.
~ll-ac-:
i
pis
wa
by the measured differences of Pu intake via food, water, and air, and are
therefore valid within the assumptions for dietary and inhalation intake.
However, the absolute quantities predicted by models 2,16,17 ; based upon the
same dietary intake values (Table 6), do not correspond with the recently
reported urine concentrations®.
Table d contains data comparing the reported
urine concentrations with the quantities predicted from the pathways and
models at New York and Bikini.
|
The reported concentration Pu in urine from the New York population is
10°
3 pci/n°.
Assuming a urine excretion of 1 2/d per person the total Pu
excreted via urine per year would then be 0.365 pCi (see Table 7).
estimates the total annual
Bennett’
intake of Pu via food, water, and inhalation to
be approximately 1.8 pCi for a person in New York.
These values then suggest
that 20% of the intake is appearing ‘in the urine.
This is a much higher per-
centage than has ever been reported '® and is higher than percentages normally
used for model predictions 7,17
Only 8% of the amount of Pu entering the
blood reaches the urine!” while 90% of the Pu in the blood is equally.
partitioned to both liver and bone 7516517
sing the latter values would
mean that the bone and liver burdens should increase by 2.1 pCi annually.
This quantity, however, is nearly equal to present New York total body |
burden accumulated since 1954".
The Pu concentrations reported for the urine
of the Bikini population would, of course, indicate body burdens 10 times
higher than those of the New York population.
€
Bennett's data! can also be used,to predict the quantity of Pu expected
tn the urine as a result of the body burden accumulated since 1954.
The
" major source of input to the blood, and subsequently to the urine, is from
turnover in the lung and lymph nodes which have half times of 500 and 1000
ee TT TEES
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ey UMad
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