US EPA

1627508 

Technical Report 

Uptake of mercury vapor in blood in vivo and in vitro from Hg - containing air 

Kudsk, FN 

1969 

HAPAB/70/00610 

Toxicol 

2-3 

HAPAB The ratio of mercury ( Hg ) concentration in the expired air to that in the inspired air was determined in four subjects. Various constant concentrations in the inspired air of 50 to 350 mcg Hg/cu m were used. The concentration of Hg in the expired air was measured by direct and continuous graphical recording with an ultraviolet photometer. This accurate technique ( error plus or minus 10% ) demonstrated that the respiratory dead space for Hg vapor in human subjects corresponds to the physiological dead space. This finding strongly indicated a complete alveolar absorption of mercury vapor in the lungs. The in vitro uptake of Hg vapor in blood and plasma was investigated by means of a simple equilibration technique similar to that used by Clrkson et al. 1961. The uptake in whole blood samples from three subjects proceeded at two rates. During the first hour the rate was approximately 0.4 mcg/hr/ml, while during the remaining part of the experimental period ( 1/2 to 13 1/2 hr ), the rate of uptake was constant for each subject's blood, but varried in the blood from individuals between 0.13 and 0.20 mcg/hr/ml. The in vitro uptake of Hg vapor in human plasma also occurred at two rates. During the first hr the rate was 0.20 mcg/hr/ml, followed by a slower rate of 0.02 mcg/hr/ ml. In similar experiments lasting up to 3 hr, the uptake of Hg in erythrocyte suspensions from different subjects was 0.17 to 0.23 mcg/hr/ ml. The addition of 0.25% glucose did not affect the rate of Hg uptake. The Hg uptake in toluene - extracted erythocyte hemolysates during an equilibration time of 2 to 5 hr was 0.60 to 1.4 mcg/hr/ml. A progressive inhibitory effect of increasing ethyl alcohol concentrations on the uptake of Hg vapor in samples of human blood was noted. In equilibration experiments of 3 hr duration, the inhibition reached a maximum of 60% at a blood alcohol concentration of 0.2%. Similar results were obtained in blood plasma with ethyl alcohol. Methyl alcohol exerted a similar inhibitory effect, but isopropyl and n- butyl alcohol were without effect. A possible involvement of the primary hydrogen peroxide - catalase complex or catalase only in the oxidation and uptake of Hg in erythrocytes was investigated, using aminotriazole as an inhibitor, either along or in combination with methylene blue and glucose as a hydrogen peroxide - generating system. Aminotriazole was without effect, but methylene blue alone, and especially in combination with glucose, caused a pronounced accelerated uptake of Hg in erythrocytes. TOXICOLOGY AND PHARMACOLOGY 70/05/00, 189 1969