List: I have often tried to puzzle through referenced studies on the various "side effects" of silver use that are often referenced in reports and literature.
Earlier today, I was seeking inspiration on how to program my up-and-coming silver bot - a net bot being designed to track down, follow and crawl links, then search through the tens of thousands of references found for interesting information. While I am still facing a programming brick wall, I found an interesting document while testing complex search strings. At first, I was unable to access the document because it was password protected. Not to be discouraged so easily, with a bit of creative effort ( wholly legal luckily ) I extracted the document in question. The document has been compiled by IPCS Inchem - "International Program on Chemistry Safety", apparently with the cooperation of the United Nations Environment Programme and the World Health Organization. Since I am uncertain WHY the sub-levels of the site required full authorization to access the document, I am going to refrain from posting it. However, I will draw from the extensive citations. This document has gone a LONG way in clarifying some confusion on where some of the "popular" referenced studies have come from, and what types of silver were actually being used to actually draw conclusions. I will share interesting notes along the way... Oyster shells were examined for silver presence. The analysis was conducted by atomic absorption spectrophotometrically. The conclusion stated that no silver existed in the hard shell ( below 1ppm ), and yet the soft tissues contained 28-82 (±10-20) ppm (Casarett and Doull, 1975; Windom and Smith, 1972). Very interesting! It was silver salts that have been exclusively used to determine what body systems/organs adsorbed silver, and in which order... Lungs, gastrointestinal tract, through nasal mucosa, conjunctiva, and skin. It is then stored in the in the reticulo-endothelial cells of the skin, mucous membranes, liver, spleen, possibly bone marrow, in basement membranes, especially those of the renal glomerulus, and presumably in muscles (Ham and Tangue, 1972; Kanai et al., 1976; Bader, 1966; Anderson, 1966; Voldrich et al., 1975). All determined exclusively via various silver salts, which at this point were not identified. It is, however, extremely unlikely that silver chloride would have been used. 110mAg was administered to rats ( oral intravenous and intraperitoneal routes ) ( an isotope? ). No doses given, but the conclusions stated that 90%+ of silver was not absorbed. Less than 1% retention after one week from the initial dose was observed in mice, rats, and monkeys.... (Fnrchner et al., 1968) "It seems that even mild degrees of liver damage considerably impair the ability of the liver to excrete quite small doses of silver (Petering, 1976). Unlike lead or mercury there is no evidence that silver is a cumulative poison (Petering, 1976)." PLEASE NOTE: It is references like THESE that cause so much confusion... Petering did not use isolated silver... Proteins, salts and silver acetate... No information was obtained on the biotransformation of silver in the animal body except that absorbed ionic silver is transformed into metallic while being deposited in tissues (Petering, 1976). HERE, it appears, is direct evidence that ionic silver does not necessarily convert soley to silver chloride in the body, unless we don't trust Peterings definition of metallic silver. However, after struggling through the document, it is evident that Petering used silver acetate to do his ionic silver study. Perhaps somebody more chemically inclined could explain how and why.... Ian? Bob? Numerous enzymes were inhibited in vitro by silver ions. High affinity to sulfhydryl and histidine imidazole groups was observed. Silver ions compete with molecular oxygen as hydrogen acceptor, resulting in inhibition of glucose oxydase (Nakamura and Ogura, 1968). Interesting, but still an in vitro study. Protargol, a silver-protein complex containing 8% silver inhibited the in vitro prostaglandin E2 synthesis by bull geminal vesicles even at concentrations of 10-7M (Deby et al., 1973). Interesting, but apparently irrelevant to our silver. Silver ion is a very toxic substance when viewed from the standpoint of its action of an inhibitor of enzymes and as a metabolic inhibitor of lower forms of life. Biochemically, the silver ion (Ag+) can act as potent enzyme inhibitor (Chambers et al., 1974). It has been reported (Wagner et al., 1975) that in vitro administration of silver dramatically decreased liver glutathione peroxidase in rats fed Se-supplemented diets with or without vitamin E. It seems therefore that silver acetate exerts its antagonistic effects on Se (silver induces Se deficiency signs) through an effect on the activity of biosynthesis of glutathione peroxidase. Much of the biologic action of silver can be attributed to the reaction of silver ion with sulfhydryl groups to produce stable silver mercaptide (Petering, 1976). THAT paragraph is interesting. Notice that silver acetate is used specifically to induce SE deficiency and vitamin E deficiency. Is this really applicable to isolated silver? Notice ALSO that if silver acetate is used, the concentrations must be extraordinarily high compared to "our" colloidal silver products. The interchange between citing "silver ions" and "silver acetate" seems VERY misleading, and is probably responsible for a WORLD of misquotes and misinterpretations. If silver ions were produced via silver acetate, then there STILL must be an incredible amount of silver present compared with a 5 - 10 ppm CS. See here: 1500 ppm Ag1 (as acetate) in drinking water for two to four weeks caused liver necrosis and death in vitamin E deficient rats. The effect was prevented by 120 ppm D- -tocophirylacetate and partially by 1 ppm Se (Diplock et al., 1967). Again, SILVER IONS VIA SILVER ACETATE. Not the same product. A further reference pointed out that a 772 ppm silver acetate was used in study. I'm certain ALL the experimenting was done with such high, and higher, levels of silver. If so, then the vitamin C and Selenium issue that is often raised is simply a study taken out of context. I see numerous references to kidney and liver retention of silver... all via silver acetate, 772 ppm. This further illustrates the point I'm trying to make: Groups of 20 chicks received 0, 10, 25, 50, 100 and 200 ppm silver during four weeks in combination with 0, 10 or 25 ppm copper in the diet. Silver at 100 ppm reduced growth in the copper deficient but not in the control chicks. At 50 ppm mortality was increased in the copper deficient group, but not in those receiving copper. 10 ppm silver reduced the haemoglobin concentration and the elastin content in the aorta in deficient chicks. These effects were completely overcome by the addition of copper to the diet (Hill and Matrone, 1970) INTERESTING! Now, at this point in the document, it is clear that all studies were done via non-isolated silver products... However, the "copper" effect is certainly interesting. Absorption of silver resembles whole body retention. It is retained in all body tissues (Hamilton et al., 1972a; Tripton et al., 1966). The silver content of the miocardium, aorta and pancreas tends to decrease with age (Bala et al., 1969) although the amount of silver in the body increases with age (Hill and Pillsbury, 1939). The concentration of silver in healthy human tissues from the United Kingdom was 1-9 µg/kg ash was found. The average silver contents in wet tissue of normal Americans was about 0.05 µg/kg (Tripton, 1963). THAT paragraph is truly exciting, because we know beyond a shadow of a doubt that isolated silver does NOT accumulate in the body as described. This simply illustrates the PROFOUND difference between the types of silvers used in studies, and their effects in the body. Regardless of type there are two forms of argyria, local and generalized. The local form involves the formation of grey blue patches on the skin or may manifest itself in the conjunctiva of the eye. In generalized argyria the skin shows widespread pigmentation, often spreading from the face to most uncovered parts of the body. In some cases the skin may become black with a metallic lustre. Heavy pigmentation of the eye structures can interfere with vision (Casarett and Doull, 1975). Except for this adverse effect argyria is solely a cosmetic problem. The slate blue colour of argyria is not entirely due as one might suspect, to the deposition of metallic silver (Petering, 1976), but largely to an increased deposition of melanin. Silver has a melanocyte-stimulating property (Rich et al., 1972). Cases of generalized argyria have occurred after ingestion or chronic medicinal application of gram quantities of silver. Silver was absorbed during prolonged (nine months) nasal application of Targesine (silver solution). It was calculated that during this time 7000 ml of solution containing 210 g silver had been used (Voldrich et al., 1975). WELL NOW! Isn't THAT interesting? Maybe the FDA should spend some time with the UN. Based on the above information, which is representative of virtually all MODERN international data on silver, I have become even more skeptical as to the claims of silver toxicity by those that quote "ambigious" sources. Chances are, they are really going back to these studies, and then quoting out of context. Now, If I get thrown in jail for grabbing this document, I'm blaming Mike. MIKEY DID IT. Seriously, though, I don't know why this information is "safe-guarded" by a professional security company ( who obviously isn't doing a very good job - Sentinel security ROFL ). Perhaps they just want you to pay for the information. I briefly explored their family of websites, and did not see any buy now buttons. I didn't see any warnings about restricted data, so I'm at a loss to why the public does not have free access to it. At any rate, I hope you all find something to take home... The Colloidal Silver Database Website http://silverdata.20m.com
