Involvement of per- and polyfluoroalkyl compounds in tumor development
Maija Pesonen1, Kirsi Vähäkangas2
1Faculty of Health Sciences, School of Pharmacy/Toxicology, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland. Maija.Pesonen@uef.fi.
Archives of Toxicology
|March 13, 2024
Summary
Per- and polyfluoroalkyl substances (PFAS) are persistent chemicals linked to tumors in animal studies. This review explores PFAS
Area of Science:
- Environmental Chemistry
- Toxicology
- Molecular Biology
Background:
- Per- and polyfluoroalkyl substances (PFAS) are widespread synthetic chemicals with high stability, found globally in the environment and human blood.
- Extensive use in industry and commerce leads to significant human and wildlife exposure, raising health concerns.
- PFAS exposure is linked to adverse effects on organs like the liver, kidney, and reproductive tissues, and has been associated with tumor development in rodents and humans.
Purpose of the Study:
- To review the involvement of PFAS compounds in tumor development.
- To focus on molecular pathways and mechanisms of PFAS-induced tumor formation.
- To examine tissues where PFAS exposure is associated with cancer, including liver, kidney, testicles, and breast.
Main Methods:
- Literature review of epidemiological and animal studies on PFAS and cancer.
- Analysis of molecular pathways and mechanisms underlying PFAS effects.
- Discussion of non-genotoxic mechanisms of PFAS carcinogenicity.
Main Results:
- PFAS exposure is associated with tumors in the liver, kidney, testicles, and breast.
- PFAS are not directly mutagenic, suggesting non-genotoxic mechanisms of action.
- The effects of PFAS are complex, influenced by concentration, structure, age, and sex.
Conclusions:
- PFAS exposure poses a risk for human health and wildlife, potentially contributing to cancer development.
- Understanding the molecular mechanisms of PFAS toxicity is crucial for risk assessment.
- Further research is needed to establish causal links and elucidate non-genotoxic pathways in tumor formation.
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