As the EPA studies show, the estimated amount of silver intake in order to be at risk for Argyria is 3.8 ( to six ) grams of silver.

One teaspoon of 5 ppm colloidal silver contains about 25 micrograms of silver, or .025 milligrams of silver. Six teaspoons, the equivalent of one fluid ounce, therefore contains .15 milligrams of silver. The EPA's critical dose for a 160 lb. adult is 1.09 milligrams daily. Taking one ounce of colloidal silver daily, according to EPA guidelines, is well below the critical daily intake for the development of argyria. Four ounces daily would equal around .6 milligrams.

However, all of this is dependent upon the body's actual retention of colloidal silver in body tissues. There is no existing data which addresses the very real differences between isolated ionic silver ( and particles sized .0003 - .05 microns in diameter), and silver compounds ( silver nitrate, silver arsphenamine , silver proteins, silver salts, silver acetate, etc. ). Can a risk assessment for argyria based on high strength ionic silver compounds be applied to low PPM isolated silver solutions and colloidal silver? This is unknown.

There is accumulating evidence which strongly suggests that neither low PPM isolated ionic silver nor minutely sized silver particles build up in the body at the same rate indicated by the compound study data. Many researchers have traditionally been unable to explain the exact risk elements associated with silver toxicity-- why one individual is at risk for argyria and why another is no, when the amount of silver ingested is the same. As some of the research data shows, however, a selenium deficiency may be a determining factor.

If selenium and other dietary factors are the sole determining factor in the risks associated with argyria ( aside from obvious massive overdoses ), then dose quantities, frequency of use, and actual silver concentration become of paramount importance in gauging risk. If dietary intake and systemic availability of needed substances exceed those required as a part of silver elimination in the body, then the accumulation of silver in the body will not be comparable to the high potency compound products, and thus the risk of argyria will not be equal.

Evidence presented in one study case conducted by Roger Altman lends credence to the idea that silver accumulation via oral use of an isolated colloidal silver product does not always occur. Needless to say, though, much further work needs to be done on the subject for definitive answers.

Some researchers believe that build up of silver in the body is caused exclusively by the concentration of silver ingested, irrespective of the actual form of silver. Therefore, it would not likely matter whether one took a silver protein that contained one milligram of silver or one milligram of silver nitrate - the risk for argyria, whatever that may or may not be, would be the same.

However, we do not believe this to be the case. We do not believe that the body itself responds the same to silver compounds as it does to isolated silver. Data inferred from the above studies indicate a wide variance in the amount of silver deposited in those whom have never taken a colloidal silver product. It is extremely unlikely that ANY of the people studied ( outside of silver-rich industrial conditions ) would have ingested large amounts of silver at any given time, and yet the variance in accumulation in body tissues infers that there are other factors involved in accumulation.