. ~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 : ey UMad ns : Y