This website is about ecotoxicology, in particular the development of ecotoxicological models. I find conceptual, mathematical and simulation models important and exciting, because they capture the general principles or the core knowledge of a scientific field and because they can make predictions.

There are also special pages dedicated to three topics:

• Toxicokinetic-toxicodynamic models
• Bioaccumulation and biotransformation
  
• Applications in risk assessment of chemicals. 

Thank you for visiting,

Roman Ashauer

Julita gave an excellent talk at the 23^rd Annual Meeting of the Society of Environmental Toxicology and Chemistry (SETAC Europe) and she won the best presentation award. Julita is part of the European project CREAM and her talk was about "Predicting toxicity to fish based on in vitro data". Congratulations Julita!

Abstract: If an organism does not feed, it dies of starvation. Even though some insecticides which are used to control pests in agriculture can interfere with feeding behavior of insects and other invertebrates, the link from chemical exposure via affected feeding activity to impaired life history traits, such as survival, has not received much attention in ecotoxicology. One of these insecticides is the neonicotinoid imidacloprid, a neurotoxic substance acting specifically on the insect nervous system. We show that imidacloprid has the potential to indirectly cause lethality in aquatic invertebrate populations at low, sublethal concentrations by impairing movements and thus feeding. We investigated feeding activity, lipid content, immobility, and survival of the aquatic arthropod Gammarus pulex under exposure to imidacloprid. We performed experiments with 14 and 21 days duration, both including two treatments with two high, one day pulses of imidacloprid and one treatment with a low, constant concentration. Feeding of G. pulex as well as lipid content were significantly reduced under exposure to the low, constant imidacloprid concentration (15 µg/L). Organisms were not able to move and feed – and this caused high mortality after 14 days of constant exposure. In contrast, feeding and lipid content were not affected by repeated imidacloprid pulses. In these treatments, animals were mostly immobilized during the chemical pulses but did recover relatively fast after transfer to clean water. We also performed a starvation experiment without exposure to imidacloprid which showed that starvation alone does not explain the mortality in the constant imidacloprid exposure. Using a multiple stressor toxicokinetic-toxicodynamic modeling approach, we showed that both starvation and other toxic effects of imidacloprid play a role for determining mortality in constant exposure to the insecticide. (Link to paper in PLOS ONE journal, open access)

Abstract: The authors present a method to predict fish survival under exposure to fluctuating concentrations and repeated pulses of a chemical stressor. The method is based on toxicokinetic-toxicodynamic modeling using the general unified threshold model of survival (GUTS) and calibrated using raw data from standard fish acute toxicity tests. The model was validated by predicting fry survival in a fish early life stage test. Application of the model was demonstrated by using Forum for Co-ordination of Pesticide Fate Models and Their Use surface water (FOCUS-SW) exposure patterns as model input and predicting the survival of fish over 485 d. Exposure patterns were also multiplied by factors of five and 10 to achieve higher exposure concentrations for fish survival predictions. Furthermore, the authors quantified how far the exposure profiles were below the onset of mortality by finding the corresponding exposure multiplication factor for each scenario. The authors calculated organism recovery times as additional characteristic of toxicity as well as number of peaks, interval length between peaks, and mean duration as additional characteristics of the exposure pattern. The authors also calculated which of the exposure patterns had the smallest and largest inherent potential toxicity. Sensitivity of the model to parameter changes depends on the exposure pattern and differs between GUTS individual tolerance and GUTS stochastic death. Possible uses of the additional information gained from modeling to inform risk assessment are discussed. (link at ET&C journal, open access)