Chemical pollution and climate change are major threats towards aquatic communities. Yet, the interactions of these stressors remain poorly understood. Especially the combination of chemical exposure and increasing heatwaves raises concern.¹ To understand the mechanisms of these stressor interactions, recent studies have explored the temperature-dependent toxicokinetics (uptake, elimination and transformation) of contaminants in aquatic invertebrates. These toxicokinetic processes define the internal concentrations in an organism and are a key connection between exposure and observed effects. However, such studies showed limitations for contaminants with strong receptor binding affinity (i.e. neonicotinoids) that were resistant towards elimination.²

In this talk, we will present a case study that examined temperature effects on the toxicokinetics of a neonicotinoid pesticide (thiacloprid) in aquatic invertebrates under laboratory and outdoor mesocosm conditions. For this purpose, a temperature dependent toxicokinetic model, including receptor-binding, was calibrated based on laboratory experiments with aquatic invertebrates exposed under static (fixed temperature and fixed exposure concentration) conditions. Additionally, experiments were performed using an outdoor mesocosm facility with a dynamic exposure (natural temperature fluctuations and exposure pulses) including a simulated heatwave (ambient temperature + 8°C).

Increasing temperature had an exponential effect on toxicokinetic rate constants. The temperature dependent toxicokinetic model showed a good fit for laboratory data (R² = 0.78 – 0.98) and allowed a correlation of temperature effects on toxicokinetics with other physiological parameters (i.e. respiration). Furthermore, the model accurately predicted tissue concentrations in the mesocosm experiment, thereby validating the model. The tissue concentrations were two times higher under heatwave conditions compared to ambient temperatures (46 vs. 25 µg kg^-1) and remained at this level even after the event of exposure due to insignificant elimination.

The presented study advanced the mechanistic understanding of the interaction of chemical exposure and changing climatic conditions. We highlight how extreme heat events can intensify risks caused by pesticides, especially when they show specific biological interactions such as strong receptor binding. These findings emphasize the need for regulatory strategies, such as dynamic models, to address the interactions of contaminants and a warming climate.

[1] Polazzo, F. et al. Change Biol. 2022, 28 (4), 1248–1267.
[2] Raths et al., Glob. Change Biol. 2023, 29 (5), 1390–1406.