A method for analysis of hexachlorophene in toilet goods was examined by thin-layer chromatography and gas chromatography. Hexachlorophene was separated from samples by extraction with hexane containing 10% ethanol and followed by column chromatography over DEAE-cellulose. The fraction obtained by elution of the column with a mixture of acetone and hydrochloric acid was submitted to alumina layers containing silver nitrate and silica gel layers. After development with petroleum ether acetic acid (88 : 12) on both layers, phenolic compounds were separated and detected on alumina layers under ultraviolet irradiation and on silica gel layers by spraying with 4-aminoantipyrine reagent. A compound was separated from some phenolic compounds by gas liquid chromatography using a gas chromatograph equipped with a flame ionization detector or an electron capture detector, and a column of SE-30 on Chromosorb G, and the limit of determination was 250 and 1 μg/ml, respectively. This method was found to be sufficiently satisfactory for determination of hexachlorophene in baby powder, cream, soap, shampoo, and hair tonic.

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Polychlorinated biphenyls (PCB) in four pairs of human adipose tissues obtained from the women by caesarean operation and human milk secreted from the subjects thereafter were analysed by gas-liquid chromatography, and relation of PCB compositions and contents among the samples was discussed. Though PCB in the tissues and milk were mainly composed of biphenyls substituted with four to eight chlorine atoms, PCB compositions were not always the same in different subjects. However, PCB in any pair of the tissue and milk obtained from the same subject had extremely similar composition. This means that in lactating women PCB in the milk were based on those accumulated in the tissue rather than those in the day's diet. The ratio of PCB levels in the milk to those in the related adipose tissues ranged from 1/50 to 1/100.

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In at least some urban areas, population exposure to elevated lead levels in the atmosphere with high motallization is associated with increased blood level of lead. Lead is known to interfere in porphyrin metabolism and the effect of motor vehicle pollution on porphyrin metabolism in lead poisoning was examined with lead-intoxicated rats with the following results : 1) Urinary excretion of coproporphyrin and δ-aminolevulinic acid was significantly higher in leadpretreated rats by their exposure to motor vehicle pollutants in a traffic lane. 2) By exposure to motor vehicle pollutants in a traffic lane, urinary excretion of coproporphyrin in lead-pretreated rats became higher than that of δ-aminolevulinic acid.

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Investigations were made on the effect of pollutants such as ethyl and phenyl-mercury, inorganic mercuric ion, cadmium ion, PCB (Kanechlor 300, 400, 500, 600), hexachlorophene, and fluoride on the activity of some enzymes, and the stability of membrane of lysosome and erythrocytes. All the organic and inorganic mercurials strongly inhibited Na⁺, K⁺-ATPase, FDP-aldolase and urease, and there were no differences among these mercurials in their inhibitory power and in the effect of sulfhydryl compounds on their inhibition. Inorganic mercuric ion disrupted potently the membranes of lysosomes and erythrocytes, but organic mercury ions did not. PCB did not inhibit the enzyme tested of simple protein, but inhibited Na⁺, K⁺-ATPase which has been known to contain phospholipids as its constituents. This inhibition was completely protected by the addition of lecithin, and PCB was comfirmed to be a lipophilic inhibitor. Hexachlorophene also showed the same type of inhibition as PCB except that it inhibited potently FDP-aldolase Fluoride was inhibitory on Na⁺K⁺-ATPase and urease activity.

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Relation between dose and absorption, and excretion of selenium was examined by short term repeated oral administration of labeled sodium selenite to rats. Male rats were divided into 4 groups of 8 rats each. To 3 groups of them, Na₂⁷⁵SeO₃ solutions (0.1 μCi/0.3 mg/2 ml/kg, 0.1 μCi/1.0 mg/2 ml/kg, 0.1 μCi/3.0 mg/2 ml/kg) were given orally every day for 35 days, and remaining 1 group was used as control. During the repeated administration, gain in body weight, whole body accumulation and excretion to urine and feces of selenium were examined. Gain in boody weight was suppressed in 3.0 mg/kg group compared with control group. At 35th day, weight of liver and kidney were markedly increased in 1.0 and 3.0 mg/kg groups, and histological changes were found only in 3.0 mg/kg group. During the time of repeated administration, the amount of whole body accumulation of ⁷⁵Se was not proportional to the dose, and the rate of daily excretion of ⁷⁵Se in the experimental groups was roughly proportional to the dose, and declined with the lapse of days in all the groups. After the termination of repeated administration of sodium selenite for 35 days, the radioactivity was excreted mainly via urine. Elimination of ⁷⁵Se was rather rapid for 10 days, became slower, and the whole body count decreased along an exponential line. The biological half lives of absorbed labeled sodium selenite were calculated from the lines obtained by plotting the whole body counting on semi-logarithmic scale, and the values in 0.3 and 3.0 mg/kg dose groups were 26 and 24 days, respectively. At 35th day, higher accumulation of ⁷⁵Se was found in the kidney, epididymis, spleen, liver, and blood in this order, but a remarkable decrease in liver and kidney was obseved 65 days after termination of the administration. In blood and hair, concentration of selenium was directly proportional to the dose.

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In order to analyse polychlorinated terphenyls (PCTs) in food wrappers rapidly, separation of PCTs from polychlorinated biphenyls (PCBs) by reverse-phase partition thin-layer chromatography (RPP-TLC) was investigated, and the method was applied to the detection of PCTs in food wrappers. The components of PCTs and PCBs were resolved on liguid paraffin layers by development with acetonitrile-acetone solvent systems, and the materials examined showed characteristic patterns composed of slightly overlapping spots. Respective perchlorinated compounds of PCTs and PCBs, o-, m-, and p-tetradecachloroterphenyls (TDCTs) and decachlorobiphenyl were also distinctly separated as well-defined spots on the thin layers, and PCTs were identified in low levels in the presence of PCBs. PCTs in food wrappers were extracted with hexane and cleaned up by Florisil column chromatography. By submitting PCT fraction directly to RPP-TLC, their presence was assumed from the pattern obtained. After perchlorination of the fraction with antimony pentachloride and extraction with benzene, PCTs were comfirmed as TDCTs in high sensitivity by RPP-TLC.

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The concentration of calcium in serum, and the amount of lead and calcium in femur of rats were determined after a single intraperitoneal administration of lead acetate, and the following results were obtained. In the case of administration of lead acetate, zinc acetate, stannous acetate, manganese acetate, or calcium acetate (0.483 mmole/kg as metal ion), lead acetate significantly increased the serum calcium concentration compared to that of other metals. Lead deposition in femur increased rapidly and reached a maximum 2 days after administration of lead (0.965 mmole/kg as metal ion). On the other hand, the amount of calcium in femur decreased by about 15% (p<0.05) of the control values one day after lead administration. The data obtained from the present experiments agree with the view that the increase of serum calcium induced by the administration of lead is caused by release of calcium into serum from the bone.

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Distribution of arsenic in blood and tissues, and excretion of arsenic in feces and urine after an oral administration of arsenic trioxide (29 mg/kg) or methylarsine sulfide (36 mg/kg) were examined in rats and rabbits. Blood level of arsenic in rats reached the maximum 3 days after a single administration of arsenic trioxide, and decreased at a slow biological half-life of 60 days, but blood concentration of arsenic in rabbits was about 1/80 of that in rats 24 hr after dosing. Distribution of arsenic in rat tissues attained the maximum 2 days, but its content was only 1% of the administered dose. Excretion of arsenic in rat feces was 68.6% during the first 4 days and a trace amount of arsenic was detected in bile. Fecal excretion of arsenic in rabbits was 62.9% and 36.2% during 7 days, respectively, when arsenic trioxide and methylarsine sulfide were given. On the other hand, urinary excretion of arsenic in the rat was only 1.8% of the dose during 30 days after arsenic trioxide administration, but the level of arsenic in rabbit urine was 5.5% and 18.2%, respectively, during 7 days after arsenic trioxide and methylarsine sulfide treatment.

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Calcium hypochlorite affects organochlorine pesticides as two different reagents, one is basic and the other, oxidative. pp'-DDT was dehydrochlorinated into pp'-DDE in basic medium, then presumably by basic action, further decomposition of pp'-DDE was observed. Heptachlor was easily hydrolyzed in water to produce 1-hydroxychlordene, which seemed to be readily oxidized. A part of Aldrin was broken up in the course of oxidation by way of Dieldrin, while most of it was degraded by way of an unidentified alcoholic substance.

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Mercury in a solution is reduced to the elemental state by tin [II], and the elemental state mercury is aerated from the solution in a single-path system mercury analyser where the absorption is measured at 253.7 nm in a quartz gas-flow cell. The following conditions are required for the detemination of mercury in sulfuric acid solution. 1) Use of a separatory funnel as a reaction vessel is convenient for shaking and bubbling many sample solutions. The funnels of almost the same volume are used, and the ratio of vapor phase to liquid phase in a funnel is 1 or a little larger than I. 2) Acidity of a sample solution should be adjusted to almost the same degree as a standard mercury solution, because the absorbance of mercury increases with higher acidity. 3) Two ml of 10% SnCl₂ solution is added to 50 ml of a sample solution, and the resulting solution is bubbled with air (2 liters/min) after shaking for 2 min. 4) Detectable range is 0.1-0.8 μg/50 ml on ×1 sensitivity and the lowest limit may be 0.01 μg/50 ml by change of sensitivity. The coefficient of variation is 2.87% at 0.5 μg/50 ml.

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