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Medical Aspects of Beryllium Use in Gemstone Enhancement

By S.K. Samuels, M.S., M.D., G.G.

At the American Gem Trade Association (AGTA) seminar in Tucson (February 7, 2003) on "Beryllium Diffusion Coloration of Sapphire," a number of comments and questions were raised about the health hazards of beryllium-treated gems. Other than the federal government's requirements for the handling of beryllium, no information was available.

Some earlier details were reported on bulk or lattice-treated stones (1) and were issued January 8, 2002 on the AGTA Web site. Another report appeared in Gems and Gemology (2). These reports suggest that one of the agents used in the treatment was beryllium, the light element Be⁴. The reason given for this treatment is to improve the color of the gem. The enhancement appears to produce color change in corundum from some localities to make the sapphire and rubies more pleasing. There currently is much consternation and confusion in the trade about the propriety of such treatments, their effect on full disclosure or lack thereof, and the effect of such treatment upon the valuation of gems. To add to the woes, there is evidence that such treatments pose a health hazard not only to the workers who process and cut the gemstones, but also to gem merchants who handle treated stones and the customer who wears such treated gems.

To address the issue of beryllium use and its medical effects, a brief literature search was made, and the results are presented here. They will help lay persons understand the medical risks beryllium poses to the jewelry industry.

This brief review shows that Be⁴ has important medical effects. Beryllium (BeO) is a silvery white metal and possesses some of the best mechanical properties of the light elements (3). The ore that is mined (in its natural state) has a chemical formula of Be₃Al₂Si₆O₁₀. It also is found in several other forms. In its oxide form (BeO), beryllium can cause illness, this effect is true whether inhaled or through skin contact.

It has been known for almost a century that miners exposed to the ore developed serious lung disease. These reports appeared in early 20th-century medical textbooks and indicated that exposed workers developed granulomatous lung disease similar to that seen in Silicosis and Pneumoconiosis, a condition of progressive lung disease leading to fibrosis, lung masses, pulmonary impairment, respiratory failure, and death. BeO is used in Uranium reactors, when plutonium is made from uranium.

Its use in high technology in the late 1940s led to the development of Chronic Beryllium Disease (CBD) in workers exposed to beryllium. CBD was found in workers who extracted and produced beryllium phosphor to make fluorescent lamps (4). In 1947, Hardy, et al., reported 17 fluorescent lamp workers with advanced pulmonary granulomatous disease. They reported that while the overall attack rate was between 1 to 16 percent, severe disease was noted in patients with low exposures, and tissue levels of beryllium do not correlate with the presence or the extent of the disease. CBD has also been reported in bystanders, as well as persons residing near beryllium processing plants (5). The list of industries that use beryllium includes:
1. aerospace foundries
2. beryllium extraction nuclear reactors
3. fabrication, smelting
4. ceramics nuclear weapons
5. dental alloys and prosthesis plating
6. electronics telecommunications
7. tool and die
To this list can be added heat-treaters of sapphires and rubies.

In 1951, Sterner and Eisenbud (6) described the immune pathogenesis of Chronic Beryllium Disease. Beryllium and other metals elicits a immunologic reactions in humans, including a delayed hypersensitivity reaction. Beryllium induces a proliferative response in the peripheral blood lymphocytes, consisting largely of T lymphocytes and CD 4 cells, along with elevations of serum immunoglobulins. (This reaction can be specific to beryllium.) In the lung, beryllium produces a active granulomatous disease. These granuloma are maintained by CD 4 cells. Some genetic factors appear to play a role; however, a detailed discussion of the subject is not germane to this paper (7). The development of CBD does not appear to be dose related. Family members who had no contact with beryllium were known to develop CBD, indicating that the exposure-response relationship is complex and that past exposure cannot be ignored.

Sterner and Eisenbud further reported on tests such as harvesting of lung cells by Broncho-alveolar lavage. They subsequently reported on other tests such as the Beryllium lymphocyte proliferation test (BLPT). These tests were carried out on workers in the ceramics industries. The tests may initially have been negative, but when followed longitudinally, the test was positive even after an interval of 15 years. They reported that beryllium induces an antigen-driven immunologic response. The results are not dose related, the threshold for sensitization to beryllium is low, but skin sensitization is high.

Given the above, it appears that workers who treat stones with beryllium are at risk for developing chronic beryllium disease. The incidence in workers exposed to beryllium is complex and is not known. Family members of beryllium miners have been known to develop CBD also. People in the jewelry trade and the end user (i.e., the customer) may also be at risk, due to the delayed hypersensitivity reaction which appears not to be dose related but, rather, related to complex genetic and other factors. This raises serious questions about acceptance of such treated material in the jewelry trade. Due to lack of details of the material used in the enhancement process, and keeping in mind that only some forms of beryllium — such as phospor, BeO and BeFe, and other analogues — can cause CBD, it is important to obtain further details about the form of beryllium used in the enhancement process. This information may also help in other ways, that may provide information leading to information that people who may have already exposed, and to access the risk it poses to those who come into contact with it in the future.

ENDNOTES

1. AGTA, Orange pink sapphire alert (2002), issued January 8. Web site.
2. T. Moses, Gem trade notes, Gems and Gemology, vol. 38, no. 3 (2002), 254-55.
3. Elements with small number of electrons.
4. H. L. Hardy and J. R Tabershaw, Delayed Chemical Pneumonitis occurring in workers exposed to beryllium compounds, J. Indust. Hygiene Toxicol. 28 (1946), 197-211.
5. Harrison, Text Book of Medicine, 424.
6. J. H. Sterner and M. Eisenbud, Epidemiology of beryllium intoxication. Arch. Indus. Hygiene Occup. Med. 4 (1951),123-57.
7. See Kathleen Kreiss, Frederick Miller, et al., Short Analytical Review. Chronic Beryllium Disease — From the Workplace to Cellular Immunology, Molecular Immunogenetics and Back, Clinical Immunology and Immunopathology, vol. 71, no. 2 (May 1994), 123-129.

Posted: April 15, 2003