Toxicological investigations in the semiconductor industry: III: Studies on prenatal toxicity caused by waste products from aluminum plasma etching processes.

The prenatal toxic effects of contaminated vacuum pump oil (Sample A) and solid waste products (Samples B and C) originating from aluminum plasma etching processes in semiconductor manufacturing were investigated. Three strains of pregnant mice with different degrees of sensitivity during organogenesis (days 6-15 of gestation) were treated daily with 1000 mglkg b.w.

Investigations of the acute toxic, cytogenetic, and embryotoxic activity of buminafos.

The organophosphorus herbicide buminafos (O,O-dibutyl-(1-butylaminocyclohexyl)-phosphonate) was tested for its acute toxic, cytogenetic, and embryotoxic activity on different strains of mice. The oral LD50 value for male NMRI mice was determined to be 3500 mg/kg. Single oral doses of 175, 1000, and 2000 mg/kg did not cause any significant enhancement in the percentage of chromosome aberrations in bone marrow cells of male NMRI mice.

Investigations on the acute toxic, cytogenetic, and embryotoxic activity of phenyl isocyanate and diethoxyphosphoryl isocyanate.

Phenyl isocyanate (I) and diethoxyphosphoryl isocyanate (II), used as intermediates in organic chemical syntheses, were tested for their acute toxic, cytogenetic, and embryotoxic activity on mice of different strains. The oral LD50 values for male CFLP mice were determined to be 196 mg/kg for I and 4080 mg/kg for II. Single oral doses of 1/40 and 1/20, respectively, of the LD50 of I (4.

Cytogenetic, genetic, and embryotoxicity studies with dimethyl 2,2,2-trichloro-1-(2,2,2-trichloro-1-hydroxyethoxy)-ethylphosphonat e, a hypothetical impurity in technical grade trichlorfon.

The hemiacetal (CH3O)2P(O)CHOCHOHCCl3)CCl3, a hypothetical contaminant in technical preparations of the organophosphorus pesticide trichlorfon, was tested for cytogenetic, mutagenic, and embryotoxic activity after ip administration to mice of different strains. A single dose of 81 mg/kg (0.2 mmol/kg) caused a significant enhancement in the percentage of chromosome aberrations in bone marrow cells of CFLP mice; a similar effect was induced by an equimolar single dose of chemically pure trichlorfon (51.

Cytogenetic and embryotoxic effects of bromophos and demethylbromophos.

The organophosphorus pesticide bromophos and the tetramethylammonium and sodium salts of demethylbromophos were tested for cytogenetic and embryotoxic activity on mice of different strains. Single intraperitoneal (ip) doses of 183.0 mg/kg (0.

Effect of dimethoate and O-demethyldimethoate on bone marrow cells of CFLP mice.

The organophosphorus pesticide dimethoate and its nonalkylating O-demethyl derivative were tested for their ability to induce chromosomal alterations in bone marrow cells of CFLP mice after ip administration. A single dose of 20 mg/kg dimethoate proved to be ineffective. However, doses of 60 mg/kg dimethoate or 69 mg/kg O-demethyldimethoate sodium salt significantly increased the aberration rates above those of the controls.

[Differences in right-left distribution of foetuses in uterus cornua and relevance of differentiated germ implantation in uterus? -experiments with laboratory mice (author's transl)].

Corpora lutea were counted in laboratory mice, and the production of the right ovary was found to be slightly higher than that of the left. Rates of implantation, consequently, were higher in the right cornu of the uterus. No right-left difference between uterus cornua was observed regarding foetal weight and sex distribution.

[Mutagenicity of dichloroacetaldehyde and 2,2-dichloro-1,1-dihydroxy-ethanephosphonic acid methyl ester, possible metabolites of the organophosphate pesticide Trichlorphon].

Dichloroacetaldehyde and 2,2-dichloro-1,1-dihydroxy-ethanephosphonic acid methyl ester which are formed solvolytically from desmethyltrichlorphone, an in vivo metabolite of the organophosphorus pesticide Trichlorphone, show in the dominant lethal test in mice at equimolar dosage (1.6 mmol/kg) a mutagenic activity comparable with that of Trichlorphon. Therefore it cannot be ruled out that the genetic effects of this pesticide may be due in part to the action of its degradation products.

[The mutagenicity of desmethyltrichlorphone in dominant lethal test on mice (author's transl)].

After i.p. administration to AB mice of 405 mg/kg desmethyltrichlorphone (sodium salt) in a single dose and 54 mg/kg daily for 3 weeks, the mutagenic effect in the dominant lethal test was at least the same as that of trichlorphone.