Combustion effluents and the human toxicology of cadmium

Abstract

Energy utilization by conventional technologies for combustion of coal, oil and waste give rise to atmospheric emissions of cadmium (Cd). Fall‐out on arable land can contribute to increases in soil concentrations of Cd. Other important sources of Cd pollution of soil are fertilizers (including sewage sludge) and direct water‐borne contamination by irrigation. From soil, Cd is taken up by plants which are used for human consumption. For the human population in general, Cd exposure is mainly via food and, in smokers, via Cd in tobacco.

After human uptake, Cd induces the synthesis of metallothionein, which binds Cd and transports it mainly to the kidney, where it is efficiently retained with a biological half‐life of more than ten years. In long‐term exposure there is accumulation of Cd in the kidney and when a critical concentration has been reached (100–300 μg/g), membrane damage occurs with subsequent losses of protein and minerals via urine. Particularly in persons with a low dietary intake of vitamin D and calcium, the renal damage favours development of a bone disease (Itai Itai disease), which has occurred in Japan. Cadmium can be carcinogenic in animals. Epidemiological evidence support the carcinogenicity of Cd, particularly when exposures are via inhalation such as in certain occupational settings. In order to avoid risks of adverse human health effects from Cd intake, it is important that Cd emissions from combustion effluents as well as other sources are kept as low as possible.

Key words:

• Cadmium
• heavy metal combustion toxicology