EUROPE: Flupyradifurone: the European Parliament blocks the Commission, in order to protect bees and children's health

[pfpcnews]

Flupyradifurone: the European Parliament blocks the Commission, in order to protect bees and our children's health

PAN Europe - September 10, 2026 - 13:04

Today, the Environment Committee of the European Parliament vetoed an attempt from the European Commission to increase Maximum Residue Levels (MRLs) of Flupyradifurone, a controversial neonicotinoid, in rapeseed (canola). Members of the European Parliament took a wise decision to protect our children's brains and pollinator populations, rather than support unsustainable agriculture.

Martin Dermine, PAN Europe Executive Director, said: "This story is repeating again and again: despite the significant scientific knowledge on the risk that neonicotinoids pose to our children's brains, the European Commission keeps trying to increase the permitted residue levels in our food. They did the same in the past with other neonicotinoids, such as acetamiprid, disregarding available scientific knowledge, and favouring industrial farming."

Flupyradifurone is a new-generation neonicotinoid that was first approved in the EU in 2015. [1] When researchers started investigating this insecticide, they realised it was toxic to bees - particularly bumble bees and wild bees.

Pauline Cervan, a Senior toxicologist at Génération Futures (France) said: "A significant number of scientific studies show that pesticides from the neonicotinoids family pass the placental barrier and directly interact with neurons from developing foetuses. Furthermore, the European Food Safety Authority raised concerns regarding indications of endocrine disruption in industry studies. Increasing European consumers’ exposure to this chemical is irresponsible."

Flupyradifurone is currently under review at EU level. The Rapporteur Member State (Greece) already concluded that, based on the available scientific information, no outdoor use should be considered safe for wild bees. Recent science further indicates that this neonicotinoid interferes with the functioning of mammalian neurons, which is in line with findings from other neonicotinoids. [2]

Martin Dermine concluded: "The European Parliament now needs to validate this vote in plenary. We trust they will support the protection of children's brains, and of pollinators, which are so vital to our food systems."

Neonicotinoids and children's brains

While the toxicity of neonicotinoids to pollinators is now well-known among citizens and decision-makers, the risk they pose to foetuses and young children is still disregarded and not prioritised. Brain development in early life stages is very sensitive to interactions with neurotoxicants. Scientific research has shown that neonicotinoids, due to their systemic properties, directly pass the placental barrier and interact with neurons within developing brains.

Currently, regulatory tests do not assess the impact of such exposure on cognitive functions which is, considering the state of scientific knowledge, unacceptable. Indeed, scientific research has already proven that exposure to pesticides during pregnancy or at early life stages leads to reduced cognitive functions, but also to an increase in the risk of developing paediatric brain tumours.

Générations Futures and PAN Europe already wrote to the European Commission to highlight the importance of more strictly regulating neonicotinoids to protect children's brains and pollinators. [3]

Acetamiprid is another neonicotinoid that is still approved in the EU, and for which there is concerning information on its neurotoxicity and its significant, chronic toxicity to pollinators. Acetamiprid is currently under review by the European Commission. According to Générations Futures and PAN Europe, it should be classified as Toxic to reproduction category 1B, considering the available scientific information on its neurotoxicity.

Contact:

Dr Martin Dermine (PAN Europe), Executive Director, martin@pan-europe.info, +32 2 318 62 55
Pauline Cervan (Générations Futures), Senior Toxicologist, pauline@generations-futures.fr, +33 7 57 18 34 22
Read more: European Parliament objection to flupyradifurone MRLs

Notes:

[1] Bayer has classified the substance as a butenolide insecticide, a new family of pesticides that was created specifically for flupyradifurone, probably to avoid the negative reputation of neonicotinoids. Since it follows the same mode of action, and is a systemic insecticide, meaning it can be absorbed by the roots or the leaves of plants, it should have been classified as a neonicotinoid. This approach was also used for sulfoxaflor (sulfoxamine), which has been banned in the meantime.

[2] Cöllen et al. (2026), Functional Expression of Nicotinic Receptors on iPSC-Derived Astrocytes and Signalling Disturbances by a Panel of Neonicotinoid Pesticides and Their Metabolites(link is external)

[3] https://www.pan-europe.info/press-relea ... and-g%C3%A...

SOURCE:
https://www.pan-europe.info/press-relea ... t-bees-and

[admin]

NOTE:

Xu L, Xu X, Wu X, Kuang H, Xu C - "Sex-dependent environmental health risk analysis of flupyradifurone" Environ Sci Technol 56(3):1841-1853 (2022)
https://doi.org/10.1021/acs.est.1c07726
"Differential metabolic pathways of FPF induced sex-based dysregulation of the hypothalamic-pituitary-thyroid axis, in which females exhibited subclinical hyperthyroidism, while males displayed abnormal hypothyroidism."

Abstract

Pesticides are used in agricultural production worldwide, resulting in widespread environmental pollution. Many diseases are closely related to exposure to pesticide residues. In this study, the association between exposure to the pesticide flupyradifurone (FPF), a substitute for neonicotinoids, and sex-dependent thyroid dysfunction was explored for the first time. Exposure using rat models revealed that the FPF metabolism is sex-dependent, with males preferring N-dealkylation and hydrolytic metabolism and females preferring hydroxylation. In particular, novel chloropyridine-site hydroxylation I and II metabolic pathways of FPF were discovered. More importantly, differential metabolic pathways of FPF induced sex-based dysregulation of the hypothalamic-pituitary-thyroid axis, in which females exhibited subclinical hyperthyroidism, while males displayed abnormal hypothyroidism. This may be attributed to the potential agonistic or antagonistic effect of FPF sex-dependent metabolites on liver thyroid hormone receptors. Furthermore, FPF exposure further mediated sex-specific dysregulation of cellular lipid homeostasis, with abnormal fatty acid β-oxidation and excessive energy expenditure in females and the risk of excessive accumulation of triglycerides in males. These results illustrate the potential risk of sex-related thyroid metabolic diseases caused by FPF and provide an important basis and support for further studies of FPF on human health and as an environmental pollutant.