ArticleEnvironment & health (Washington, D.C.)2025
Long-Term Maternal Exposure to Triclosan Provokes Pulmonary Fibrosis in Mouse Offspring.
Article in Environment & health (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Phenolic Endocrine-Disrupting Chemical Exposure and Systemic Biomarker Variability in Patients with Lung Cancer.Medicina (Kaunas, Lithuania) · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triclosan (TCS) is a broad-spectrum antibacterial agent that is widely used as an additive in personal care products. Due to its extensive application, TCS has been frequently detected in human samples, posing potential health risks. To investigate the adverse effects on offspring following maternal exposure to TCS, 4-week-old female mice were exposed to TCS via daily gavage until the end of lactation. The results showed that the birth weight, 21-day survival rate, and skeletal length of offspring were all significantly reduced. Morphological examinations revealed distinct inflammatory infiltrations in the liver, kidney, and spleen of the F1 mice. However, the lungs exhibited abnormal alveolar cells, interstitial hyperplasia, and thickened vascular walls. Further investigations uncovered fibrosis, collagen deposition, fibroblast proliferation, and myofibroblast augmentation in the lungs of the mouse offspring. The enhancement of apoptosis, necroptosis, and pyroptosis in the lungs indicated the involvement of PANoptosis in pulmonary injury. RNA sequencing analysis predicted that the Hedgehog and PI3K-Akt signaling pathways might be the potential toxicological mechanisms underlying maternal TCS exposure-induced pulmonary damage in mouse offspring. This study highlights the toxic effects of TCS on offspring and provides special insights into the health risks associated with TCS exposure.
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