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BRIEF RESEARCH REPORT article

Front. Toxicol.
Sec. Regulatory Toxicology
Volume 6 - 2024 | doi: 10.3389/ftox.2024.1438890
This article is part of the Research Topic Emerging topics on chemical safety assessment View all 6 articles

Neonicotinoid pesticides: evidence of developmental neurotoxicity from regulatory rodent studies

Provisionally accepted
Jennifer B. Sass Jennifer B. Sass 1*Nathan Donley Nathan Donley 2Bill Freese Bill Freese 3
  • 1 Natural Resources Defense Council, New York, United States
  • 2 Center for Biological Diversity (CBD), Oakland, California, United States
  • 3 Center for Food Safety - Washington DC, Washington, United States

The final, formatted version of the article will be published soon.

    Neonicotinoid insecticides are widely used, environmentally persistent, and are detected in drinking water, foods, human urine, breast milk, amniotic and cerebrospinal fluids, and the brains of treated rodents. Here we provide the first comprehensive assessment of unpublished rodent developmental neurotoxicity (DNT) studies on five neonicotinoids sponsored by neonicotinoid manufacturers. Statistically significant shrinkage of brain tissue was observed in high-dose offspring for five neonicotinoids: acetamiprid, clothianidin, imidacloprid, thiacloprid, and thiamethoxam. A decreased auditory startle reflex was reported for acetamiprid at all doses and was statistically significant in the mid- and high-dose offspring, and for clothianidin in juvenile high-dose females. No mid- or low-dose brain morphometric data were submitted for acetamiprid, imidacloprid, or thiacloprid. Thiamethoxam mid- and low-dose brain morphometric data were provided to the U.S. Environmental Protection Agency (EPA) upon request. Only partial mid-dose brain morphometry data were submitted for clothianidin, but no low-dose data. Nonetheless, EPA set the mid-dose as the study’s No Adverse Effect Level (NOAEL) for failing to find a definitive NOAEL for acetamiprid, clothianidin, imidacloprid, thiacloprid and thiamethoxam. We conclude that perinatal exposure to neonicotinoids and their metabolites induces adverse, nicotine-like neurotoxic effects in rodent bioassays, and that the exposure limits set by EPA for human exposure are either not protective or not supported by available neurotoxicity data. We propose regulatory changes to empower EPA to better protect public health from developmental neurotoxins like neonicotinoids.

    Keywords: pesticide, Neurotoxic, DNT, Neonicotinoid, EPA - Environmental Protection Agency, neurodevelopment, Developmental, Brain

    Received: 26 May 2024; Accepted: 05 Sep 2024.

    Copyright: © 2024 Sass, Donley and Freese. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Jennifer B. Sass, Natural Resources Defense Council, New York, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.