Soil contamination with radiocaesium (Cs) has a long‐term radiological impact because it is readily transferred through food chains to human beings. Plant uptake is the major pathway for the migration of radiocaesium from soil to human diet. The plant‐related factors that control the uptake of radiocaesium are reviewed. Of these, K supply exerts the greatest influence on Cs uptake from solution. It appears that the uptake of radiocaesium is operated mainly by two transport pathways on plant root cell membranes, namely the K+ transporter and the K+ channel pathway. Cationic interactions between K and Cs on isolated K‐channels or K transporters are in agreement with studies using intact plants. The K+ transporter functioning at low external potassium concentration (often <0.3 mM) shows little discrimination against Cs+, while the K+ channel is dominant at high external potassium concentration with high discrimination against Cs+. Caesium has a high mobility within plants. Although radiocaesium is most likely taken up by the K transport systems within the plant, the Cs:K ratio is not uniform within the plant. Difference in internal Cs concentration (when expressed on a dry mass basis) may vary by a factor of 20 between different plant species grown under similar conditions. Phytoremediation may be a possible option to decontaminate radiocaesium‐contaminated soils, but its major limitation is that it takes an excessively long time (tens of years) and produces large volumes of waste.
Total concentrations of metals in soil are poor predictors of toxicity. In the last decade, considerable effort has been made to demonstrate how metal toxicity is affected by the abiotic properties of soil. Here this information is collated and shows how these data have been used in the European Union for defining predicted-no-effect concentrations (PNECs) of Cd, Cu, Co, Ni, Pb, and Zn in soil. Bioavailability models have been calibrated using data from more than 500 new chronic toxicity tests in soils amended with soluble metal salts, in experimentally aged soils, and in field-contaminated soils. In general, soil pH was a good predictor of metal solubility but a poor predictor of metal toxicity across soils. Toxicity thresholds based on the free metal ion activity were generally more variable than those expressed on total soil metal, which can be explained, but not predicted, using the concept of the biotic ligand model. The toxicity thresholds based on total soil metal concentrations rise almost proportionally to the effective cation exchange capacity of soil. Total soil metal concentrations yielding 10% inhibition in freshly amended soils were up to 100-fold smaller (median 3.4-fold, n = 110 comparative tests) than those in corresponding aged soils or field-contaminated soils. The change in isotopically exchangeable metal in soil proved to be a conservative estimate of the change in toxicity upon aging. The PNEC values for specific soil types were calculated using this information. The corrections for aging and for modifying effects of soil properties in metal-salt-amended soils are shown to be the main factors by which PNEC values rise above the natural background range.