The continuous aerobic transformation of synthetic cyanide waste-water, amygdalin solutions and almond seed extract containing cyanide was investigated in several fluidized bed reactors. Various inocula consisting of activated sludge or soil slurry were used. Successful inoculation was achieved with simple soil slurry. No significant influence was found between the performance of the systems inoculated with a cyanide contaminated soil and a garden soil. The performance and stability of the reactors with respect to degradation rate were tested for a range of cyanide loading conditions, with feed containing only cyanide, and with different additional carbon sources, as well as various C : N ratios at a hydraulic retention time of 24 h. No growth with cyanide as the sole source of carbon and nitrogen was observed. The system with lactate as the organic C-source was capable of operating at cyanide concentrations of 16o ppm cyanide with a conversion rate of o.125 kg cyanide/m 3 d. Ammonia was the end product and the effluent concentration was o.5 ppm CN-. The systems with ethanol as the organic C-source could degrade only o.o5 kg cyanide/mSd, whose feed concentration was 6o ppm cyanide. Amygdalin, an organic cyanide-containing compound present in stone fruit seeds, was fed as a model substrate. Degradation rates up to LZ kg COD/m3d couId be measured with no free or organically bound cyanide in the effluent, These rates were limited by oxygen transfer, owing to the large amount of degradable COD. The further investigations with almond seed extracts, confirmed the applicability of the aerobic process to treat food-processing waste streams having low concentrations of cyanide with high COD content.
1 Introduction
Cyanide is one of nature's most toxic substances. The fatal doses for human adults are 1-3 mg/kg body weight if indigested, lOO-3OO ppm if inhaled, and lOO mg/kg body weight if adsorbed [1]. At normal pH and temperature, CN-is toxic to most species in freshwater or marine environments at a level of o.1 ppm. Cyanide toxicity is essentially based on an inhibition of the oxygen-transport metabolism.