Evidence map›Paper›PMID 40128328›Full record

ArticleArchives of toxicology2025

New insights into the effects of PFOS exposure on rat lung development: morphological, functional, and single-cell sequencing analysis.

Jiali Mo, Jingye Zuo, Lin Yu, Huishan Zhang, Shuting Weng, Leping Ye

Abstract read
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Article in Archives of toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Jiali MoDepartment of Pediatric Pulmonology, Children's Medical Center, Peking University First Hospital, Beijing, 102627, China.
Jingye ZuoDepartment of Pediatric Pulmonology, Children's Medical Center, Peking University First Hospital, Beijing, 102627, China.
Lin YuDepartment of Pediatric Pulmonology, Children's Medical Center, Peking University First Hospital, Beijing, 102627, China.
Huishan ZhangDepartment of Pediatric Pulmonology, Children's Medical Center, Peking University First Hospital, Beijing, 102627, China.
Shuting WengDepartment of Pediatric Pulmonology, Children's Medical Center, Peking University First Hospital, Beijing, 102627, China.
Leping YeDepartment of Pediatric Pulmonology, Children's Medical Center, Peking University First Hospital, Beijing, 102627, China. yeleping@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-1319-5607

Funding

National High Level Hospital Clinical Research Funding 2023IR03National Natural Science Foundation of China 81971424National Natural Science Foundation of China 82371708
6 · The paper itself

Abstract

Perfluorooctane sulfonate (PFOS), a widely persistent environmental pollutant, has been demonstrated to disrupt lung development in animal models. However, its cellular and molecular mechanisms remain insufficiently understood. This study examines the effects of prenatal PFOS exposure on lung development and function in offspring rats. Pregnant rats were exposed to PFOS at concentrations relevant to both environmental and occupational exposures, with doses of 0, 0.01, 0.1, and 1 mg/kg/day from gestational day 11-20. We primarily evaluated morphological changes, pulmonary function, bronchoalveolar lavage fluid composition, and alterations in trace element and fatty acid metabolism at postnatal days 0, 4, 14, 21, and 60. Single-cell RNA sequencing was employed to profile cellular and molecular responses in the lungs. Our results show that PFOS exposure leads to dose-dependent reductions in alveolar development, increased pulmonary injury, fibrosis, and impaired lung function. PFOS also changes lung cell composition, particularly affecting structural and immune cells, and shifts immune responses from innate to adaptive immunity. Differential gene expression analyses revealed the upregulation of Fam111a and downregulation of Stk35, implicating these genes in PFOS-induced lung injury and repair processes. In addition, pathway analyses demonstrated suppression of immune-related signaling pathways and disruption of cell adhesion and phagocytosis, which may exacerbate lung tissue injury. These findings provide novel insights into the developmental toxicity of PFOS and highlight its potential long-term health risks.

Indexed as

Alkanesulfonic AcidsEnvironmental PollutantsFluorocarbonsLungPrenatal Exposure Delayed EffectsAnimalsBronchoalveolar Lavage FluidDose-Response Relationship, DrugFemaleMaleMaternal ExposurePregnancyRatsRats, Sprague-DawleySingle-Cell AnalysisAlkanesulfonic AcidsEnvironmental PollutantsFluorocarbonsperfluorooctane sulfonic acidImmune responseLung developmentPerfluorooctane sulfonatePrenatal exposureSingle-cell RNA sequencing

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Registered trials

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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.