We examined the epidemiology of chronic beryllium disease among a stratified, random sample (n = 895) of nuclear weapons workers using the blood beryllium lymphocyte transformation (BeLT) test and chest radiograph for case identification. Of 18 new cases of beryllium sensitization, 12 had beryllium disease, and three more developed pulmonary granulomas on lung biopsy over the succeeding 2 yr. Beryllium-sensitized cases did not differ from noncases in age, gender, race, ethnicity, smoking, most respiratory symptoms, spirometric or radiographic abnormalities, or job tenure. The six sensitized cases without initial disease differed from beryllium disease cases in having greater pack-years of smoking. Sensitization occurred among workers with inadvertent or bystander exposure, such as a secretary and security guard. However, beryllium sensitization risk was higher for machinists (4.7%) and for persons reporting measured overexposure (7.4%, odds ratio 5.1); exposure beginning before 1970 (3.6%, odds ratio 2.7); consistent beryllium exposure (3.4%); and sawing (4.7%) or band sawing (6.0%) of beryllium metal. We conclude that both individual susceptibility to sensitization and exposure circumstances are important in developing disease.

We examined the prevalence of beryllium sensitization in relation to work process and beryllium exposure measurements in a beryllia ceramics plant that had operated since 1980. We interviewed 136 employees (97.8% of the workforce), ascertained beryllium sensitization with the beryllium lymphocyte proliferation blood test, and reviewed historical industrial hygiene measurements. Of eight beryllium‐sensitized employees (5.9%), six (4.4% of participating employees) had granulomatous disease on transbronchial lung biopsy. Machinists had a sensitization rate of 14.3% compared to a rate of 1.2% among other employees. Machining had significantly higher general area and breathing zone measurements than did other processes in the time period in which most beryllium‐sensitized cases had started machining work. Daily weighted average (DWA) estimates of exposure for machining processes also exceeded estimates for other work processes in that time period, with a median DWA of 0.9 μ/m3. Machining process DWAs accounted for the majority of DWAs exceeding the 2.0 μg/m3 OSHA standard, with 8.1% of machining DWAs above the standard. We conclude that lowering machining process‐related exposures may be important to lowering risk of beryllium disease. © 1996 Wiley‐Liss, Inc.

Objectives-To describe relative hazards in sectors of the beryllium industry, risk factors ofberyllium disease and sensitisation related to work process were sought in a beryllium manufacturing plant producing pure metal, oxide, alloys, and ceramics. Methods-All 646 active employees were interviewed; beryllium sensitisation was ascertained with the beryllium lymphocyte proliferation blood test on 627 employees; clinical evaluation and bronchoscopy were offered to people with abnormal test results; and industrial hygiene measurements related to work processes taken in 1984-93 were reviewed. Results-59 employees (9.4%) had abnormal blood tests, 47 of whom underwent bronchoscopy. 24 Beryllium exposure leads to cell mediated immunological sensitisation in a small percentage of workers exposed to beryllium aerosols, dusts, or fumes; of the sensitised workers, many have granulomatous lung disease.' Prevention of beryllium disease depends on knowledge of risk factors which can be modified. Although inborn genetic factors are associated with risk of disease in those exposed to beryllium,4 these cannot be changed in an existing workforce exposed to beryllium. In contrast, work related risk factors offer the opportunity to lower risk of beryllium disease and to understand the exposure characteristics associated with high disease rates. In our previous studies of plant workforces exposed to beryllium, we found risks of beryllium sensitisation or disease related to work processes in three plants representing single sectors of the beryllium industry. These include machining of beryllium metal,' grinding, dicing, and drilling of beryllia ceramics,' dry pressing, and research and development in a plant which manufactured beryllia ceramics historically.' We report here the results of epidemiological and exposure surveillance in a plant which encompasses most sectors of the beryllium industry in production of beryllium metal, alloys, and beryllium oxide from which ceramics were made historically. We sought to describe risks of beryllium disease related to work processes which could provide opportunities for future study of exposure variables conferring excess risk. Understanding of qualitative and quantitative exposure-response relations is critical to prevention of disease in the many sectors of the beryllium industry.The plant opened in 1953 to produce beryllium-copper alloy, which is cast and fabricated into tubes, wire, sheet, plates, and metal parts before shipment to other factories to become finished products. Beryllium metal operations were developed in about 1957 in buildings and under management which were largely separate from alloy operations. Beryllium metal is produced from beryllium hydroxide through a chemical process. The two component areas involved in beryllium metal production are the pebble plant, which contains fluoride and reduction furnaces, and vacuum melting.' As the crystalline structure of cast beryllium metal is unsuitable for many applications, the metal is partitioned into differing grade...

The blood beryllium lymphocyte proliferation test is used in medical surveillance to identify both beryllium sensitization and chronic beryllium disease. Approximately 50% of individuals with beryllium sensitization have chronic beryllium disease at the time of their initial clinical evaluation; however, the rate of progression from beryllium sensitization to chronic beryllium disease is unknown. We monitored a cohort of beryllium-sensitized patients at 2-year intervals, using bronchoalveolar lavage and repeated transbronchial lung biopsies to determine progression to chronic beryllium disease as evidenced by granulomatous inflammation in lung tissue. Fifty-five individuals with beryllium sensitization were monitored with a range of 2 to 5 clinical evaluations. Disease developed in 17 sensitized individuals (31%) within an average follow-up period of 3.8 years (range, 1.0-9.5 years). Thirty-eight of the 55 (69%) remained beryllium sensitized without disease after an average follow-up time of 4.8 years (range, 1.7-11.6 years). Progressors were more likely to have worked as machinists. We found no difference in average age, sex, race or ethnicity, smoking status, or beryllium exposure time between those who progressed to chronic beryllium disease and those who remained sensitized without disease. We conclude that beryllium sensitization is an adverse health effect in beryllium-exposed workers and merits medical follow-up.