge based on the epidemiological workplace studies, basic research on the role of the immune response to beryllium, and clinical research on the diseases that ensue, and addresses the recent developments in CBD detection and diagnosis. The chapter emphasizes CBD, since this is now the most common form of beryllium toxicity, continuing to occur in 2% to 16% of exposed workers.

Beryllium Copper Alloy (2%) Causes Chronic Beryllium Disease, by R.C. Balkissoon, MD, DIH, MSc, and L.S. Newman, MD, MA, Journal of Occupational and Environmental Medicine, pgs 304-308.

We describe two newly confirmed cases of chronic beryllium disease who presented to our clinic from a facility that only used 2% beryllium copper alloy. These cases illustrate that the 2% beryllium copper alloy continues to cause chronic beryllium disease and that appropriate preventive measures must be taken to control exposures and educate industries and their workers about the hazards of beryllium alloys.

Beryllium: A Chronic Problem, Environmental Health Perspectives, Volume 102, Number 6-7, June-July 1994

In its early stages, CBD may be completely asymptomatic, as observed in apparently healthy individuals with lung X-ray abnormalities. In other cases, CBD may begin with nonspecific respiratory symptoms, including mild shortness of breath and cough, but no recognizable changes on chest films. Gradually, the majority of patients develop symptoms more characteristic of chronic disease: cough, burning, chest pain, progressive shortness of breath (dyspnea) wit exertion, weakness, fatigue, dyspnea at rest, and, characteristic of advanced disease, anorexia, weight loss, acrocyanosis, and clubbing of finger and toe bones. Signs of right heart failure and cor pulmonale (enlargement and strain of the right side of the heart due to increased pressure in the pulmonary artery from lung damage) may also be detected in advanced cases. CBD’s clinical course is extremely variable. Some individuals remain stable for many years, others progress more precipitously, developing severe respiratory symptoms within a few months. The majority experience a slow inexorable decline in pulmonary function. Mortality from CBD occurs in an estimated one-third of cases. "Most clinicians are taught that beryllium disease is a dinosaur," states Lee S Newman of the Occupational and Environmental Medicine Division, National Jewish Center for Immunology and Respiratory Medicine, in Denver. "But the chronic form of the disease is far from extinct. In fact, with increasing usage of beryllium in industry, the absolute number of cases can be expected to increase as well.’

Aerosols Generated During Beryllium Machining, John W Martyny et al, Journal of Occupational and Environmental Medicine, Volume 42, Number 1, January 2000, pgs 8-18

Some beryllium processes, especially machining, are associated with an increased risk of beryllium sensitization and disease. Little is known about exposure characteristics contributing to risk such as particle size. This study examined the characteristics of beryllium machining exposures under actual working conditions. Stationary samples, using eight-stage Lovelage Multijet Cascade Impactors, were taken at the process point of operation and at the closest point that the worker would routinely approach. Paired samples were collected at the operator’s breathing zone by using a Marple Personal Cascade Impactor and a 35-mm closed-faced cassette. More than 50% of the beryllium machining particles in the breathing zone were less than 10 micrograms in aerodynamic diameter. This small particle size may result in beryllium deposition into the deepest portion of the lung and may explain elevated rates of sensitization among beryllium machinists.

Pneumoconiosis and Exposures of Dental Laboratory Technicians, William N Rom et al, American Journal of Public Health, November 1984, Volume 74, No. 11, pgs 1252-1257

One hundred and seventy-eight dental laboratory technicians and 69 non-exposed controls participated in an epidemiological respiratory study. Eight technicians who had a mean of 28 years grinding nonprecious metal alloys were diagnosed as having a simple pneumoconiosis by chest radiograph. Mean values for per cent predicted FVC and FEV were reduced among male nonsmoker technicians compared to male nonsmoker controls; after controlling for age, there was also a reduction in spirometry with increasing work-years. An industrial hygiene survey was conducted in 13 laboratories randomly selected from 42 laboratories stratified by size and type of operation in Salt Lake City, Utah metropolitan area. Personal exposures to beryllium and cobalt exceeded the Threshold Limit Values (TLVs) in one laboratory. Occupational exposures in dental laboratories need to be controlled to prevent beryllium-related lung disorders as well as simple pneumoconiosis.

Lung Cancer Incidence Among Patients With Beryllium Disease: A Cohort Mortality Study, Kyle Steenland, Elizabeth Ward, Journal of the National Cancer Institute, 83: 1380-1384, 1991

We have conducted a cohort mortality study on 689 patients with beryllium disease who were included in a case registry. An earlier mortality study on 421 of these patients was limited to males and resulted in a determination of a nonsignificant twofold lung cancer excess based on only seven lung cancer deaths. We have extended this earlier study by including females by adding 13 years of follow-up. Comparison of the 689 beryllium disease patients with the U.S. population resulted in a lung cancer standardized mortality ration (SMR) of 2.00 (95% confidence interval = 1.33-2.89) based on 28 observed lung cancer deaths. Adjustment for smoking did not change these results. All causes of mortality were also significantly elevated (SMR = 2.19), largely because of the very high rate of deaths due to pneumoconiosis (primarily beryllium disease) (SMR = 34.23; 158 deaths). No other causes of death were significantly elevated. The excess of lung cancer was consistent for both sexes and did not appear to increase with duration of exposure to beryllium or with time elapsed since first exposure to this element. The case registry included those with acute beryllium disease, which resembles a chemical pneumonitis, and those with chronic beryllium disease, which resembles other pneumoconiosis. The lung cancer excess was more pronounced among those with acute disease (SMR = 2.32) than among those with chronic disease (SMR = 1.57).

Development of an Eight-Hour Occupational Exposure Limit for Beryllium, Paul W Wambach, Richard M Tuggle, Applied Occupational and Environmental Hygiene, Volume 15(7): 581-587, 2000

This article recommends an 8-hour occupational exposure limit (OEL) for beryllium. It responds to growing concerns about the continuing incidence of chronic beryllium disease despite the long-standing OEL for beryllium: 2 micrograms of beryllium per cubic meter of air,, 8-hour time-weighted average (TWA). Current 8-hour TWA beryllium OELs are not based on chronic beryllium disease toxicology and an increasing number of studies report incidence of chronic beryllium disease at exposure levels apparently below 2 micrograms/m3. The experience of the beryllium-exposed population of Lorain, Ohio, in the late 1940s and the ambient air regulatory standards derived from that event provide evidence that establishing a protective level is possible. These levels are used as the basis for a new recommended beryllium exposure standard. A correspondingly protective 8-hour TWA level of 0.1 micrograms/m3 has been derived, which, for commonly encountered workplace conditions (in terms of geometric standard deviation and percent-compliance), should provide long-term mean exposure protection comparable to that received by the unaffected Lorain subpopulation and provided by the Environmental Protection Agency (EPA) ambient standard. It is concluded that an exposure limit of 0.1 micrograms/m3 combined with exposure monitoring to assure a high rate of day-to-day compliance would provide better control of both long-term mean exposure levels and short-term levels than do current occupational exposure limits. The health data available, while certainly not conclusive, support further reductions in exposure levels to help minimize the incidence of chronic beryllium disease.

Beryllium Contamination Inside Vehicles of Machine Shop Workers, Wayne T Sanderson et al, Applied Occupational and Environmental Hygiene, Volume 14: 223-230, 1999

Inhalation of beryllium particles causes a chronic, debilitating lung disease—chronic beryllium disease (CBD)—in immunologically sensitized workers. Evidence thata very low concentrations of b eryllium may initiate this chronic disease is provided by incidences of the illness in family members exposed to beryllium dust from workers’ clothes and residents in neighborhoods surrounding beryllium refineries. This article describes the results of a cross-sectional survey to evaluate potential take-home beryllium exposures by measuring surface concentrations on the hands and in vehicles of workers at a precision machine shop where cases of CBD had recently been diagnosed. Many workers did not change out of their work clothes and shoes at the end of their shift, increasing the risk of taking beryllium home to their families. Wipe samples collected from workers’ hands and vehicle surfaces were analyzed for beryllium content by inductively coupled argon plasma-atomic emission spectroscopy (ICP-AES). The results ranged widely, from nondetectable to 40 micrograms per cubic foot on workers’ hands and up to 714 microcrams per cubic foot inside their vehicles, demonstrating that many workers carried residual beryllium on their hands and contaminated the inside of their vehicles when leaving work. The highest beryllium concentrations inside the workers’ vehicles were found on the drivers’ floor, indicating that workers were carrying beryllium on their shoes into their vehicles. A safe level of beryllium contamination on surfaces is not known, but it is prudent to reduce the potential for workers to carry beryllium away from the work site.

Chronic Beryllium Disease in a Dental Laboratory Technician, by R Kotloff, Paul Richman, J K Greenacre, and M Rossman, American Review of Respiratory Disease, 1993; Volume 147, p 205-207.

Workers involved in the manufacture of dental prostheses are exposed to a number of potentially harmful substances capable of inducing lung disease. In this report, we describe a dental laboratory technician who developed chronic beryllium disease as a result of exposure in the workplace. The diagnosis of chronic beryllium disease was suspected from the clinical, radiographic, and histologic features and confirmed by the in vitro proliferation of lung lymphocytes to beryllium salts. The potential risks of beryllium use in the dental industry have been recognized for some time, but this is the first documentation of chronic beryllium disease in this population of workers. Since chronic beryllium disease may be easily confused with sarcoidosis, awareness of this occupational association is essential in preventing misdiagnosis and in providing appropriate management.

Lung Granulomatosis in a Dental Technician, by P Brancaleone, B Weynand, P Devuyst, D Stanescu, and T Pieters, American Journal of Industrial Medicine, 34:628-631, 1998

Various types of pneumoconiosis have been reported in dental technicians such as silicosis, asbestosis, hard metal disease, and the so-called "dental technician's pneumoconiosis," in which Cr-Co-Mo alloys could play a role. Dental technicians are, indeed, exposed to various dusts and other forms of chemicals when polishing and grinding prosthetics and during casting operations. Mineralogic studies on bronchoalveolar lavage (BAL) and/or lung biopsies can be helpful in making the diagnosis of occupational lung disease. The particularity of the case we report is the exposure to several harmful occupational agents and the presence in the lung of non-caseating granulomas.

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