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LINEAR ALKYLBENZENE SULFONATE (LAS) - UNEP Chemicals

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OECD SIDS <strong>LINEAR</strong> <strong>ALKYLBENZENE</strong> <strong>SULFONATE</strong> (<strong>LAS</strong>)<br />

3.1.6 Genetic Toxicity<br />

In vitro Studies<br />

Several in vitro bacterial (Ames) tests have been conducted on <strong>LAS</strong> using Salmonella typhimurium<br />

TA 98, TA 100, TA 1535, TA 1537, and TA 1538 strains with and without metabolic activation at<br />

test material concentrations up to 5000 µg/plate (Schoeberl 1993a; Inoue et al. 1980; Sunakawa et<br />

al. 1981). Results were negative in all studies, while the positive and negative controls gave the<br />

expected results. Similarly, results with and without activation were negative in a recombination<br />

assay using Bacillus subtilis at concentrations up to 50 µg/plate and in an E. coli reverse mutation<br />

assay (Inoue and Sunakawa 1979).<br />

A transformation test with Syrian hamster embryo (SHE) cells without metabolic activation also<br />

showed negative results (Inoue et al. 1980).<br />

In vivo Studies<br />

In vivo mammalian bone marrow cytogenetic studies on <strong>LAS</strong> exposure are available in which mice<br />

received either oral gavage doses up to 800 mg/kg bw/day (Inoue et al. 1977) or dietary doses up to<br />

1170 mg/kg (Masabuchi et al. 1976). Rats were also given dietary doses up to 450 mg/kg bw/day<br />

(Masabuchi et al. 1976). In all studies, there was no significant difference in the incidence of<br />

chromosomal aberrations between the treated groups and the control groups. A dominant lethal<br />

assay with mice is also available in which male mice received <strong>LAS</strong> in the diet at a dose of 300 mg/kg<br />

bw/day for 9 months before being mated with untreated females (Masabuchi et al. 1976). There were<br />

no significant differences in fertility, the mortality of ova and embryos, the number of surviving<br />

fetuses, or the index of dominant lethal induction between the experimental groups and the control<br />

group. Three male mice each given a single intraperitoneal injection of 100 mg/kg bw <strong>LAS</strong> showed<br />

no differences in the incidences of polychromatic erythrocytes with micronuclei in the bone marrow<br />

between the control and treatment group (Kishi et al. 1984). The reliability of each of the in vivo<br />

studies reported here was not assignable because the original study reports were not available for<br />

review. However, they had been evaluated by the International Program of Chemical Safety (IPCS<br />

1996) and therefore are considered reliable.<br />

Conclusion<br />

No indication of genetic toxicity for <strong>LAS</strong> is evident in any of the studies conducted.<br />

3.1.7 Carcinogenicity<br />

Several studies looked at the potential for tumorigenicity in rats. In the most documented study<br />

(Buehler et al. 1971), four groups of Charles River weanling rats, divided by sex, were given 0.5,<br />

0.1, and 0.02% (10, 50, 250 mg/kg bw/day) <strong>LAS</strong> in their food for 2 years. Following completion of<br />

those studies, five male and five female rats from each of the parental groups (F1b and F2b) and all<br />

survivors were selected for necropsy. Gross examination of all animals for pathology did not reveal<br />

any abnormalities. No consistent dietary induced changes that could be considered a toxic response<br />

were observed. Animals that showed significant loss of weight, development of tumors, or other<br />

evidence of abnormalities were sacrificed and tissues examined. The incidence of tumors and the<br />

common incidental diseases were similar in all dieting groups.<br />

Other rat studies had similar results with drinking water exposures up to 200 mg/kg bw/day for 24-<br />

26 months (Tiba 1972; Endo et al. 1980) or dietary exposures up to 300 mg/kg bw/day for up to 24<br />

months (Fujii et al. 1977; Yoneyama et al. 1977). No effects were observed on survival, body<br />

weight gain, or general histopathology and hematological endpoints. Slight increases in liver and<br />

<strong>UNEP</strong> PUBLICATIONS 29

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