About 8% of patients attending contact dermatitis clinics have given allergic skin reactions when patch tested with palladium compounds (usually the chloride). Palladium chloride was a potent skin sensitizer in guinea pigs, and various palladium compounds have been shown to induce sensitization in guinea pigs, mice, rabbits and cats. One worker developed asthma as a result of occupational exposure to palladium chloride. Certain palladium compounds, including the chloride, were irritant to rabbit skin. Palladium chloride and tetramminepalladium hydrogen carbonate (TPDHC), but not palladium monoxide, were severely irritating to the rabbit eye.

The acute oral toxicities of the metal itself and of its monoxide were low in rats, whilst that of the sulphate was moderate. A moderate to low acute oral toxicity was indicated for the chloride in rats and mice. The diacetate had a low acute oral toxicity in mice. In rats, TPDHC had a moderate acute oral toxicity and a low acute dermal toxicity. Alterations in liver enzyme systems and tissue changes in the gastro-intestinal tract, liver, kidneys and lungs were seen on acute oral administration of palladium or its compounds to rodents. By acute intravenous injection, a range of palladium compounds induced cardiovascular effects in rats, whilst palladium chloride damaged the heart, kidneys, bone marrow and liver of rabbits. A limited study involving lifetime ingestion of palladium chloride by mice provided evidence of tissue changes in the kidneys and equivocal evidence of carcinogenic activity. In shorter studies, repeated oral exposure of rats to the chloride resulted in altered liver enzyme activities while the monoxide reduced liver protein levels. Repeated ingestion of TPDHC produced tissue changes in the spleen and gastric lining of rats. In Soviet studies, rats repeatedly ingesting palladium or “chloropalladosamine” showed effects on the blood and tissue changes in the kidneys, while repeated dermal application of “palladium hydrochloride” [palladium chloride?] evidently induced liver and kidney degeneration in rabbits.

In mice, single oral treatment with TPDHC, or single subcutaneous injection of palladium metal or the monoxide, did not induce genotoxic effects (micronuclei or dominant lethal mutations). In human white blood cells in culture, palladium chloride, TPDHC and ammonium tetrachloropalladate (II) (but not several other palladium compounds) induced chromosome damage. Palladium chloride did not induce DNA damage in a (comet) assay using human blood cells. The chloride and another palladium salt were apparently inactive in another genotoxicity assay (transformation of mouse cells in vitro). In (sometimes limited) Ames bacterial tests, no evidence of mutagenicity was found for a range of palladium compounds (including the chloride), though one complex compound was reportedly mutagenic. The same complex compound also gave evidence of DNA-damaging ability in bacteria (in a “rec” assay). Another complex palladium compound, which was not an Ames mutagen, was mutagenic in other bacteria. A range of palladium compounds, including the chloride, did not damage bacterial DNA (in an SOS chromotest). Palladium chloride gave some evidence of an ability to interact with isolated mammalian DNA.

Date of Publication: 2007

Number of Pages: 28

CAS Number*: 7647-10-1























Format: PDF available for immediate download

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