Neurotoxicity of chlorpyrifos and chlorpyrifos-oxon to Daphnia magna

Abstract

Chlorpyrifos (CPF) is a widely used broad-spectrum organophosphate insecticide. CPF elicits neurotoxic effects in exposed organisms by inhibiting the activity of acetylcholinesterase enzymes (AChE), which prolongs nerve transmission and results in neurotoxic symptoms and death at high doses. While CPF is capable of eliciting neurotoxic effects, chlorpyrifos-oxon (CPFO) is the primary neurotoxicant agent. Aquatic organisms bioactivate CPF to CPFO through the Cytochrome P450 phase I metabolic pathway following exposure to CPF. Additionally, in the environment, CPF transforms to CPFO, primarily through photo-oxidation. As both compounds can be transported in air and water to aquatic ecosystems, there is the potential for exposure to non-target organisms. The potential for adverse impacts on aquatic receptors depends on patterns of exposure and toxicity of individual compounds and the mixture. To study the neurotoxicity of these compounds, a 48 h acute and 21 d chronic Daphnia magna bioassay was conducted independently with CPF and CPFO. Acute bioassay results show a median lethal concentration (LC50) of 0.76 μg L-1 for CPF and 0.32 μg L-1 for CPFO, suggesting that CPFO is 2.4 times more acutely toxic to D. magna. Acute assay results were also used to derive Benchmark Dose Levels of 0.58 μg L-1 for CPF and 0.25 μg L-1 for CPFO. However, neither compound elicited an effect on reproduction or growth at relevant chronic exposures. As D. magna are a small and relatively sensitive species, and the AChE inhibition adverse outcome pathway is highly conserved, these results may be cautiously extrapolated in assessing adverse impacts on aquatic receptors.1