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Diss Factsheets

Administrative data

Description of key information


Key value for chemical safety assessment

Additional information

Oral and dermal

No oral or dermal repeated dose studies with DMS were reported.



In a two-week inhalation study in rats (Frame 1993) DMS was found to induce nasal epithelial cell proliferation at all concentrations tested (0.5, 3.7 and 6.3 mg/m36hr/day 5 d/wk). The 2.0- 3.7 fold increase in 2-bromo-5’-deoxyuridine (BrdU) incorporation in nasal epithelium is larger than could be expected from DNA repair only. In respiratory epithelium BrdU incorporation was statistically increased in the highest exposure group only. At the two highest exposure concentrations lesions of the nasal and respiratory epithelium were found, including erosion, ulceration, and atrophy, which increased in severity with exposure concentration and decreased in severity from anterior to posterior regions. Hypertrophy, hyperplasia, and squamous metaplasia were observed in the respiratory epithelium only. The study, however, is insufficiently reported to allow any conclusion on the impact of the observed cell proliferation on the possible carcinogenic action of DMS (seeCarcinogenicity).

In a carcinogenicity study, rats, mice, and hamsters were exposed to 2.6 mg/m3DMS (6 hr/d, 2d/wk)7, 10.5 mg/m3once every two weeks or a sublethal dose for about 15 months (Schlögel, 1972). This study is reviewed in section It is considered not suitable for evaluation as repeated dose study according to the guidelines, because no haematology, no clinical biochemistry and very limited histopathological examinations were performed.

Inflammation of the nasal cavity was seen in rats that were exposed to DMS (15.7 and 25.2 mg/m3, 1 hr/d, 5 d/wk for 130 days) in a study of Druckrey (1970) (seeCarcinogenicity).

It is reported that repeated inhalative exposure of rats and guinea-pigs for 4 months to 2.64±0.43 mg/m3induced changes in nervous system function, liver (fatty degeneration of single hepatocytes), kidney (degeneration of single renal tubuli), respiratory organs (bronchitis), and peripheral blood parameters. All changes except of bronchitis were reversible after a recovery period. A 4 month-exposure to 0.29±0.02 mg/m3induced only marginal changes. According to the authors these changes were without toxicological relevance (increased body weight, decreased hippuric acid elimination). No morphological changes could be found. In both concentration groups no effects on reproductive organs, spermatogenesis and sperm morphology were detected (Molodkina et al., 1986).

This study is considered not suitable for evaluation as repeated dose study because of the very limited reporting of study design and results. There are e.g. no data on number of animals per group, exposure duration per day, and a list of parameters studied is lacking. Furthermore the results were not substantiated with quantitative data. The conclusion of the authors that 0.29 mg/m3is the NOAEL for repeated-dose toxicity of DMS in their studies is not suppported. In another part of the repeated-dose inhalation studies with rats (exposure 4 months) and mice (exposure 2.5 months), reported in the same publication, and performed to assess the genotoxic activity of DMS, it is found that concentrations of 0.24 mg/m3and higher induce an increase in the percentage of bone marrow cells with chromosome aberrations. (see Genetic toxicity)

Justification for classification or non-classification