ArticleEnvironment & health (Washington, D.C.)2024
Insights into Triclosan-Induced Endocrine Disruption: Evidence from the National Health and Nutrition Examination Survey and Zebrafish Models.
Article in Environment & health (Washington, D.C.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed.
- Mechanism of liver fibrosis induced by life-long triclosan exposure in offspring rats: an adverse outcome pathway framework validated by in vivo and in vitro experiments.Archives of toxicology · 2026Article
- Association Between Organophosphate Flame Retardant Exposure and Trouble Sleeping: Integrating Epidemiological Evidence with Mechanistic Insights.International journal of molecular sciences · 2026Article
- Long-Term Maternal Exposure to Triclosan Provokes Pulmonary Fibrosis in Mouse Offspring.Environment & health (Washington, D.C.) · 2025Article
- Nontargeted Toxicological/Chemical Analysis in Complex Mixtures for Risk Assessment and Key Driver Discovery.Environment & health (Washington, D.C.) · 2025Article
- Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triclosan (TCS) has garnered significant attention due to its widespread use and associated endocrine-disrupting effects. However, its impact on the neuroendocrine system and underlying mechanisms remain poorly understood. Here, we established correlations between TCS exposure and serum sex hormone levels in participants of the National Health and Nutrition Examination Survey (NHANES). Additionally, we investigated TCS's influence on the neuroendocrine system using adult zebrafish exposed to environmentally relevant concentrations of TCS (0.361-48.2 μg/L) for 21 days. Assessment of reproductive and neurotoxicity included histopathological examination and behavioral tests. Transcriptomics, proteomics analyses, and biochemical detection were employed to elucidate mechanisms underlying TCS-induced neuroendocrine disruption. Significant correlations were found between TCS exposure and estradiol, testosterone, and sex hormone-binding globulin levels in NHANES participants. In addition, TCS exposure inhibited ovary development and spermatogenesis in zebrafish. Transcriptomics and proteomics analysis revealed gender-specific key signaling and metabolism-related pathways implicated in TCS-induced reproductive toxicity. Moreover, TCS exposure induced nervous system impairment, as evidenced by histological changes and altered motor behavior, possibly associated with oxidative damage. Correlation analysis further highlighted the potential connection between endocrine system disruption and nervous system impairment following TCS exposure. Overall, this study provided evidence supporting TCS-induced endocrine disruption and offered insights into its underlying mechanisms.
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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.