Ecotoxicological hazard assessment currently relies on a rather small number of standardized laboratory tests using species from different trophic levels (autotrophs, primary and secondary consumers). These standard tests measure apical toxicological endpoints such as lethality, and give emphasis to acute effects of high exposure concentrations

Limitations of this primarily descriptive approach are evident: on the one hand, apical endpoints provide little insight into the underlying toxic processes and mechanisms, which complicates grouping of chemicals on the basis of common modes of action, as well as effect extrapolation across species (Eggen et al., 2004; Breitholtz et al., 2006; Segner, 2011); on the other hand, there is an ongoing debate if apical endpoints inform on the ecological consequences of toxic effects, since propagation from individual-level effects to population-level effects is not linear but varies due to other factors including phenotypic plasticity, life history strategy, resilience/elasticity processes, or individual variations within populations (Kooijman, 1998; Rose, 2000; Calow and Forbes, 2003; Relyea and Hoverman, 2006; Segner, 2007).

Despite these caveats, the current ecotoxicological testing paradigm in use appears to work well to assess toxic hazards arising from high concentrations, short-term exposures, and non-specifically acting chemicals. The question, however, is whether it still works well for low concentrations, long-term exposures and specifically acting compounds, or whether such scenarios require the additional consideration of sub-organism responses and traits.

Regards
Lucie Morgan,
Journal Coordinator,
Journal of Ecology and Toxicology.