Summary
3
1.4
Environmental levels and human exposure
In contrast to the large body of information concerning concen-
trations of metals such as lead or nickel in the environment, there is
little information on palladium. Concentrations of palladium in surface
water, where it is detected, generally range from 0.4 to 22 ng/litre (fresh
water) and from 19 to 70 pg/litre (salt water). Concentrations reported
in soil rang e from <0.7 to 47 µg/kg. These soil samples were all
collected from areas near major roads.
Concentrations reported in sewage sludge range from 18 to
260 µg/kg, although a concentration of 4700 µg/kg has been reported
in a sludge contaminated by discharges from the local jewellery
industry. Drinking-water samples usually contain no palladium or
<24 ng palladium/litre. The few data available show that palladium can
be present in tissues of small aquatic invertebrates, different types of
meat, fish, bread and plants.
The general population is primarily exposed to palladium through
dental alloys, jewellery, food and emissions from automobile catalytic
converters.
The human average dietary intake of palladium appears to be up
to 2 µg/day.
In analogy to platinum, ambient air levels of palladium below
110 pg/m
3
can be expected in urban areas where palladium catalysts are
used. Therefore, the inhalative palladium uptake is very low. In road-
side dust, soil and grass samples, a slight accumulation of palladium
has been detected, correlating with traffic density and distance from
the road.
Oral exposure in the general environment is very important and
may occur by daily direct contact of the gingiva with palladium dental
alloys. Skin exposure may occur by contact with jewellery containing
palladium.
Dental alloys are the most frequent cause of constant palladium
exposure. The corrosive behaviour of palladium-containing dental
alloys in the mouth can be influenced by the addition of other metals
EHC 226: Palladium
4
(such as copper, gallium and indium) and processing of the alloy.
Palladiu m–copper alloys with high copper content may be less
corrosion-resistant than palladium alloys with low copper content.
Palladium release from palladium-containing dental restorations shows
substantial individual variation depending on the dental condition, the
material involved and personal habits (e.g., gum chewing). Clinical data
for iatrogenic exposure are of limited value, as the few case-studies
have methodological deficiencies, such as limited numbers of tissue
samples and poorly matched control groups. It is, therefore, difficult to
make an accurate quantitative statement regarding daily intake, and the
proposed value of
#
1.5–15 µg palladium/day per person thus remains
a crude estimation.
There is some informa tion on palladium levels in the general
population, where levels in urine were in the range of 0.006–
<0.3 µg/litre in adults.
M o s t occupatio n al exposures to palladium (salts) occur during
palladium refining and catalyst manufacture. There are few exposure
measurements, ranging from 0.4 to 11.6 µg/m³ as an 8-h time-weighted
average. No recent data are available for biological monitoring of
workers exposed to palladium and its salts.
Dental technicians may be exposed to peaks of palladium dust
during processing and polishing of dental casting alloys containing
palladium, especially if adequate protective measures (dust extraction
or aspiration techniques) are not taken.
1.5
Kinetics and metabolism in laboratory animals and
humans
Only few data are available on the kinetics of metallic or ionic
palladium.
Palladium(II) chloride (PdCl
2
) was poorly absorbed from the
digestive tract (<0.5% of the initial oral dose in adult rats or about 5%
in suckling rats after 3–4 days). Absorption/retention in adult rats was
higher following intratracheal or intravenous exposure, resulting in
total body burdens of 5% or 20%, respectively, of the dose
Summary
5
administered, 40 days after dosing. Absorption after topical application
was observed but not quantified.
After intravenous administration of different palladium com-
pounds, palladium was detected in several tissues of rats, rabbits or
dogs. The highest concentrations were found in kidney, liver, spleen,
lymph nodes, adrenal gland, lung and bone. For example, 8–21% of the
administered d o s e of palladium(II) chloride or sodium tetr a c h l o r o -
palladate(II) (Na
2
PdCl
4
) has been found in the liver or kidney of rats
1 day after dosing. After a 4-week dietary administration of palla-
dium(II) oxide (PdO), measurable levels have been found only in the
kidney of rats.
Only scarce data are available on the distribution of palladium
from dental restorations in human tissues or fluids (e.g., in serum and
saliva: about 1 µg/litre).
Transfer of small amounts of palladium to offspring via placenta
a nd milk was seen with single intravenous doses of palladiu m ( I I )
chloride in rats.
Information on the elimination and excretion of palladium is scarce
and refers mostly to palladium(II) chloride and sodium tetra-
chloropalladate(II), which were found to be eliminated in faeces and
urine. Urinary excretion rates of intravenously dosed rats and rabbits
ranged from 6.4 to 76% of the administered dose during 3 h to 7 days.
Elimination of palladium in faeces ranged in these studies from traces
to 13% of the administered dose. Following oral administratio n o f
palladium(II) chloride, >95% of palladium was eliminated in faeces of
rats due to non-absorption. Subcutaneous or topical treatment with
palladium(II) sulfate (PdSO
4
) or other palladium compounds resulted in
detectable concentrations of palladium in the urine of guinea-pigs and
rabbits.
Half-lives calculated for the elimination of palladium from rats
(whole body, liver, kidney) ranged from 5 to 12 days.
Mean retention values determined at three time intervals (3 h, 24 h,
48 h) in rats injected intravenously with
103
PdCl
2
showed little change
with time for kidney, spleen, muscle, pancreas, thymus, brain and bone.
24>
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