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EC number: 233-823-0
CAS number: 10377-52-3
The stratum corneum provides its
greatest barrier function against hydrophilic compounds, whereas the
viable epidermis is most resistant to highly lipophilic compounds. Due
to the hydrophilic character of lithium phosphate and the barrier
function of the stratum corneum against salts, the dermal absorption of
lithium phosphate is expected to be very poor. It is supported by an
acute dermal toxicity study that revealed an LD50 value >3000 mg/kg bw
without any local or systemic effects for the structural and chemical
similar compound lithium carbonate. The assumption that absorption is
negligible is further confirmed by the results of an EPISKIN assay (OECD
439) and two Corrositix test with lithium phosphate. The tests showed
that lithium phosphate is not irritating or corrosive to the
skin. Further, no sensitization was observed in the local lymphnode
assay (LLNA) with the read-across substance sodium
Resorption after oral uptake:
Upon oral uptake, lithium phosphate
will reach the stomach in form of lithium ions and phosphate ions.
Lithium ions and phosphate ions will be readily and almost completely
absorbed from the gastrointestinal tract due to their low molecular
weight (< 500 g/mol). Additionally, the low log Pow of both ions favors
them for absorption by passive diffusion and therefore they can cross
lipophilic membranes. They are also small and water soluble enough to be
carried through the epithelial barrier by the bulk passage of water. A
weight of evidence approach was performed with read-across data from
lithium sulfate and lithium nitrate. The available read-across data
showed LD50 values >300 mg/kg (cat. 4, H302). Because phosphate is an
essential element, and phosphate ions are a natural constituent of food,
phosphate has less toxicological relevance.
Resorption after inhalation:
The vapour pressure of lithium
phosphate is negligible (Modifies Gain method: 4.88E-022 Pa at 25 °C)
and therefore exposure to vapour is toxicologically not relevant if the
substance is handled at room temperature. If lithium ions reach the
lung, resorption after inhalation is assumed to be low due to the very
low log Pow. Thus, upon inhalation, the bioavailability of lithium
phosphate is expected to be low.
Distribution, Metabolism and
does not bind to protein and as a small cation it is quickly distributed
throughout the body water both intra- and extracellularly, replacing
normal cations (as K+, Na+). Lithium ion effects in the cell level are
presumed to be related to interferences with processes that involve
these ions such as renal tubular transport and ion channels involved in
neurotransmission. Lithium has a large volume of distribution of 0.6-0.9
L/kg (42 L for a 70 kg adult, which is the total body water). Because of
its large volume of distribution, lithium shifts into the intracellular
compartment of cells. With long-term use, the intracellular
concentration of lithium increases, which thereby results in increased
total body lithium load. The intracellular concentration is not
reflected by the plasma level, which measures only the extracellular
fluid concentration. Organ distribution is not uniform: Lithium is
rapidly taken up by the kidney (there is obviously a clear interaction
between lithium and sodium excretion/retention altering the electrolyte
balance in humans). Penetration is slower into the liver, bone and
muscle. Its passage across the blood-brain barrier is slow and
equilibration of the CSF lithium level reaches only approximately half
the plasma concentration.
primary route of excretion is through the kidneys. Lithium is filtered
by the glumeruli and 80 % of the filtered lithium is reabsorbed in the
tubules, probably by the same mechanism of sodium reabsorption. Lithium
is excreted primarily in urine with less than 1 % being eliminated with
renal clearance of lithium is proportional to its plasma concentration.
The excretion of lithium ions is considered to be fast. About 50 % of a
single dose of lithium is excreted in 24 hours and about 90% in 48
hours. However, trace amounts can still be found 1 to 2 weeks after the
ingestion of a single lithium dose. A single oral dose of lithium ion is
excreted almost unchanged through the kidneys. A low salt intake
resulting in low tubular concentration of sodium will increase lithium
reabsorption and might result in retention and intoxication. Renal
lithium clearance is under ordinary circumstances, remarkably constant
in the same individual but decreases with age and also when sodium
intake is lowered.
to the fast excretion, bioaccumulation is not to be assumed. Lithium is
not metabolised to any appreciable extent in the human body. In
conclusion, lithium in human body is quickly distributed and unchanged
excreted. Bioaccumulation can be excluded.
is taken up daily as it is naturally present in many foods including
dairy products, meat and cereal grains. The normal concentration of
phosphorus in plasma is 3-4.5 mg/dL. Once absorbed, phosphate in the
extracellular fluid may exchange with the pool in bone. The skeleton is
continuously remodeled, with typically 200 mg of phosphate entering and
leaving the skeleton. But the principal mechanism by which the body
regulates extracellular phosphate balance is renal phosphate excretion.
About 700-900 mg phosphate per day are excreted via kidneys (Prasad and
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