Exposure study on chemosensory effects of epsilon-caprolactam in the low concentration range.

OBJECTIVE: Aim of the study was to examine possible chemosensory effects of epsilon-caprolactam in the low concentration range relevant to indoor environmental conditions. METHODS: Twenty healthy subjects (10 male, 10 female) aged from 21 to 38 years were exposed for 6 h, respectively, to 0, 0.15, 0.5 and 5 mg/m3 epsilon-caprolactam vapours in a randomized and double-blind method. As a measure of trigeminal stimulation of the eye, blink frequency was video-recorded four times per day and evaluated by using a new semi-automatic, computer-assisted method compared to baseline recording and manual counting. Digital slit lamp photographs were taken at the same time to examine conjunctival hyperaemia. A standardized ophthalmologic grading scale was used to measure redness of the eyes objectively. Active anterior rhinomanometry compared nasal resistance before and after exposure. Subjective ratings of discomfort and mental orientation were assessed using the German version of the Swedish Performance Evaluation system (SPES). As a measure of personality traits, positive and negative affectivity was determined (PANAS). RESULTS: Six hour exposures to epsilon-caprolactam revealed no significant dose-response relationship concerning blink frequency, nasal resistance and redness of the bulbar conjunctiva. Subjective ratings of discomfort (sum scores) significantly increased only at the highest concentration of 5 mg/m3. However, the increase in discomfort was only moderate, ranging between "not at all" and "somewhat". Significant increases of the subjective detection of malodour (subscore) already occurred at 0.15 mg/m3, showing no adaptation over time. Irritation of the eyes or upper airways was not reported. CONCLUSIONS: Exposure to epsilon-caprolactam vapour did not elicit any acute health effects in a concentration range up to 0.5 mg/m3. Even at the highest concentration of 5 mg/m3, we could only find a slight increase in subjective symptoms, mainly due to an unincisive increase of perception of malodour.

Investigations in mice on the potentiation of resistance to infections by a new immunostimulant compound.

BM 12.531, 2-[2-cyranaziridinyl-(1)]-2-[2-carbamoylaziridinyl-(1)]-propane, a new immunostimulant compound, increased the resistance of mice to infection with Candida albicans. Because BM 12.531 had no fungistatic activity in vitro, it is proposed that the therapeutic effect of BM 12.531 is caused by the stimulation of cell-mediated immunity. Administration of cyclophosphamide alone increased the mortality among mice infected with C. albicans and Pseudomonas aeruginosa, but when BM 12.531 was then administered to these animals, the mortality was reduced. Among mice with acute Escherichia coli infection, a synergistic effect of chloramphenicol and BM 12.531 was demonstrated.

Animal experiments on the compensation of the immunosuppressive action of cyclophosphamide by 2-[-2-cyanaziridinyl-(1)-]-2-[-2-carbamoylaziridinyl-(1)]-propane BM 12 531.

BM U2 531, the 2-[2-Cyanaziridinyl-(1)-]-2-[-2-carbamoylaziridinyl-(1)-]-propane, the further development of BM 06 002 is able to compensate the immunosuppressive action of Cyclophosphamide and to increase the carcinostatic action of Cyclophosphamide. These properties are demonstrated 1. by a leucocytosis induced after application of BM 12 531 in rats 2. by a quick restauration of leucocyte depression induced by Cyclophosphamide in rats and dogs 3. by an increase of resistance against an infection (candida albicans) in mice 4. by an increase of antitumour effect of Cyclophosphamide against a DS-carcinosarcoma in rats.

Experimental investigations on increased resistance to infections with Candida albicans and Staphylococcus aureus Smith by 4-imino-1,4-diazobicyclo-(3.1.0)-hexane-2-on BM 06.002 (prop. INN imexon) in mice.

BM 06.002 increases the resistance of mice to experimentally induced chronic infection with Candida albicans. Furthermore, BM 06.002 leads to increased resistance in the case of experimentally induced infection with Staphylococcus aureus Smith, when a subtherapeutic dose of sulfadiazine is applied. In mice immunosuppressively pretreated with hydrocortisone, BM 06.002 effectuates immunorestauration.