Biological and hepatotoxic effects of palladium. An overview on experimental investigations and personal studies

• Published in: The International journal of risk & safety in medicine Vol. 8; no. 2; p. 149
• Main Authors: Hildebrand, H F, Floquet, I, Lefèvre, A, Véron, C
• Format: Journal Article
• Language: English
• Published: Netherlands 1996
• ISSN: 0924-6479
• DOI: 10.3233/jrs-1996-8203

Workers are occupationally exposed to Pd and Pd-complexes during the refining process, in particular in Pt-refineries. The metal is increasingly used as component in fine jewellery, is commonly present in dental alloys, and is also employed in telecommunication systems.In view of the toxicity of Pd when absorbed and anticipating the possible entry of some of this material into man's environment from the use of automotive catalitic converters, the retention, tissue distribution, excretion and placental transfer of Pd were determined by several authors following different administration routes in animal experiments. Most investigations on Pd and the Pt group metals were performed with simple and complex salts (chlorides and water-soluble ammoniacal compounds of Pt, Ir, Os, Pd, Rh and Ru). The highest retention for Pd was obtained following intravenous dosing, and the lowest retention occured after oral administration. Following a single oral dose, almost all Pd is excreted in the faeces, whereas after i.v. injections, similar quantities are excreted in both urine and faeces. Tissues containing the highest concentrations were the kidneys, spleen and liver. Following i.v. dosing of pregnant rats, a small amount is found in the fetuses.Pd and its compounds are considered to have hepatotoxic and nephrotoxic effects, acting by way of the -SH groups on complex biosystems: proteins, enzymes, etc. Oral administration of PdCh2 has obvious effects on the hepatic mono-oxygenase system and causes notable decreases in hepatic content of cytochrome-P450. Pd++ salts have also metabolic effects on a lot of other enzymes by inhibiting the activity of prolyl-hydroxylase, creatine kinase, aldolase, succinic dehydrogenase, carbonic anhydrase and alkaline phosphatase. These studies suggest that Pd may interfere with energy metabolism, acidlbase and electrolyte eqUilibria. In addition, Pd significantly increases the hepatic Se content and has a strong interaction within the Se-Hg competition. Proposed exposure limit for Pd compounds is 0.03 mg/m3.It is highly important to make the difference between soluble Pd-salts and metallic Pd. Although simple and complex Pd-salts have obvious hepatotoxic and nephrotoxic effects, no biological incidences have been demonstrated for metallic Pd. This is important especially for its increasing use in dental alloys. Our own experiences on cell culture systems with powders of pure metallic Pd and Pd-containing dental alloys have never shown any influence on the cell viability and on the induction of inflammatory effects. Its biocompatibility is comparable to that of Au, Pt or Ti.In the last few years, however, Pd has caused a lot of controversial discussion with respect to its sensitizing effects. The present state-of-the-art of this problem is that Pd sensitization may coincide with Ni sensitization.