The neonicotinoid alternative sulfoxaflor causes chronic toxicity and impairs mitochondrial energy production in Chironomus kiinensis.

Abstract Unintentional environmental consequences caused by neonicotinoids reinforce the development of safer alternatives. Sulfoxaflor is considered such an alternative. However, ecological risk of sulfoxaflor remains largely unknown. Here, we investigated the acute and chronic toxicity of sulfoxaflor to a benthic invertebrate, Chironomus kiinensis. Sulfoxaflor showed lower lethality than imidacloprid to midges, with LC50 values of 84.1 (81.5-87.3), 66.3 (34.8-259), and 47.5 (29.5-306) μg/L for 96-h, 10-d, and 23-d exposures, respectively. Conversely, sulfoxaflor significantly inhibited C. kiinensis growth and emergence in chronic exposures when concentrations were above 20 μg/L. Effects on energy production were assessed through in vitro tests using mitochondria isolated from C. kiinensis. Sulfoxaflor disrupted mitochondrial state-3 respiration, meanwhile, adenosine triphosphatase (ATPase) activity and adenosine triphosphate (ATP) production were both inhibited in a dose-dependent manner. The observed mitochondrial dysfunction may be related to the decreased organismal growth and emergence, which could further influence biodiversity. Interestingly, sulfoxaflor uptake in C. kiinensis was detected even after emergence, implying its potential to be transported along food webs and among environmental compartments. This study provides thorough investigations on the toxicity of an emerging neonicotinoid alternative to Chironomidae. Data derived from the current study are useful to inform future ecological risk assessment and benefit problem-solving to the overall agriculture-environment nexus.