This will be in several posts due to the length. Regarding Argyria. You have a concern about silver particle size increasing the risk of Argyria. From what I have been able to determine, Argyria is caused by silver salts and not elemental silver. The following excerpts are from Appendix 9 of "Spacecraft Water Exposure Guidelines for Selected Contaminants: Volume 1". Free download of book available at http://www.nap.edu/catalog.php?record_id=10942). I strongly recommend downloading and reading Appendix 9 if you are interested in silver toxicity.
1) Silver was used on the US and Russian Space Stations: "Human exposure to silver usually occurs by inhalation of silver-containing dust in the environment or by dermal contact to jewelry or photographic materials containing silver. Silver has been the primary agent used to disinfect potable water processed from humidity condensate in the Russian Mir space station. Silver will also be used in the humidity-conden sate water-processing assembly in the Russian service module (SM) to support the crew during the early phases of assembly of the International Space Station (ISS). The Russian and U.S. crew members aboard the early assembly missions of the ISS will consume water containing silver at about 0.5 milligrams (mg)/L. Moreover, silver will be added electrolytically in the Russian water supplies carried to the ISS via Progress resupply vehicles during the ISS assembly phase. The concentrations of silver in the archived water samples from the cold and hot water galleys of various Mir missions ranged from 8 :g/L to 670 :g/L, although the target concentration was 500 :g/L. That probably indicates that the mechanism of silver addition did not work reliably, or there was a silver demand in the system after it had been added. During the Mir missions, when U.S. astronauts lived in the Mir space station for 3-6 months (mo), the fuel-cell water transferred from the shuttle was deiodinated and silver was added as silver salts to support the crew drinking water requirements. The residual iodine precipitated some of the silver, which caused very low silver concentrations in some samples. The common salts that were used to maintain silver in solution were formate and fluoride. If the crew uses water recovered from the humidity condensate, the forms of the silver salts will depend on the salts of calcium and magnesium added as mineralizing agents to improve the organoleptic properties. Because that has been proprietary, the exact forms are not known." 2) Silver deposition in tissue appears to be caused by silver salts, not elemental silver: "Even though silver salts are not metabolized in the typical sense, silver salts that are transformed are reduced to metallic silver. It was suggested (ATSDR 1990) that the deposition of silver in tissues is the result of precipitation of insoluble silver chlorides and silver phosphates and that those silver salts are transformed to silver sulfides by forming complexes with amino or carboxyl groups in proteins or are reduced to metallic silver by reduction with ascorbic acid (Danscher 1981). Buckley et al. (1965) identified silver particles deposited in the dermis of a woman with argyria as silver sulfide. Similarly, Berry and Galle (1982) reported that deposits of silver in the internal organs of rats were identified as silver sulfide. Silver seems to interact with other metal salts, especially with selenium in the diet (Berry and Galle 1982, as cited in ATSDR 1990)." 3) A number of argyria cases are discussed. Here is an example. Note that the argyria in this instance may have been due to a blocked biliary excretion pathway. "A 47-y-old woman with a 2-y history of blue-gray discoloration of neck and face (argyria) reported the onset of discoloration after the use of 32 lozenges per day for 6 mo. ... In addition, according to East et al. (1980), other investigations believed that the use of the lozenges did not result in any significant level of absorption of silver. That indicates that with repetitive doses, the overall body retention might be higher, perhaps due to the saturation of the only biliary excretion pathway, resulting in increased distribution to tissues and poor excretion. Hence, the high percentage of retention could be a gross overestimate of what might result from chronic small doses." 4) The amount of silver needed to cause argyria is not predictable. "Gaul and Staud (1935) analyzed 70 cases of argyria where subjects had been exposed to silver either in a colloidal form or had it injected intravenously as a medication (e.g., silver arsphenamine for syphilis). Ten males and two females received a total of 31-100 intravenous injections of silver arsphenamine over a period of 2 to about 10 y. This amounted to a total exposure dose of 4-20 g of silver. No definite threshold could be identified for the incidence of argyria; some developed the condition after a total dose of 4 g of silver, while it appeared in others only after 20 g. Using a biospectrometric analysis of skin biopsies, the authors concluded that the skin discoloration was proportional to the amount of silver present. Based on the lowest level.4 g of silver arsphenamine.the EPA working group on silver (EPA 1992) calculated that argyria might occur at a total body burden approximately equivalent to 1 g or above." 5) Vitamin E and selenium may influence the toxicity of silver. "Factors That Influence Silver Toxicity Diplock et al. (1967) reported that vitamin E and selenium in the diet could significantly influence the toxicity of silver. When weanling Norwegian hooded rats fed a basal vitamin-E deficient diet were provided drinking water containing silver at 970 mg/L (as silver acetate), all rats developed liver necrosis within 2-4 wk and died. In another group, when selenium was added at 1 ppm to the vitamin-E deficient diet, and the drinking water contained silver acetate, only four of nine rats died. In another group that was fed a diet containing vitamin E and was sacrificed after 50 d of silver exposure, no liver necrosis was found. Bunyan et al. (1968) reported similar observations in rats exposed to silver at 650 mg/L (as silver acetate) in drinking water. Liver necrosis was seen when the dietary selenium was reduced. Necrosis was induced at much lower doses of silver (80 mg/L). Vitamin E appeared to reverse that effect. Also, Grasso et al. (1969) reported that when silver (silver acetate) was fed either in the diet (at 130-1,000 ppm, or 4-33 mg/kg/d) or in drinking water (97.5 mg/kg/d) to vitamin-E deficient rats, fatal necrosis was noted. Alexander and Aaseth (1981) reported that depletion of liver GSH by diethyl maleate decreased biliary excretion of silver into the bile. Selenite also inhibited the biliary excretion of silver and increased its retention in the tissues. It was suggested that selenite formed an insoluble complex with silver that retarded biliary excretion. It is not clear if that is in any way related to the effect of selenium-containing diets in reducing the GSH peroxidase (see Wagner et al. 1975, described above). To be continued. - Steve N -- The Silver List is a moderated forum for discussing Colloidal Silver. Instructions for unsubscribing are posted at: http://silverlist.org To post, address your message to: [email protected] Address Off-Topic messages to: [email protected] The Silver List and Off Topic List archives are currently down... List maintainer: Mike Devour <[email protected]>
