Pesticide residues in food — 2006: Toxicological ... - ipcs inchem

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(TA1535, TA100, TA1537, TA98 and TA102). The study complied with test guideline OECD 471.
Six concentrations of up to 5000 μg/plate were used in the presence and absence of a metabolic
activation system (Aroclor 1254-induced rat liver S9). The initial test was performed in triplicate
using the plate incorporation procedure, and the results were confirmed in an independent assay
using the preincubation (20 min) method. Doses up to and including 158 μg per plate did not
cause any bacteriotoxic effects. Total bacteria counts remained unchanged and no inhibition of
growth was observed. At higher doses, the substance had only a weak, strain-specific bacteriotoxic
effect. Oing to the weakness of this effect, this range could nevertheless be used for assessment
purposes. Precipitation was observed at 5000 μg per plate. Evidence of mutagenic activity of
thiacloprid-sulfonic acid amide was not seen. No biologically relevant increase in the mutant
count, in comparison with the negative controls, was observed. The positive controls (sodium
azide, nitrofurantoin, 4-nitro-1,2-phenylene diamine, mitomycin C, cumene hydroperoxide and
2-aminoanthracene) had a marked mutagenic effect, as was seen by a biologically relevant increase
in mutant colonies compared to the corresponding negative controls (Herbold, 2003c).
The mutagenic potential of thiacloprid-sulfonic acid amide (purity, 96.6%; dissolved in
deionized water) was tested in a test for gene mutation at the Hprt locus in Chinese hamster
V79 cells in vitro. The study complied with test guideline OECD 476. Six concentrations of up
to 4000 μg/ml were used in the presence and absence of a metabolic activation system (Aroclor
1254-induced rat liver S9). In the presence and absence of metabolic activation, thiaclopridsulfonic
acid amide induced no relevant decreases in survival to treatment or decreases in relative
population growth. Precipitation of thiacloprid-sulfonic acid amide in the culture medium was also
not observed. However, thiacloprid-sulfonic acid amide was tested up to its limits of solubility and
up to and greater than 10 mmol/l, the requested limit concentration. In the presence and absence
of metabolic activation, there was no biologically relevant increase in mutant frequency above
that of the vehicle controls. Ethyl methanesulfonate and dimethylbenzanthracene induced clear
mutagenic effects and demonstrated the sensitivity of the test system and the activity of the S9 mix
(Herbold, 2003d).
The clastogenic potential of thiacloprid-sulfonic acid amide (purity, 96.6%; dissolved in
deionized water) was investigated in a test for mammalian chromosome aberration in Chinese
Hamster V79 cells in vitro. The study complied with test guideline OECD 473. Cells were exposed
in the absence and in the presence of S9 mix for 4 h to thiacloprid-sulfonic acid amide at a
concentration of 250, 500, 1000, 2000 or 4000 μg/ml. Cultures at all concentrations were harvested
18 h after the beginning of the treatment. In addition, cells treated at 1000, 2000 and 4000 μg/ml
were harvested 30 h after the beginning of the treatment. In the absence of metabolic activation,
an additional experiment was performed using continuous treatment for 18 h, harvesting at the
same time, and thiacloprid-sulfonic acid amide concentrations of 1000, 2000 and 4000 μg/ml. On
the basis of their cytotoxicity, which was additionally determined 8 h after the beginning of the
treatment, concentrations were selected for reading of metaphases. In the presence and absence of
metabolic activation, no cytotoxic effects were observed. Precipitation in the medium did not occur.
Therefore, for all treatment conditions, thiacloprid-sulfonic acid amide concentrations of 1000,
2000 and 4000 μg/ml were chosen for reading. The highest concentration of 4000 μg/ml exceeded
the requested maximum concentration of 10 mmol/l. None of the cultures treated with thiaclopridsulfonic
acid amide in the absence and in the presence of metabolic activation showed biologically
relevant or statistically significant increased numbers of aberrant metaphases. The positive controls
mitomycin C and cyclophosphamide induced clastogenic effects and demonstrated the sensitivity
of the test system and the activity of the S9 mix used (Herbold, 2003e).
THIACLOPRID X-X JMPR 2006