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

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plate incorporation procedure, and the results were confirmed in an independent assay using
the preincubation (20 min) method. No biologically or statistically significant increase in the
number of revertant colonies was seen in any strain at any concentration. No bacteriotoxicity
was observed. Appropriate positive controls (sodium azide, nitrofurantoin, 4-nitro-1,2-phenylene
diamine, cumene hydroperoxide and 2-aminoanthracene) produced significant increases in
revertant colonies (Herbold, 1995e).
The mutagenic potential of thiacloprid-sulfonic acid Na-salt (purity, 95.1–95.2%; 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 3200 μg/ml were used in the presence and absence of a metabolic activation system (Aroclor
1254-induced rat liver S9). Under both activation conditions, no cytotoxic effects were induced.
No precipitation of thiacloprid-sulfonic acid Na-salt in the medium was observed. However,
thiacloprid-sulfonic acid Na-salt was tested up to its limits of solubility under culture conditions.
Thiacloprid-sulfonic acid Na-salt induced no biologically relevant increases in mutant frequencies.
The positive controls ethyl methanesulfonate and dimethylbenzanthracene had a marked mutagenic
effect, as was seen by a biologically relevant increase in mutant frequencies when compared with
the corresponding negative controls and thus demonstrated the sensitivity of the test system and
the activity of the S9 mix used (Herbold, 2003a).
The clastogenic potential of thiacloprid-sulfonic acid Na-salt (purity, 95.2%; dissolved in
deionized water) was tested in an in vitro mammalian chromosome aberration test using Chinese
Hamster V79 cells. The study complied with test guideline OECD 473. Cells were exposed for 4 h to
thiacloprid-sulfonic acid Na-salt at a concentration of 0, 800, 1600 and 3200 μg/ml in the presence
and absence of a metabolic activation system (Aroclor 1254-induced rat liver S9). Duplicate cultures
were used at each concentration. Cells were harvested at 18 h (all concentrations) and at 30 h (0 and
3200 μg/ml). An additional experiment was performed in the absence of metabolic activation using
continuous treatment for 18 h, harvesting at the same time, and thiacloprid-sulfonic acid Na-salt at a
concentration of 0, 800, 1600 or 3200 μg/ml. From each of two parallel cultures 100 metaphases were
examined for chromosome aberrations. In the absence of metabolic activation, cytotoxic effects were
observed at 3200 ug/ml after 18 h of treatment. In all other groups treated with thiacloprid-sulfonic
acid Na-salt, no cytotoxic effects were observed. None of the cultures treated with thiacloprid-sulfonic
acid Na-salt in the absence and in the presence of metabolic activation showed biologically relevant
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, 2003b).
(iii)
Thiacloprid-sulfonic acid amide
In a study of acute oral toxicity, two groups of three female non-fasted Wistar (Hsd/Cpb:
WU) rats were given thiacloprid-sulfonic acid amide (purity, 96.6%) as a single dose at 2000 mg/kg
bw in demineralized water by gavage. The study complied with test guideline OECD 423. The
dose of 2000 mg/kg bw was tolerated without mortalities, effects on weight development and
gross pathology. Clinical signs (decreased motility, decreased reactivity, spastic gait, laboured
breathing, uncoordinated gait, lateral position, rolling over and closed eyelids) were evident at 1 h
after treatment and lasted for up to 2 days. According to OECD guideline 423, the LD 50
cut-off of
thiacloprid-sulfonic acid amide is 5000 mg/kg bw and higher (Renhof, 2003).
The mutagenic potential of thiacloprid-sulfonic acid amide (purity, 96.6%; dissolved
in deionized water) was investigated in a test for reverse mutation in Salmonella typhimurium
THIACLOPRID X-X JMPR 2006