Two groups of male and female Sprague-Dawley rats (50 animals/group per sex) were treated with either 15.37 or 46.77 μmole of 1,1,2-TCE in DMSO/rat for 2 years. The animals were treated once a week by s.c. injection of test compound in the skin of neck. Two groups of controls received either DMSO or no treatment at all. The incidence of benign mesenchymal and epithelial tumors was not significant when compared with either DMSO-treated or untreated controls. The animals treated with 46.77 μmole 1,1,2-TCE significantly developed sarcomas when compared with the untreated controls. In a further experiment, either 40 μmole or 160 μmole 1,1,2-TCE was injected into male Wistar rats and the metabolites, TdGA and HEMA, were determined in 24-h urine samples. Comparative studies were carried out giving equimolar amounts of chloroethanol and 2-chloroacetaldehyde diethyl acetal. Analysis of the metabolites showed that no detectable HEMA was excreted in urine after treatment of rats with 1,1,2-TCE or chloroethanol. TdGA was excreted in urine much more among chloroacetaldehyde-treated animals than among 1,1,2-TCE- or chloroethanol-treated rats.

A new specific method for urinary delta-aminolevulinic acid (ALA-U) measurement in man as a serial screening method for health control in occupational lead exposure was compared with a recommended, selective test (DAVIS method). The new test can be run fully automated, and the cost of material per sample is much lower than in the DAVIS method. ALA values obtained with this specific method were lower than those measured with the DAVIS method (= DAVIS values) in each case due to the elimination of interfering urinary compounds. In DAVIS values below the biological tolerance level (BAT level) of 15 mg/l, the percentage of interfering compounds varied between 10 and 80%; above BAT level, these components represented about 20% of the total amount of ALA-U. A strong correlation can be demonstrated between specifically measured ALA values and the enzyme activity of ALA-dehydratase (ALA-D) in blood at lead levels (Pb-B) below 35 μg/dl (r = -0.768 for ALA-U/log ALA-D; n =18).

Quantitative analysis of the dose-dependent urinary excretion of acrylonitrile and its metabolites was carried out in male Wistar rats following inhalation exposure of the animals to 1, 5, 10, 50 and 100 ppm acrylonitrile for 8 h. Quantitative analysis of acrylonitrile in urine was performed by gas chromatography. The urinary metabolites cyanoethyl mercapturic acid, S-carboxymethyl cysteine and hydroxyethyl mercapturic acid were measured by a modified amino acid analysis, and thiodiglycolic acid by GC-MS. The excretion pattern of the compound and its metabolites was dependent on the exposure level; it is concluded that urinary determination of the unmetabolized acrylonitrile and two of its metabolites, cyanoethyl mercapturic acid and thioglycolic acid, may be useful for biological monitoring of industrial exposure.

Either 40 μmole or 160 μmole 2,2′-DDE was injected into male Wistar rats and the metabolites, TdGA and HEMA, were determined in the 24-h urine specimens. Comparative investigations were carried out giving equimolar amounts of chloroethanol and 2-chloroacetaldehyde diethyl acetal. In a further step, inhalation experiments were performed to determine urinary excretion of the two metabolites after an 8-h exposure of male Wistar rats to 10, 50, 100, and 500 ppm 2,2′-DDE and to 50, 200, und 1000 ppm vinyl chloride.