Epigenetic impacts of the acaricide flumethrin on honeybees (Apis mellifera)

  • Environ Pollut. 2026 Jun 1:398:128049. doi: 10.1016/j.envpol.2026.128049.
Xue Wang  1 ,  Suzhen Qi  1 ,  Mu Ding  2 ,  Wei Zhang  3 ,  Aidi Huang  1 ,  Changlu Sun  1 ,  Man Fan  4 ,  Liming Wu  5 ,  Miao Wang  6
Affiliations
  • 1. State Key Laboratory of Resource Insects, Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, 100093, China.
  • 2. College of Biotechnology, Beijing University of Agriculture, Beijing, 100096, China.
  • 3. Innovation Center of Pesticide Research, Department of Applied Chemistry, College of Science, China Agricultural University, Beijing, 100193, China.
  • 4. State Key Laboratory of Green Pesticide, Key Laboratory of Green Pesticide and Agricultural Bioengineering, Guizhou University, Guiyang, 550025, China.
  • 5. State Key Laboratory of Resource Insects, Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, 100093, China. Electronic address: [email protected].
  • 6. State Key Laboratory of Resource Insects, Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, 100093, China. Electronic address: [email protected].
PMID: 41933828 DOI: 10.1016/j.envpol.2026.128049
Abstract

Epigenetic modifications facilitate organismal adaptation to environmental toxins. While the toxicity of the acaricide flumethrin toward honeybees has been documented, the mechanisms underlying its effects on epigenetic modifications remain unclear. Risk screening revealed a high prevalence of flumethrin residues in honeybee colonies and notable bioaccumulation in honeybee brains following oral exposure. Flumethrin exposure at 10 μg/L (the minimum detected residue level) significantly altered the global levels of multiple epigenetic modifications-including RNA m6A, Am, m5C, m7G, and DNA 5 mC and 6 mA-along with the expression of related genes. m6A-seq demonstrated that flumethrin significantly altered m6A methylation on transcripts crucial for neuronal activity and memory within the Hedgehog and Hippo signaling pathways. Critically, m6A methylation modulated the transcripts of 12 odorant receptors, correlating with flumethrin-induced olfactory sensitivity deficits confirmed by electroantennography. Additionally, flumethrin altered methylation on transcripts encoding stress sensors and immune modulators in the FOXO and MAPK signaling pathways, triggering defense responses. The induced epigenetic marks and m6A-mediated transcripts, including EDD1, PI3K, Ptc, FOXO, Jra, and Argk, can be regarded as potential biomarkers for neurotoxicity assessment in honeybees. Our findings provide novel mechanistic insights into flumethrin toxicity and support a framework for epigenetic biomarkers in assessing environmental risks to honeybees.

Keywords
Epigenetic modification; Neurotoxicity; Olfactory deficit; RNA m(6)A methylation; Toxicity defense; m(6)A-seq.
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