Monochloressigsäure, Natriummonochloracetat
MAK-Begründung, Nachtrag
Andrea Hartwig1 (Vorsitz der Ständigen Senatskommission zur Prüfung gesundheitsschädlicher Arbeitsstoffe, Deutsche Forschungsgemeinschaft)MAK Commission2
1 Institut für Angewandte Biowissenschaften, Abteilung Lebensmittelchemie und Toxikologie, Karlsruher Institut für Technologie (KIT), Adenauerring 20a, Geb. 50.41, 76131 Karlsruhe, Deutschland
2 Ständige Senatskommission zur Prüfung gesundheitsschädlicher Arbeitsstoffe, Deutsche Forschungsgemeinschaft, Kennedyallee 40, 53175 Bonn, Deutschland
Abstract
The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area has re‐evaluated monochloroacetic acid [79‐11‐8] together with sodium monochloroacetate [3926‐62‐3] considering all toxicological endpoints. Monochloroacetic acid is a strong acid and dissociates in biological media. Therefore, also data for sodium monochloroacetate are used to evaluate the systemic toxicity.
Monochloroacetic acid is corrosive to the eyes but there are no inhalation studies from which a NOAEC for local effects can be derived. Therefore, a maximum concentration at the workplace (MAK value) of 2 mg/m3 (0.5 ml/m3), which has been set for the better investigated phosphoric acid, is also established for monochloroacetic acid. As irritation is the critical effect, monochloroacetic acid is classified in Peak Limitation Category I. By analogy with phosphoric acid, an excursion factor of 2 is set.
In chronic studies in rats, a NOAEL for sodium monochloroacetate of 3.5 mg/kg body weight and day for males was found for depressed body weight gain and diminished liver and kidney weights. After toxicokinetic scaling, extrapolation to humans and application of the preferred value approach, a MAK value of 2 mg/m3 for the inhalable fraction is set. Since systemic effects of sodium monochloroacetate are critical, it is assigned to Peak Limitation Category II. From the half‐life of 3 hours in rat plasma, an excursion factor of 2 is derived.
In a study with monochloroacetic acid in rats, the NOAEL for developmental toxicity was 70 mg/kg body weight. This dose corresponds to a concentration of 121 mg/m3 at the workplace, which is about 60 times as high as the MAK value of 2 mg/m3. Therefore, damage to the embryo or foetus is unlikely when the MAK value is not exceeded and monochloroacetic acid and its sodium salt are classified in Pregnancy Risk Group C. Monochloroacetic acid is DNA‐damaging in vitro at concentrations which are also cytotoxic, but it is not an alkylating agent. Overall, the acid and its sodium salt are not regarded as genotoxic and they are not carcinogenic in rats and mice. Monochloroacetic acid in concentrations which are not irritating to the skin is not taken up via the skin in toxicologically relevant amounts. The sodium salt, however, is expected to penetrate the skin in amounts contributing to toxicity and is therefore designated with “H”. Both compounds are not expected to be sensitizers.
