Latent pesticide effects and their mechanisms

Abstract

Short pulses of toxicants can cause latent effects that occur long after the contamination event and are currently unpredictable. Here, we introduce an analytical framework for mechanistically predicting latent effects considering interactive effects of multiple stressors and hormetic effect compensation. We conducted an extensive investigation using high temporal resolution microcosm data of the mayfly Cloeon dipterum exposed to the pyrethroid pesticide esfenvalerate for 1 h. For 6 pesticide concentrations and 3 food levels we identified daily general stress information and predicted their synergistic interactions using the Stress Addition Model (SAM). Our analysis revealed that, especially at low concentrations, latent effects contributed most to the overall effect. At low concentrations ranging from 1/100 to 1/10,000 of the acute LC50, resulting in a 30–15 % mortality, latent effects prevailed, accounting for 92 % to 100 % of the observed effects. Notably, the concentration causing 15 % mortality 29 days post-exposure was 1000 times lower than the concentration causing the same mortality 4 days post-exposure, emphasizing the time-dependent nature of this Latent-Effect-Amplification (LEA). We identified both acute mortality and latent effects of pesticides on emergence. Furthermore, we observed pesticide-induced compensation mechanisms at both individual and population levels, transforming the initial monotonic concentration-response relationship into a hormetic, tri-phasic response pattern. Combining these processes enabled a quantification of the underlying causes of latent effects. Our findings highlight that short-term pesticide exposures can lead to latent effects of particular significance, especially at low effect concentrations.