* Ag: antigalling, Ca: castability, Co: electrical conductivity, Cr: corrosion resistant, D: use discontinued, Ds: dimensional stability, Er: electrical resistivity, Fo: formability, Hc: heat conductivity, Hr: heat resistant, Lw: light weight, Nm: neutron moderator, No: naturally occurring (as emerald and aquamarine), Ns: non-sparking, Sf: stiffness, Sp: springiness, St: strength, Wr: wear resistant, Xt: X-ray transparent.

Beryllium:

Toxicity, Etc...

by Anthony Theo Jr. Dore

Beryllium is a highly toxic metal and if exposed to it, at or above the threshold values, it can lead to a chronic beryllium disease (CBD) (i.e. berylliosis) or an acute beryllium disease. Toxic exposure to beryllium is most often thru an inhalation pathway. Beryllium has a variety of effects. Some beryllium combines with a protein and is deposited in the liver, spleen and kidneys, but the beryllium when bound with a biological protein, a hapten, can result in the chronic form of the disease which is believed to be a delayed hypersensitivity immune response. The major toxicological effects of beryllium are on the respiratory tract,specifically the lungs and their alveoli.

Beryllium and its unique characteristic led to it being used widely in a variety of industries prior to is know toxic effects. Today it is know that beryllium is a highly toxic material which results in devastating toxic effects on the lungs. There has been drastic increases in the regulation in beryllium use so as to protect those that directly handle and work with the metal. With theses regulations, beryllium is fairly safe to work with and use in a variety of products and industries. In the following text, there will be a description of beryllium confusing history and toxic effects on the respiratory system of man.

Beryllium has the symbol Be. In the older chemical literature, beryllium is called glucinium after the Greek word glykys meaning sweet, because of Vauquelin's initial description and observation of Beryllium. Beryllium's atomic number is 4, its atomic weight is 9.01 and in its pure metal form it melts at 1278 degrees Celsius.

The Beryllium element, an alkaline earth metal which belongs to group II of the periodic table, was first discovered in 1798 by L.M. Vauquelin. Vauquelin,a French chemist, was doing work with aluminum and noticed a white powder that was nothing like that of aluminum or any of its derivatives. Vauquelin named this mystery powder, gluinium because of its sweet taste was like that of glucose. In 1828, Wohler, a German metallurgist reduced it to its metallic form and renamed it beryllium.(figure 2)

There was no commercial application of beryllium until 1918 when Cooper patented a beryllium-aluminum alloy, which turn into the 'jump-start', into extending beryllium's application.

Following Cooper's patent of the beryllium alloy, Charles II in 1921, was intrigued by beryllium's light weight, extreme stiffness, high heat absorption and interesting nuclear cross section. Charles II was looking at beryllium and its unique characteristics to try and see if there was any potential for it to be used in any industrial practices. It turned out that Charles II was on to something.

Several properties account for beryllium metal's considerable value in modern industry. It has a very high stiffness to weight ratio and low density and it has the strength of steel without steel's weight. It also has a low coefficient of thermal expansion, has an unusually high melting point and has good thermal and electrical conductive properties. Also, alloys containing beryllium are corrosive resistant and small amounts of beryllium in an alloy gives this alloy a higher resistance to metal fatigue. These properties make the beryllium metal very useful in the aerospace, nuclear power, and electronics industries, along with the automobile and computers industries. (If you weren't reading this on the web, this is where you would be turning to figure 1)

The raw material from which beryllium was first refined was supplied from domestic deposits of beryl ore. With a domestic resource of beryl ore (beryllium), beryllium was immediately exploited for the first time industrially in the phosphors for fluorescent lights.

Brush II and C.Baldwin Sawyer started Brush Laboratories (1921), one of the first laboratories to further understand and explore commercial/industrial uses for beryllium. In 1926, the true value of beryllium was discovered. Beryllium was perfect as a precipitation hardener in cooper and nickel. Corson patented a beryllium-cooper-nickel alloy in United States. In Germany, around the same time as Corson's patent, Siemens, the German electrical components company, patented binary alloys of beryllium-cooper-cobalt in Germany.

The Beryllium Corporation of America, founded by Lester Hofheimer in 1927, was the first commercially producing company of beryllium-containing materials. Andre w Gahagan, decided to get into the beryllium industry in 1929 and formed the Bery llium Development Corporation, and later, gained control of the Beryllium Corporation of America and changed its name to the beryllium corporation(Berylco) in the year 1932. The patents and founding of several beryllium corporations sky-rocket ed between the years 1921, when Brush Laboratories was started to 1932 when Andre w Gahagan was trying to start a small monopoly.

Initially, in the 1930s,small amounts of Be-cooper alloys, Be-oxide compounds an d metallic beryllium were made but their growth in production was stimulated dramatically, through the increased demand of beryllium-cooper products used in World War II. Along with the increased demand of World War II, a third US producer of beryllium related products, manufactured beryllium oxide mainly for their use in the fluorescent lamp industry. Beryllium was starting to truly expand in its applications from metallic alloys to their use in fluorescent lights.

During and immediately following the second world war, a lot of research was being done in the area of nuclear fission and beryllium physical and chemical characteristics, lead to beryllium being of great interest to the nuclear scientists. This work, as well as all the previous work in the metallic alloys and fluorescent light industries, was done prior to any valid knowledge of the potential hazards of beryllium. Therefore, all this work was done without the use of any protection or precautions, which came back to due some serious damage to those who worked with beryllium directly and the industry.

As early as the 1930s, the period when beryllium products were being made in a high quantity, there were reports of a beryllium related disease which appeared in the European medical literature. These claims/reports went basically unnoticed or disregarded in the United States supposedly because the findings failed to show a clear and direct relationship of beryllium causing the disease. This may be the sole reason but bearing in mind that the United States was heavily dependent on these beryllium products in their military efforts of World War II, as well as being heavily invested in the beryllium alloys, there may have been other heavily weighing factors which the government did no want to explain so they choose to simply say that the European literature was scientifically unsound.

The beryllium related disease was first reported in Germany in 1933. This report stated that beryllium induced lung disease and was recognized as the cause of numerous cases of disability and death among beryllium workers. As well as this report from Germany, a fluorescent light company in Massachusetts reportedly had a few cases of a similar disease in the thirties and forties. Dr. Howard Van Ordstr and wrote the first paper on beryllium toxicity in the United States in 1943 and included three cases of "chemical pneumonia in workers extracting beryllium oxide. Interestingly enough, this important finding of Dr. Van Ordstrand, was overshadowed by the United States Public Health Service Bulletin, known as the Fairhall report.(10) The Fairhall Report stated that beryllium was toxicologically inert and speculated that the toxicity associated which beryllium was caused by the fluorides or oxyflourides in the compounds.(10) This among other errors and misconceptions were made in the exploration of beryllium's use which lead to various controversies and confusions while beryllium was initially being exploited. case and point, the Fairhall Report!

The reason for the gross mistakes in the research warranting the Fairhall Report is believed to be in the poor planning, and the questionable animal experiments along with the fact that there was a clear ignorance of the more appropriate and applicable human case reports. It took thirty years of the more knowledgeable scientists continually pointing out the blatant mistake of the Fairhall Report before the United States Public Health Service issued a document recanting the original finding of the Fairhall Report. During this thirty year time period, the Fairhall Report was considered valid and exact by the industry and manufacturers because after all, these finding were released by a government agency. So the manufacturers for thirty years or more, believed this report with 'blind faith'. It wasn't for approximately approximately fifteen years that the true hazards and standards for using beryllium were initially established.

With beryllium research being so contradictory and confusing as to the direct relationship of beryllium and the questionable disease many organizations and agencies were reluctant in issuing regulation on the use of beryllium. As an example, the State of California which is known for its strict governmental regulation and oversight, the scientific advisory panel of the State of California, in connection with proposition 65, addressed the problems by saying that,"...Beryllium is a good example of a chemical that for which the scientific data is very ragged, patchy and contains a lot of holes. Therefore, it is going to be very difficult to make any kind of regulatory or scientific decision based on the information that is available regarding its oral administration, its inhalation administration or administration by pulmonary routes."(12) This was stated in 1987, so even after the correction of the Fairhall Report there were still contradicting findings as to the exact hazards in dealing with beryllium. Various findings may have been clear as to the hazards of beryllium but they may not have been convincing enough to warrant governmental regulation. This being in 1987, the issue may have not been directly related to whether or not beryllium was hazardous but it may have been addressing more the uncertainty of beryllium's carcinogenic potential. This will be address further into the text and will show that beryllium's potential hazards are confusing and uncertain, at least for a period of time.

After the Van Ordstrand paper and the Fairhall Report, Van Ordstrand reported on 170 cases of dermal and respiratory illnesses among beryllium workers including five fatal cases of pneumonia. It is now recognized that beryllium can cause two types of lung injury:(1) an acute chemical pneumonitis, and (2) a chronic inflammatory lung lesion characterized by granuloma formation which is indistinguishable histopatyhologically from sarcoidosis.(figure 4

In 1946, Hardy and Tabershaw reported 17 cases of "delayed chemical pneumontis" among fluorescent lamp workers exposed to beryllium compounds. Of the 17, the first four all came from the same fluorescent lamp plant which led to the conclusion that it was an occupational lung disease. Further investigation and studies led to the delayed lung disease being called, chronic beryllium disease (CBD).As well as the chronic beryllium disease, there is also an acute illness which was initially mentioned in one of Van Ordstrand's earlier investigations of 1943.

Along with the 17 case findings of Hardy and Tabershaw(1946), other cases of CBD and 'neighborhood' cases were arising in Lorain, Ohio.

In Lorain Ohio, there was a beryllium processing plant and its workers as well people in the area around the plant were showing signs of the beryllium disease. This was interesting in that several of the individuals with the beryllium disease, never were employed in the beryllium plant and they had never knowingly been exposed to beryllium. Why then were these people if never exposed to beryllium, having symptom of the beryllium disease and how were they being exposed? What was found, was that the fumes and exhaust form the processing of the beryllium, were contaminating the air outside the plant and exposing the surrounding area to apparently toxic levels of beryllium. The amount of toxic material needed to induce berylliosis is in the range of milligrams to micrograms, and its onset can be from years to decades after exposure.

This lead to the establishment of 'out-plant' standards for beryllium which are still to this day in effect. This type of 'out-plant' regulation was the first of its kind and was 25 years before any other type of regulation was imposed for plant production and air pollution(1940s). According to Farber and Wilson(1961), the Lorain incident, "represents the first reported epidemiological study of a chronic disease due to air pollution in which beryllium has been established as the etiological agent."(5) Beryllium was ahead of its time as far as being regulated, although its disease and rapid growth of applications warranted such regulation.

Eisenbud, was the principle investigator of the Lorain Incident and through his work, it was decide that there should be some type of limits for beryllium exposure. What he decided was that there was a need for two separate limits based on the premise that the acute disease was a direct dose-response, and the chronic disease which appeared to be a selective response of the immune system. Essentially what was derived from his findings was that to prevent being afflicted with the acute disease, a single exposure ceiling level was needed and to keep from getting the chronic beryllium disease, a long term average exposure was need for those that constantly worked with beryllium.

This led to the 'Eisenbud levels' for beryllium exposure;

(1)to control acute disease, an in-plant maximum concentration of 25 ug beryllium/m3 of air measured,

(2) to control the chronic disease, an in-plant concentration of not to exceed 2 ug/m3 of air averaged over an eight hour day and third, in light of the Lorain incident, to protect the general public in the vicinity of a beryllium plant, a concentration not to exceed 0.01 ug/m3 of air as a monthly average concentration.

Eisenbud's level seemed so reasonable and valid for the time that, the first two, were adopted by the American Industrial Hygiene Association, the American Conference of governmental Industrial Hygienists and there American National Standards Institute. These profound levels were also, in 1972, used as a consensus standard by the Occupational Safety and Health Administration. Eisenbud's third level was adopted by the United States Environmental Protection Agency in 1974 as a National Emissions Standard for Hazardous Air Pollutants and in Section 112 of the Clean Air Act.

{As an aside, in recalling our lecture in class given by Dr. Gordon on respiratory toxicology, bearing in mind that beryllium is such a highly toxic material, should it's exposure levels be changed to an one hour time frame as opposed to theeight hour exposure limit enforced presently? I only bring this up due to Dr. Grodon's mention of the debate presently going I in California about changing the threshold limit values of ozone from it's present eight hour time frame to a one hour time frame. Although, the ozone has peak levels during the day and lower levels during the night and early morning prior to rush hour.}

Interestingly, up until 1984, the vast amount of research literature on the pulmonary effects of beryllium and its compounds, there was no specific article/report directly addressing the 'effectiveness' of the threshold limits whichwere adopted in 1949, based on Eisenbuds findings and recommendations. Otto P. Preuss states in a 1984 paper, A Contribution to the Epidemiology of Beryllium Disease that, " The validity of the TLV of 2ug/m3 of air and a thirty minute peak value of 25ug for the prevention of disease has generally been accepted on the basis of overall impressions. However, to date it has never been confirmed in a published study."

The conclusions made by Preuss through his own observations, retrospectively, are as follows:

1. Exposure to dusts or fumes from pure beryllium metal and beryllium alloys will not cause acute beryllium disease.

2. The high selectivity of CBD, and our knowledge that the lymph cells of diseased individuals show evidence of sensitization, justifies the assumption of immune mechanism as its cause.

3. Sensitized individuals still require minimum exposures for the development of disease.

4. No new cases of CBD have occurred whenever the adopted TLV of 2ug was maintain.

So even with out the 'validation' Preuss said Eisenbud's labels were lacking, they still were correct and effective in decreasing the number of CBD cases.

With all the new regulation and strict levels being established, a lot changes in the beryllium industry on a whole were taking place. Various plants were closing due to the increased awareness of the hazardous potential of beryllium and the search for alternatives to beryllium led to the decrease in the number of products using beryllium in its production. This was during the 1948-49 time period. In time, 1960-1980, the beryllium industry reemerged and overall, the Eisenbud level proofed to be effective in lowering the number of CBD reports, in light of the increase of beryllium production and the number of employees. This data was collected in 1983.(2) Still with the decrease in the number of beryllium disease cases, reports of the disease still continue to occur, despite the generalized adoption of current air standards. Granted the majority of these reports are due to accidental exposure to spills and/or unmaintained equipment.(4)

In 1975 OSHA tried to get the level for the average daily concentrations of beryllium from 2ug to 1ug and also to reduce the maximum concentration from25ug to 5ug. This was done in light of the finding that beryllium was also considered a cancer causing agent and needed further and stricter regulation but this was never passed, because of, once again the lack of sufficient evidence.

The use of beryllium containing materials is expanding from the traditional high technology applications in electronics, aerospace, communications and nuclear devices to such consumer products as household appliances, business machines and automobiles and even recreational equipment like golf clubs. (another figure that you can't see is referenced here)

Beryllium is not an essential element in the body and its compounds form insoluble precipitates at acid pH which make them rarely absorbed from thegastrointestinal tract. However, contact with water-soluble beryllium salts may result in acute dermatitis or lesions if they come into contact with a mucous membrane. The most dangerous way that beryllium gets into the body via inhalation through the respiratory tract with the effects being predominantly on the lungs, particularly the alveoli.

Beryllium effects are the most serious in the lungs, after it gets absorbed, it can be distributed throughout the body. Beryllium detection can be done through blood and urine analysis but, these methods of analysis can only be used as a way to determine or confirm if there has been exposure to beryllium, but not the extent of the exposure. The lungs are engaged in a constant struggle with the environment, with each breathe we take. We constantly inhale unwanted particles, aerosols and gases, most of which are not harmful but others injure the lungs through their effects on the immune system or other mechanisms. Exposure to a chemical by inhalation can have two effects; it can have an effect on the lung tissue and on distantorgans that are reached after the chemical enters the body's blood stream after being inhaled.

The inhalation of beryllium is usually encountered in the smelting and manufacturing operations and has also been associated, not conclusively, with cancers of the respiratory tract. Clearance of inhaled beryllium is multiphasic, half is cleared in about two weeks; remainder is removed slowly and a residuum becomes fixed in the tissue probably within fibrotic granulomata. Chelating agents, for example, aurintricarboxylic acid has been found to be effective in rats and mice if given parenterally within eight hours after intravenous injection of an otherwise lethal dose of beryllium sulfate.(1) Despite these findings, chelating agents are ineffective in chronic beryllium poisoning cases.

People who have been exposed to beryllium and are showing ill effects, can be treated with meso-2,3-dimercaptosuccinic acid (DMSA) or 2,3-dimercaptopropane 1-sulfonate (DMPS), two chelating agents, at a dose of 50 mg/kg, and show asignificant mobilization of beryllium into feces which is reflective of a decrease in hepatic, renal and spleen levels of beryllium.(1) In this work there was no mention as to the effects of DMSA and DMPS on beryllium in the lungs although there was mention of these chelating agents having no effect on decreasing the levels of beryllium in the blood.(1) With these findings in mind, it seems unlikely that the chelating effects of DMSA and DMPS on chelating beryllium out of the lung would be successful.

Beryllium has effects on various organs of the human body of whichthe lung are beryllium primary target. The skin or dermal effects of beryllium exposure is contact dermatitis and this is the most common type of a beryllium-related toxic effect. Exposure to soluble beryllium compounds may result in papalovesicular lesions of the skin, which is a delayed type hypersensitivity reaction and cell mediated.

It is now recognized that beryllium can cause two types of lung injury: (1) an acute chemical pneumonitis and (2) a chronic inflammatory lung lesion characterized by granuloma formation.(figure 3

Acute beryllium disease was first documented in beryllium workers by Weber and Engelhardt in Germany in the 1933. Acute tissue reactions induced by beryllium are characterized by nonspecific inflammation similar to that caused by other mucosal irritants. The first reports of this disease in the United States was by Van Ordstrand in 1943 which drew attention to beryllium's possible health hazards. It was found that acute beryllium disease was due to dust or fumes of soluble beryllium salts which are the products of beryllium oxide and metallic beryllium production.

There are two types of acute beryllium disease: (1) which has a very rapid and severe course, 'fulminating', which develops within 72 hours after a massive exposure and the second, which is considered an insidious version that takes several days to develop and is seen after someone has been exposed to a lower concentration of beryllium. Acute Chemical Pneumonitis or acute pulmonary disease from inhalation of beryllium or one of its insoluble compounds in finely dispersed forms is , as mentioned earlier, a fulminating inflammatory reaction of the entire respiratory tract. Acute reaction involves the nasal passages, pharynx, bronchial airways and the alveoli. In the most severe cases, there is an acute fulminating pneumonitis. Severity of the acute disease in generally has a dose related relationship to the concentration of beryllium, unlike that of the chronic disease. There have been deaths as a result of the acute disease, but recovery is generally complete after a period of several weeks or even months. Usually, recovery is less than one year.(figure 3

The signs of acute beryllium exposure are, a nonproductive cough, chest pain, cyanosis and a sharp drop in the vital functioning and capacity of the lungs. Also included in with the acute disease, is that there may be some edematous distension and round cell infiltration of the septa, and it is the proteinaceous material, distension and desquamated alveolar cell, monocytes and lymphocytes and plasma cells within the alveoli that characterize the acute diseases process.(5)

Of the 224 reported acute chemical pneumonitis people, 10% resulted in death with all of the reported deaths having the fulminating type of acute chemical pneumonitis. In contrast, the insidious type, had no reported fatalities and were completely recovered from four to twelve weeks. The standard treatment for the acute beryllium disease is not very specific. It includes, the immediate removal from further exposure, bed rest and the administration of oxygen. An extreme example of the acute condition is that of an eighteen year old boy who was employed for only thirty-eight days in a beryllium plant and died 19 days later of illness.(12)

Since the acute beryllium disease has virtually been placed in check through increased regulation and preventive measures, research in the area of beryllium toxicity has shifted to the chronic beryllium disease and its immunological aspects. Most cases of beryllium lung disease are in North America with approximately 900 cases in the USA case register since 1951.(12)

Using blood testing, it was found that the beryllium ion is bound to a protein to form beryllium antigen which induces the cell-mediated beryllium hypersensitivity reaction. This can be determined in vitro by an increase of lymphoblast transformation and also an inhibition of macrophage migration.(6) One of the adverse effects of beryllium poisoning has been the once postulated, but now agreed, disruption of the bodies immune system by berylliosis,s mechanism of disease. The overall fatality rate from chronic beryllium disease, no matter what the length on the latency period between known exposure and the first signs or symptoms is about 33%.(2) A key finding is that there is an inverse relationship between the latency period and the fatality rate, as the latency period increases, the fatality rate decreases.

Chronic Granulomatous Disease(CBD) or Berylliosis's symptoms include, shortness of breath, if severe, this is accompanied by cyanosis and clubbing of the fingers (hypertrophic osteoarthropathy) a characteristic that is a manifestation of chronic pulmonary disease).(6) Chronic beryllium disease, is quite different from that of the acute form. Pulmonary X-rays show miliary mottling, a haziness to "snow-flurry" effect of exposed lungs.(figure 5) Histopathologically, the lung tissue shows interstitial granulomatosis. Pulmonary granulomas involve the lung interstitum and tend to be found along the bronchovascular bundles involving blood vessels or bronchi/bronchioles and may also involve the pleura. A characteristic of the lungs being exposed to toxic levels beryllium, is the irreversible onset of fibrosis and the resulting damage to the lungs alveoli. Another key distinction between the acute and chronic disease is unlike that of the acute disease, berylliosis dose not have a dose-response relationship between the extent of exposure and the severity of the disease. More specifically, in the chronic beryllium disease, the lung is seen to have diffuse inflammation as well as the formation of noncesating granulomas. CBD is usually unrecognized upon onset and it usually requires a repeated or long exposure. CBD's primary target is the lung but the granulomatous inflammation may involve other organs such as the lymph nodes, skin, salivary glands, liver, spleen, kidney , bone and muscle. The fibrotic nature of CBD is mediated by proliferation of CD4 positive helper/inducer T cells under the influence of lung tissue beryllium and beryllium-specific T cell clones.(1)(figure 6)

In the early stages of the chronic disease, these are composed of fluid, lymphocytes and plasma cells, Then as the disease progresses, they become organized with the proliferation of fibrosis tissue and then eventually form small fibrosis nodules. In late stages, the lesions progress, interstitial fibrosis increases with the loss of functioning alveoli and the impairment of effective air-capillary gas exchange and an increasing respiratory dysfunction. The later stages or advanced form of berylliosis, is also accompanied by a decrease in life expectancy.

Examples of the chronic side of beryllium disease are, a girl, who appeared heal thy after not working in a beryllium plant for two years, showed x-rays changes in her lungs and in three to four weeks was gasping of air and cyanotic. Also, a man gave a normal chest x-ray after four years not being around beryllium, but later showed x-ray abnormalities and was in respiratory distress fourteen months later.(12)

CBD reactions to beryllium are believed to involve the immune system through formation of an antigen by a beryllium ion combining with a protein (a hapten) or other natural body substance. H. S. Van Ordstrand initially summarized the idea of CBD as being a disease of hypersensitivity but was this idea of CBD being a such a disease was first hypothesized by Sterner and Eisenbud in 1951. In looking solely at beryllium, being of such small weight and size, alone it is unable to induce an immune response therefore it is likely that the immune response to beryllium is induced through a hapten-beryllium complex. Unable to induce an immune response therefore it is likely that the immune response to beryllium is induced through a hapten-beryllium complex. Therefore, the pathogenesis of chronic beryllium disease, it is thought to be that of an antigen-driven reaction, associated with a delayed hypersensitivity (type 4) response.(1) This was established on the 48 to 72 hour period before the beryllium patch lesions appear, the prominence of gramulomas, and the accumulation of the beryllium-specific helper/inducer T cells.(6)

The idea of chronic beryllium disease is caused by beryllium complexing with a hapten is supported by the work and observations that T lymphocytes in the lung and blood of afflicted people show a proliferation response in vitro when exposed to beryllium and lung T cells from people with chronic beryllium disease do not respond to common recall antigens or to other metals.(8)

Most of the research on CBD, suggest that the lung lymphocytes in people with CBD obey the same basic immunologic mechanisms seen in other diseases that have a predominant cell-mediated immune response. Upon exposure, the T lymphocytes recognizes the beryllium-hapten complex and the cell enters the cell cycle and proliferates. It is also believed that there is a small family of T lymphocytes in the lung of CBD afflicted people, that can recognize beryllium as an antigen. It has also been seen that strain differences in susceptibility to beryllium gives evidence that there are also genetic factors which are important in the response to beryllium exposure leading to chronic beryllium disease. In looking at the genetic aspect of CBD, there are also several lines of research that provide evidence that suggests a genetic susceptibility that contributes to the risk of CBD.

Detection of any valid genetic factors that may predispose a person exposed to beryllium to getting the chronic beryllium disease would aid in screening and the need for added precaution necessary to ensure the health of this person.

Richeldi and co-workers have described a genetic marker in beryllium workers who have chronic beryllium disease which resulted from the inhalation of the metal beryllium.(8)(figure 6) These afflicted workers exhibit the amino acid glutamate in a potentially critical location, that being position 69, in a cell-surface glycoprotein that plays a role in antigen recognition. Although, of the total population tested, all of which had CBD, only thirty percent have the glutamate in position 69. What they are proposing is that this glutamate at position 69 in the genetic sequence in the major histocompatibility complex allele HLA-DPB1 identifies people who, if are exposed to beryllium, are at an increased risk of developing CBD.(8) (figure 6)

The presentation of the beryllium antigen requires the presence of the major histocompatibility complex II molecules, which are subject to genetic variation among different people. These components of MHC II are known to be involved in the susceptibilities to a few auto immune diseases and also in T cell responses to nickel and gold. This leads to the possibility that a person risk can be predicted. With this, there is still no definite light shed on the association of CBD with the MHC allele HLA-DPB1-Glu69 and the mechanism of CBD.(figure 6)

CBD continues to occur in industry at an average of approximately two percent among people exposed to beryllium oxides, metal alloys and ceramics in the aerospace, nuclear weapons, precision metal machining, electronics and automotive industries.(11) A considerable amount of progress has been made in understanding the course of chronic beryllium disease, despite this fact, further research into the exact mechanisms of disease causation and determinants of susceptibility to the harsh effects of beryllium on the lungs is needed.(figure 8)

The obvious effect of beryllium on the respiratory system, primarily the lungs, is well document but classifying of beryllium as a clear carcinogen is encountering basically the same trials and tribulations that were encountered in establishing the direct correlation of beryllium to the acute and chronic pulmonary diseases. With there being so may different institutions and regulatory agencies monitoring the effects of toxic materials and their carcinogenic potentials, each has a separate set of guidelines they use in establishing the classification of materials as to their carcinogen potential. Overall, beryllium is not, specifically, known as a human lung carcinogen although there is suspicion that it might be has been the center of recent debate.

As was mentioned earlier, in 1975, OSHA concluded that, "beryllium should be treated as posing a carcinogenic threat to man." This was based on scientifically unsound research, which was why OSHA's efforts to have beryllium considered a carcinogen failed. Even prior to OSHA's claim, the National Institute of Occupational Safety and Health (NIOSH), in 1971, 1972, stated that, there was an increased risk for getting lung cancer with exposure to beryllium but this finding was also not statically significant. Problems in the experimental modeling of OSHA's and NIOSH research were not scientifically sound.(figure 9)

Along with OSHA and NIOSH, the International Agency for Research on Cancer (IARC) stated that,"Beryllium should be considered suspect of being carcinogenic to humans." The IARC classifies beryllium as having 'limited' carcinogenic effects. Even the Environmental Protection Agency has looked into the carcinogenic potential of beryllium but return to say that its findings also were,'inadequate' to classify beryllium as a carcinogenic agent. The EPA's stand, is that the evidence and research data, is currently inadequate to draw a conclusion as to the carcinogenicity of beryllium in humans. One of the problems of distinguishing beryllium as a definite carcinogen it that its cancer-causing ability has been found to be highly species specific.(11) Along with the fact that all the data collect thus far on beryllium carcinogenic potential has been seen to have various methodical problems.

Yes, I'm dead serious.

Consumer Factsheet on: BERYLLIUM

List of Contaminants

As part of the Drinking Water and Health pages, this fact sheet is part of a larger publication:

National Primary Drinking Water Regulations

This is a factsheet about a chemical that may be found in some public or private drinking water supplies. It may cause health problems if found in amounts greater than the health standard set by the United States Environmental Protection Agency (EPA).

What is Beryllium and how is it used?

I'll take the money line.

Beryllium (+141) $5000


Oh wait.

Just make the check out to "cash"

Beryllium, as has been discussed has had a very controversial history as to it toxic potential, in the beginning to its present day controversy as to its carcinogenic potential. Beryllium is a very valuable material to various industries and it over regulation may in fact be unfair to its use and benefactors. But in the same breath, is it not better to be somewhat conservative when it comes to the lives and health of hard working employees and as in the case of the Lorain incident, the innocent by stander? It seems apparent the the government and the other regulatory agency are being very cautious in coming to a conclusion as to beryllium's carcinogenic potential after their previous mistake, the Fairhall Report which proved to be a major mistake in the assessment of beryllium and the relation to the pulmonary disease. All in all, with the proper regulation and precaution, beryllium has continued to be a huge part of various industries with little to no cases of ill effects to its workers that are careful and respectful of beryllium and its hazardous potentials. The next hurdle for beryllium is it classification as a carcinogen or not. Let's hope the correct research is being done in a timely fashion so as to not end up repeating history. Although, it has been said that history tends to repeat itself.

Works Cited

1. Flora, S.J.S., Seema Mathur, R. Mathur., Effects of meso-2,3-dimercaptosuccini

c acid or 2,3-dimercaptopropane 1 sulfonate on beryllium-induced

biochemical alterations and mental concentration in male rats., Toxicology