Since halogenated organic compounds have been detected in drinking water, great interest has been directed toward the identification of products from chemical oxidation processes. To get water treatment processes which provide safe and delicious tap water, it is nessesary to have knowledge of the intermediate and end products formed during ozonation. It is also of great interest whether the products are potential toxic or precursors of other toxic compounds which could be produced if the ozonated effluent is subsequently chlorinated to provide residuals for disinfection. It is in general known that ozonation for a short or long time is effective for reducing mutagenicity, but uncomplete ozonation creates compounds which show more mutagenicity than the origin. Many researchers have found aromatic, phenolic, aliphatic mono and di-carboxylic acids, aldehydes and ketones to be present in the ozonation products. However, we do not know all the intermediate and end product formed during ozonation. This is due to the fact that ozone reaction is very complex because ozone itself is unstable, the concentratrion of product is too small for analysis and the number of products are too big. This report consists of four parts : 1) the two types of ozonation reactions ; (a) direct reactions of ozone with the organic compound and (b) free radical reactions of ozone which involve a hydroxyl free radical intermediate. 2) the oxidability of ozone ; (a) removal characteristic of COD_Cr and TOC and (b) comparison with the combination of UV radiation or nuclear radiation. 3) the reaction mechanisms of ozone with organic compounds. 4) the reaction products formed during ozonation and their mutagenicity directly or indirectly.

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The color reaction between o-hydroxyhydroquinonephthalein (Qnph) and aluminum (III) was examined in the presence of various surfactants alone or in combination (cationic, anionic, nonionic and amphoteric surfactants) in weakly acidic media. A simple, rapid and sensitive spectrophotometric determination of aluminum (III) (0-2.0 μg of aluminum (III) in a final volume of 10 ml, at 555 nm) was developed by using the Qnph-aluminum (III) complex in a mixed micelle system of zephiramine (tetradecyldimethylbenzylammonium chloride) as a cationic surfactant and Brij 35 (poly (oxyethylene) dodecylether) as a nonionic surfactant. This proposed method (apparent molar absorptivity of 2.1×10⁵ l·mol^-1·cm^-1) showed good reproducibility, and the influence of foreign ions was reduced to 1/4-1/10 of that in the previous method with Qnph alone in weakly basic media. The method was used for the determination of aluminum (III) in pharmaceutical preparations (aspirin aluminum). Further, since aluminum may leach out of aluminum packaging of the kind widely used for instant foods, this proposed method was applied to the assay of aluminum (III) in biological specimens (calf serum and human urine), and in leaching solution used on aluminum foil. The recovery was good, and it was found that the leaching solution contained significant amounts of aluminum (III).

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Maximal incorporation of labeled carbon from ¹⁴C-CCl₄ into isolated rat hepatocytes occurred 5 min after exposure to ¹⁴C-CCl₄. The radioactivity (expressed as unit per milligram of protein) in the microsomal fraction was found to be higher than that in the nuclear, mitochondrial or soluble fraction of the cell. Exposure of liver microsomes of rats pretreated with phenobarbital (PB), 3-methylcholanthrene (3 MC) or polychlorinated biphenyls (PCBs) to CCl₄ inactivated cytochromes P-450 and b₅, and aminopyrine N-demethylase, aniline hydroxylase and glucose-6-phosphatase. The contents of the two cytochromes and the activities of the three microsomal enzyme declined to levels similar to those in CCl₄-exposed microsomes from rat liver untreated with the inducers of microsomal enzymes. The contents of lipid peroxide in microsomes of rats pretreated with PB and PCBs were increased by exposure to CCl₄ more than those in untreated and 3 MC-pretreated rat liver microsomes. Piperonyl butoxide, which inactivates cytochrome P-450, suppressed the destruction of cytochrome and the production of lipid peroxidation induced by CCl₄, while cysteine had no effect on the reduction of the two cytochrome contents, the inactivation of the three microsomal enzymes or the production of lipid peroxide. These results suggest (1) that the species of cytochrome P-450 induced by PB and PCBs mainly participate in the biotransformation of CCl₄ to trichloromethyl radical, and are involved in the inactivation of P-450 and the initiation of lipid peroxidation by CCl₄, (2) that a CCl₄ metabolite, probably trichloromethyl radical, causes the destruction of cytochrome P-450 and lipid peroxidation, and (3) that the formation of phosgene does not play a significant role in the inactivation of cytochrome P-450 and microsomal enzymes by CCl₄.

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In order to confirm that the accumulation of environmental chemical pollutants may be different between fresh-and sea-water fishes, mullet (Mugil cephalus), an estaurine sea-water fish, was acclimated to fresh-water, to examine the intakes of chlordane and pentachlorophenol-Na (PCP-Na) and also the acute lethal toxicity of PCP-Na. The accumulation of chlordane in the liver of fresh-water-acclimated mullet was approximately four times higher than that of sea-water mullet. The accumulation of PCP in the liver was also higher in fresh-water mullet than in sea-water mullet. The LC₅₀ of PCP-Na was about six times lower in fresh-water mullet than in sea-water mullet. These results well-coincided to the previously reported observation on an euryhaline fresh-water fish, tilapia (Tilapia nilotica). The difference thus found between fresh-and sea-water fishes suggests that chemicals are accumulated and metabolized differently in the fishes of both water areas. This difference might be an important factor for the ecological evaluation of chemical pollutants.

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Uptake of cadmium into the lung and chemical forms in the lung supernatants of rats were studied after intratracheal instillation of cadmium chloride to find the mechanisms why the lung is sensitive to the metal by exposure through the airways. Male Wistar rats (10 weeks old ; body weight, approximately 270 g) were instilled intratracheally with cadmium chloride at a dose of 2.5 μg Cd/rat (0.4 ml in physiological saline). The animals were killed 1/6, 1/3, 2/3, 1, 2, 3, 6, 12, 24 and 48 h after the instillation. The lungs were homogenized in the same volume (w/w) of 0.1 M Tris-HCl buffer (pH 7.4, 0.25 M glucose ; bubbled through with nitrogen gas) using a Polytron homogenizer in an atmosphere of nitrogen gas after removing air in the lungs under reduced pressure. More than 90% of cadmium was retained in the lung 10 min after the instillation. However, the concentrations of the metal in the supernatants (170000 g for 60 min) were less than 50% in the homogenates before 12 h after the instillation. The supernatants were subjected to analysis for the distributions of cadmium, copper, iron, phosphorus, sulfur and zinc by high performance liquid chromatography-inductively coupled argon plasma-atomic emission spectrometry (HPLC-ICP). Cadmium bound to metallothionein was less than 50% in the supernatants within 12 h after the instillation. Two distinct cadmium peaks were observed other than metallothionein on an Asahipak GST-520 column by HPLC-ICP within 3 h after the instillation. The rapid uptake into the lung and low inducibility of metallothionein in the lung may explain the high susceptibility of the lung to cadmium.

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We examined anaerobic biodegradations of sodium linear alkylbenzenesulfonate (LAS), sodium alkyl sulfate (AS), sodium alkylpoly (oxyethylene) sulfate (AES), sodium alkylphenyl (oxyethylene) sulfate (NES), sodium α-olefinsulfonate (AOS), sodium salt of fatty acid (Soap), alkyl poly (oxyethylene) ether (AE) and p-alkylphenyl poly (oxyethylene) (APE) by bacterial sources from sewage sediments. In the course of biodegradation, the productions of H₂, H₂S, CO₂ and CH₄ were determined. Assuming that the final products were CO₂ and CH₄, the results of the anaerobic biodegradabilities of surfactants were as follows : (AS, Soap)>AE>(APE, AES, NES)>(AOS, LAS). These results indicated that the surfactant having benzene ring, branched alkyl chain or ethoxylate chain [-(EO)n-] was resistant to anaerobic biodegradations. The biodegradability of surfactants was also influenced by the structure of hydrophilic group. When the hydrophobic group was identical, the extent of biodegradation decreased in the following order : -OSO₃Na>-(EO)_nH>-(EO)_nSO₃Na, -SO₃Na.

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A high-molecular-weight protein that binds cadmium primarily before the induction of metallothionein (MT) in rat liver was identified chromatographically. Female Wistar rats were injected intravenously with a single dose of 0.4 or 1.0 mg Cd/kg body weight and sacrificed 0.5 and 3 or 0.5 h, respectively, after the injection. The liver supernatants were subjected to gel filtration analyses on Sephadex G-75 and Asahipak GS-520 columns, the former being used as a conventional column and the latter as an HPLC column. Cadmium (Cd) in the eluate was determined simultaneously with copper, iron, phosphorus, sulfur and zinc on an inductively coupled argon plasma-atomic emission spectrometer (ICP). Cadmium was eluted as a sharp peak at a retention time of 13.2 min accompanied with minor peaks at 11.5 min (broad peak), 14.5 min (MT) and others on a GS column before induction of MT at the low Cd dose. The major peak at 13.2 min from a GS column corresponded to the Cd peak eluted at V_e/V_o=1.20 on a Sephadex column. This major Cd-binding protein was separated on a cation exchange column and identified as a constitutive zinc-and sulfurcontaining protein without other metals. The Cd-binding zinc protein was identical with the Cd-binding protein of 40000 daltons that had been detected by competitive binding assay using a western blotting technique.

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Determination of tris (1, 3-dichloroisopropyl) phosphate (TDCPP), a flame retardant, in commercial curtains and carpets was examined. TDCPP was extracted by refluxing in methanol, purified by deactivated alumina column chromatography and determined by gas chromatography with a flame photometric detector (FPD). Concentration of TDCPP in 35 commercial curtains analyzed ranged as follows : ND (not detected)-3300 μg/g in 16 polyester fibers, ND-40.5 μg/g in 10 acrylic and modacrylic fibers, ND in 7 other fibers. Concentrations of TDCPP in 12 commercial carpets analyzed ranged ND-660 μg/g.

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A new post labeling method with high performance liquid chromatography (HPLC) was developed for the determination of"free"malonaldehyde (MA) and"bound"MA (pyrimidopurinones) in biological materials. The system involves separating free and bound MAs on the column, heating the eluate with thiobarbituric acid (TBA) through a Teflon [○!R] tubing, and measuring the absorbance at 532 nm. The instrument detection limit of the TBA reactants (MA, pyrimidopurinones) was approximately 0.1 nmol. The MA values found in the meat samples by the HPLC method were 36-47% of those found by the conventional TBA method. The effects of acids, solvents and metal compounds on the TBA reaction were also investigated.

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Hexamine has been mainly employed as a standard substance for the formaldehyde determination by the acetylacetone (AA) and chromotropic acid (CA) method, and formalin by the 4-amino-3-hydrazino-5-mercapto-1, 2, 4-triazole (AHMT) method in"Standard Method of Analysis for Hygienic Chemists"authorized by the Pharmaceutical Society of Japan. Formaldehyde in the test solution prepared by steam distillation of formalin was determined by these three methods, and the data obtained were not coincident with each other. Formalin was employed for the standard substance instead of hexamine in the AA and CA method, so there were no any difference in the data. Formalin should be utilized as the standard substance for the determination of formaldehyde in the AA and CA method just as in the AHMT method.

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Concentrations of cyanide ion in untreated and treated water discharged from chemical laboratories were determined sixty-nine times from July 1986 to December 1986. The average concentrations of cyanide ion in the untreated and treated water were 0.010 mg/l and 0.007 mg/l, respectively. These values are very low in comparison with the allowance limit provided by the regulation of Kobe City on waste water (0.7 mg/l). Even though the amount is very small, the existence of cyanide ion in the treated water cannot be disregarded because of its high toxicity. It was found that the cyanide ion in the treated water was formed by the reaction of phenol with nitrous acid.

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