Forty-two subjects working maximally for 15 years in a ferrite core manufactory were examined of their health. Nineteen of them were mainly exposed to about 9 mg/m3 (geometric mean) of the mixed dust of Fe2O3 (70%), ZnO, MgO and MnCO3. Sixteen of them were exposed to about 3 mg/m3 of spineled ferrite dust of Fe2O3 and so on. The others were exposed to less than 0.7 mg/m3 of the spineled ferrite dust. A significant change of chest X-ray film characterized by small round opacity was found in 4 subjects out of 33, who were exposed for 5 years or more. The two out of the four were exposed to the ferrite dust. When compared to the control group, workers of ferrite manufactory had significantly higher rate of constant coughing (almost 50%), about two times higher incidence rate of respiratory disease, and about two times more frequent hospital visit. While the neurological examination, pulmonary function, and zinc content in urine and blood revealed no abnormalities.
The activities of Na+, K+-ATPase and acetylcholinesterase (AChE) in the red cell membrane were determined in workers exposed to mercury. The values for Na+, K+-ATPase activity in red cell membranes from the exposed wor-kers were significantly lower than those obtained from the controls (t-test, p<0.01). The AChE activity in the exposed workers was also significantly lower than that in the controls (p<0.05). Significant correlations were found between mercury concentrations in the blood and red cell Na+, K+-ATPase activity (r=-0.576, p<0.001) and AChE activity (r=-0.376, p<0.05). No clinical signs of chronic mercury poisoning were found in the present investigation. This seems to suggest that when excessive exposure to mer-cury occurs Na+, K+-ATPase activity and AChE activity in the red cell membrane decrease before clinical signs appear.
Pregnant mice fed methylmercury alone or methylmercury and selenite simultaneously for 30 precoital days and thereafter up to Day 18 of gestation were examined for organ and tissue mercury concentrations and embryonic and fetal death. Coadministration of selenite increased maternal liver mercury concentrations and decreased maternal kidney mercury concentrations. When the two groups were combined, the death rate, defined as the number of total embryonic and fetal deaths per total number of implants, was significantly correlated with organ mercury concentrations in the maternal brain, liver, blood, uterus, amniotic membrane, amniotic fluid and fetal liver. The highest correlations were found with the maternal blood and amniotic fluid. When the two groups were separated, the extent of correlation became greater in the methylmercury alone group and smaller in the coadministration group. Nevertheless, correlation coefficients of as large as some 0.9 were observed in both groups for the maternal blood and amniotic fluid. From the significant difference in the two dimensional distribution (the mercury concentration vs. the death rate) and the above results in these two tissues, the dose-response relationship and its modification by selenite were discussed.
In this 30-day study, the distribution and excretion, and the biological half-time (B.H.T.) of chromium in selected organs of the rat were studied and the results obtained showed a characteristic difference between hexavalent (Cr VI) and trivalent (Cr III) chromium compounds. The rate of retention at the site of a single injection of Cr III was 88.7% (after 24 hrs) whereas that of Cr VI was 6.4%. After the administration of Cr VI, 232.73 μg or 36% of the total chromium injected was excreted into the urine within 7 days while 48.45 μg or 8.0% was excreted after Cr III administration. The amount of chromium excreted in the feces within 7 days after the injection of Cr VI was 89.17 μg or 13.9%, while the amount of chromium excreted was 146.96 μg or 24.2% of the Cr III administered. The results of calculation of B.H.T. in several organs after a single administra-tion of Cr VI were as follows. The lung showed two components represented by two kinds of regression lines. The calculated B.H.T. was 60.2 hours (2.5 days) and 501.6 hours (20.9 days). The liver showed three components, 2.4 hours, 52.8 hours and 376.2 hours (15.7 days) ; the kidney had two components, 52.8 hours and 250.8 hours (10.5 days); the brain also showed two components, 4.4 hours and 231.52 hours (9.6 days); the heart showed two components, 66.9 hours and 334.42 hours (13.9 days) ; the testis also showed two components, 4.58 hours and 300.9 hours (12.5 days); and the blood had only one component, 334.4 hours (13.9 days).
Male SD strain rats were subjected to 5 hr inhalation exposure to CrCl3. 6 H2O aerosol (13.3 mg Cr/m3, particle size<2 μm), killed at intervals of 1, 2 and 7 days after exposure and Cr contents in the total organ, high-molecular-weight fraction (Cr-HMW) and low-molecular-weight, Cr-binding substance (LMCr) were determined in the lungs and liver. Total Cr contents in the lungs stayed at a level approximately 8 to 25 times higher than those in the liver. Sephadex gel filtration revealed that only 3 to 10% of the total Cr was retained in LMCr in the lungs in contrast to 56 to 71% in the liver. The percentages of Cr-HMW in the total lung and liver Cr were 60 to 70% and 15 to 25%, respectively. Cr-HMW and total Cr contents in the lungs showed a slow and comparable decrease after exposure. In contrast, LMCr in the lungs gradually increased in parallel with LMCr in the liver, showing levels approximately equal to the latter. A statistically significant correlation was observed only between LMCr in the lungs and each of Cr-HMW, LMCr and total Cr contents in the liver. A linear one-compartment kinetic model gave estimates of the biological half-times of 12.8 days for lung Cr and 1.2 days for liver Cr. These results suggest that LMCr in the lungs is in equilibrium with Cr in the rest of the body and participates in the movement of Cr from the lungs to other organs. The long half-time possibly resulting in the accumulation of Cr in the lungs may be explained by the slow rate of LMCr synthesis in the lungs.
In rats given a subcutaneous injection of 0.5 mg of Cd/kg, 6 days/ week for 15 weeks, daily excretion of cadmium in the urine and feces was determined. The relationship between cadmium accumulation and the excretion was studied in terms of cadmium toxicity. Urinary excretion of cadmium was markedly affected by cadmium toxicity, but fecal cadmium was scarcely affected. A linear relationship was obtained between the accumulation of cadmium and its urinary excretion only before the onset of renal damage. A linear relationship between the cadmium accumulation and fecal excretion was seen throughout the whole experimental period. The present experiment reveals that the main route of cadmium excretion is the feces before both renal and hepatic damage occur, but it is the urine thereafter.