Since my previous post regarding Hexavalent Chromium (CRVI), it's been nagging in the back of my mind. I don't know why, though.
Anyway, I looked it up further. Shoot, I forgot to take note of where I'm copying this from, but I'll post it anyway:
...."Because of structural similarity to phosphate, which is transported into all types of cells, if Cr(VI) does reach a cell, it can enter it. Once Cr(VI) enters the cell, it is chemically transformed to the more stable Cr(III). This does not mean, however, that the cell is necessarily safe from adverse effects. One of the major reasons Cr(III) does not cause toxic effects is that, unlike Cr(VI), it has a poor ability to enter cells. However, inside the cell Cr(III) has the capacity to damage DNA. Two decades' worth of research by the late Karen Wetterhahn, a chemist at Dartmouth Medical School in Hanover, New Hampshire, and De Flora on the uptake and reduction of Cr(VI) by cells indicates that Cr(VI) acts as a "Trojan horse" for delivering DNA-damaging Cr(III) into cells.
The process by which Cr(VI) is reduced to Cr(III) can cause many forms of DNA damage: oxidative DNA lesions such as strand breaks, chromium-DNA adducts, DNA-DNA interstrand cross-links, and DNA-protein cross-links. (An adduct is a modification of a biological molecule--in this case, DNA--caused by the covalent attachment of a chemical, such as chromium; cross-links are a specific class of adduct.) Research by Steven Patierno, a professor of pharmacology and genetics and of environmental occupational health at The George Washington University in Washington, D.C., and colleagues first identified a potential mechanism of genotoxicity for intracellular Cr(III). Those studies, published in the March 1994 issue of Molecular Carcinogenesis and the November 1994 and July 1996 issues of Carcinogenesis, indicate that Cr(III)-induced DNA-DNA interstrand cross-links are the lesions responsible for blocking DNA replication.
Recent work by Costa and colleagues looked at the possible mutagenicity of certain Cr(III)-induced DNA adducts. In an article published in the 15 April 1998 issue of Nucleic Acids Research, the scientists found that Cr(III)-glutathione cross-links exhibited the greatest mutagenicity of the adducts studied, with a mutation frequency five times greater than background. This observed mutagenicity complements other studies on Cr(III)-dependent DNA lesions, which demonstrate the importance of a Cr(III)-dependent pathway in Cr(VI) carcinogenicity. Additional studies are investigating the relative importance of oxidative and Cr(III) pathways in genetic damage caused by exposure to Cr(VI). ...."
So, then I thought I'd research some more on relationships between CrVI and MS. Instead, I found this. This is an excerpt:
Before the Subcommittee on Public Health
Committee on Health, Education, Labor, and Pensions
United States Senate
ATSDR's Role in Environmental Health Tracking
Henry Falk, M.D., M.P.H.
Agency for Toxic Substances and Disease Registry
U.S. Department of Health and Human Services
March 6, 2002
"I am Dr. Henry Falk, Assistant Administrator of the Agency for Toxic Substances and Disease Registry (ATSDR). ATSDR is a sister agency to the Centers for Disease Control and Prevention (CDC). Congress created ATSDR in the Superfund legislation to assess the public health impact of Superfund sites to nearby populations, and to determine the relationship between exposures to hazardous substances and disease.
We also should develop new tracking of diseases thought to have some relationship to environmental exposures. For example, currently no tracking exists for critical neurologic diseases such as multiple sclerosis or Parkinson's, nor immune system diseases such as lupus and other autoimmune diseases, nor developmental diseases such as autism or other neurodevelopmental diseases. Nor do any tracking systems exist for diseases known to be caused by exposure to specific hazardous substances like asbestos. ...
... ATSDR has begun to address one of these diseases -- multiple sclerosis (MS) -- around multiple Superfund sites. In an article just published in Neurology, ATSDR researchers found nationally a 50% increase in MS in women for the period of 1991 - 1994, versus an earlier time period of 1982 - 1986. To address local concerns, ATSDR in cooperation with state and local public health partners, has initiated a number of studies. In El Paso, Texas a cluster of MS cases was investigated. Based on available background estimates, preliminary results show the number of MS cases among former students at one school to be twice as high as expected. In another effort, we are funding programs in Ohio, Missouri and Texas to investigate MS prevalence rates in Lorain County, Ohio; Independence and Sugar Creek, Missouri; and a 19-county area around Lubbock, Texas. These studies will use neurologists' medical records as the primary data source to determine age- and sex- specific MS prevalence rates in these areas. ATSDR conducts these efforts through a cooperative agreement program, and has established such relationships with more than 30 state health departments. ...."
I wonder how that tracking is coming along?