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Chapter 8

The Toxicology of Silver

Silver has no trace metal value and should be regarded as a xenobiotic element in the human body. Argyria and argyrosis resulting from the precipitation of silver sulfide or silver selenide in dermal tissues of the skin and eye respectively are the principle side effects associated with prolonged exposure to high levels of occupational silver or colloidal silver consumption. Neither is health threatening. The putative mechanisms of argyrosis involving selenium are discussed. In vitro toxicity studies show that silver is toxic to isolated cells but that changes seen are not consistent with silver being ether mutagenic, carcinogenic or teratogenic. This is verified experimentally and clinically.

Experimental models using live animals have proved to be of limited value in evaluating silver toxicity.

Silver ionises following ingestion and inhalation to be absorbed through intestinal and respiratory mucosae. Ag+ in a protein complex is metabolised to soft tissues and bone. The liver is the most important organ involved in silver excretion, but is not subject to more than transitory enzymic changes following high silver uptake by any route. Silver is excreted in the urine but renal changes are minimal, inert silver precipitates locate in lysosomal vacuoles. Renal pathology has been observed in patients treated with intra-renal injection of dilute silver nitrate to alleviate infections and haemorrhages. Measurement of urinary silver is a poor indication of silver uptake. Silver is precipitated in bone where Ag+ displaces Ca++ from hydroxyapatite with the potential risk of osteoporosis, but the extent of this problem is not known.

Although discoloration of the skin is an indication of silver exposure, the tissue is not subject to functional impairment or pathological damage. Minimal concentrations of blood silver and induction of signs of signs of argyria are not known. Although dermal in distribution, argyria can be removed by surgical dermabrasion, and the prognosis is good. Silver is toxic to keratinocytes in culture but in the intact stratum corneum, keratin provides an effective barrier against percutaneous silver absorption. Delayed hypersensitivity and allergy to silver occur in jewellers, patients treated with silver -containing dressings, and occupations associated with silver, but the extent of the problem is not known. Solar radiation is important in the induction of argyria and allergic responses. Silver absorption does not lead to alterations in melanocytes or melanin production.

Silver has been associated with risks of leucopenia and neutropenia in children treated with silver sulfadiazine for severe burns. Whilst this hazard is now discounted, there is evidence that silver nitrate is a cause of electrolyte disturbances and may lead to methaemaglobinaemia. This not related to silver but to reduction of the nitrate anion. Silver nitrate is still valuable as strong caustic in the cauterisation of verucae, warts and excessive granulations, but this therapy is safe and therapeutically beneficial.

Print publication date: 07 May 2010
Copyright year: 2010
Print ISBN: 978-1-84973-006-8
PDF eISBN: 978-1-84973-179-9
From the book series:
Issues in Toxicology