4.8 Article

High Tolerance and Delayed Responses of Daphnia magna to Neonicotinoid Insecticide Imidacloprid: Toxicokinetic and Toxicodynamic Modeling

Journal

ENVIRONMENTAL SCIENCE & TECHNOLOGY
Volume 55, Issue 1, Pages 458-467

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acs.est.0c05664

Keywords

sensitivity; exoskeleton adsorption; distribution; pulse exposure; carry-over toxicity

Funding

  1. Guangdong Provincial Department of Science and Technology [2019B151502020]
  2. National Natural Science Foundation of China [U1901220, 41773101]
  3. Fundamental Research Funds for the Central Universities [21617452]

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Species sensitivity to neonicotinoids varies among aquatic invertebrates. Daphnia magna shows high tolerance to imidacloprid in short-term exposure, but delayed and carry-over toxicity present challenges under repeated pulse exposures. Slow damage recovery significantly enhances the toxicity of imidacloprid, despite fast depuration from soft tissues. Integrating delayed and carry-over toxicity quantification is necessary in assessing the risk of neonicotinoids to aquatic invertebrates.
Species sensitivity to neonicotinoids has been shown to be highly variable among aquatic invertebrates. Toxicokinetic and toxicodynamic (TKTD) models were constructed to mechanistically elucidate the susceptibility of Daphnia magna to imidacloprid. D. magna was highly tolerant to single short-term exposure to imidacloprid (96-h LC50 of 8.47 mu g/mL), but delayed and carry-over toxicity occurred under repeated pulse exposures. Kinetic distribution of imidacloprid between exoskeleton and soft tissues of D. magna was evaluated using a newly developed method. Approximately 84% imidacloprid was distributed to soft tissues but was rapidly depurated from the tissue (t(1/2) of 1.2 h), resulting in low bioaccumulation and high tolerance. TKTD modeling also successfully simulated the survival of D. magna after pulsed exposures. The calculated recovery time was 45 d, indicating significant delayed and carry-over toxicity of the insecticide. While complete elimination of imidacloprid only took about 5 h (TK), slow damage recovery (45 d) caused slow organism recovery (TD). Consequently, although D. magna was tolerant to imidacloprid due to fast depuration from soft tissue, long damage recovery time significantly enhanced the toxicity under repeated pulse exposures. Our study highlights the necessity of integrating delayed and carry-over toxicity quantification in assessing the risk of neonicotinoids to aquatic invertebrates.

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