The Beryllium Thread

[Simplex3]

I'm putting this in here so that it won't hang around the top of the lounge while I cut and paste information in to post after post.

This is part of my ongoing offseaon attempt to get us ranked on the first page of some search engine(s) when nerds search for "beryllium".

Before you PM me with "Why?", the answer is simply that I am sitting around reading log files at work and cutting and pasting into this thread requires absolutely NO mental stress.

[Simplex3]

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)

[Simplex3]

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)

[Simplex3]

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)

[Simplex3]

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.

[Simplex3]

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.

[Simplex3]

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)

[Simplex3]

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)

[Simplex3]

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)

[Simplex3]

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.

[Simplex3]

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)

[Simplex3]

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.

[Simplex3]

Originally Posted by chagrin

Dude, I am just curious, are you serious about why you are posting this?

Yes, I'm dead serious.

[Simplex3]

Consumer Factsheet on: BERYLLIUM

[Simplex3]

List of Contaminants

[Simplex3]

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