ReviewPeerJ2026
Breakdown products of the fungicide Fludioxonil may account for observed environmental impact: potential implications for human health.
Review in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Fludioxonil fungicide has been shown to rapidly degrade in the environment into a perfluoroalkyl substance (PFAS) breakdown product. Fludioxonil has been previously associated with both health and environmental damage, but a clear mechanism has not been proven and reports of toxic effect have been troublingly inconsistent. Methodology: This review collects references from 2012-2025 detailing the extent of ecological impact and human health effects ascribed to fludioxonil. An effort was made to focus on points of similarity to shed light on potential mechanisms. Results: It is found that prior observations of toxic effect may be explicated by an elicitation of oxidative stress. We illustrate here that a primary breakdown product of fludioxonil includes a maleimide moiety, a chemical structure capable of irreversibly binding biological thiols like glutathione (GSH). This is relevant because damaging this key component of cellular anti-oxidant defense is known to be causal for increased oxidative stress. Conclusions: A mechanism of toxicity based on GSH depletion is consistent with previously unexplained toxicity issues ascribed to this fungicide, emphasizing the potential threat to both agriculture-adjacent aquatic biomes (from fish to phytoplankton) and human health.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.