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Toward a mechanistic understanding of poly-and perfluoroalkylated substances and cancer

Boyd, Raya I., Ahmad, Saeed, Singh, Ratnakar, Fazal, Zeeshan, Prins, Gail S., Madak Erdogan, Zeynep, Irudayaraj, Joseph, Spinella, Michael J.·2022·Cancers
DOI 10.3390/cancers14122919PMC PMC9220899
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Abstract

Poly- and perfluoroalkylated substances (PFAS) are chemicals that persist and bioaccumulate in the environment and are found in nearly all human populations through several routes of exposure. Human occupational and community exposure to PFAS has been associated with several cancers, including cancers of the kidney, testis, prostate, and liver. While evidence suggests that PFAS are not directly mutagenic, many diverse mechanisms of carcinogenicity have been proposed. In this mini-review, we organize these mechanisms into three major proposed pathways of PFAS action—metabolism, endocrine disruption, and epigenetic perturbation—and discuss how these distinct but interdependent pathways may explain many of the proposed pro-carcinogenic effects of the PFAS class of environmental contaminants. Notably, each of the pathways is predicted to be highly sensitive to the dose and window of exposure which may, in part, explain the variable epidemiologic and experimental evidence linking PFAS and cancer. We highlight testicular and prostate cancer as models to validate this concept.

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Figure 1 Chemical structures of Poly- and perfluoroalkylated substances. Structures are based on 2D structures from PubChem accessed 5 June 2022 and assembled in Chem-space.com accessed 5 June 2022.
Figure 1 Chemical structures of Poly- and perfluoroalkylated substances. Structures are based on 2D structures from PubChem accessed 5 June 2022 and assembled in Chem-space.com accessed 5 June 2022.CC BY · PubMed Central
Figure 2 Proposed mechanisms of potential PFAS cancer promotion. PPAR-dependent and -independent reprogramming of metabolism, epigenetics, and endocrine disruption are represented as interconnecting, mutually reinforcing pathways of potential PFAS tumor promotion. The precise details of how PFAS influences these pathways are still uncertain, as is the impact of other proposed PFAS mechanisms, including immunosuppression and oxidative stress.
Figure 2 Proposed mechanisms of potential PFAS cancer promotion. PPAR-dependent and -independent reprogramming of metabolism, epigenetics, and endocrine disruption are represented as interconnecting, mutually reinforcing pathways of potential PFAS tumor promotion. The precise details of how PFAS influences these pathways are still uncertain, as is the impact of other proposed PFAS mechanisms, including immunosuppression and oxidative stress.CC BY · PubMed Central

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Metadata

Authors
Boyd, R. I., Ahmad, S., Singh, R., Fazal, Z., Prins, G. S., Madak Erdogan, Z., Irudayaraj, J., & Spinella, M. J.
Affiliations
  • Department of Comparative Biosciences, University of Illinois, Urbana-Champaign, Urbana, IL 61802, USA
  • Department of Bioengineering, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA
  • Departments of Urology, Pathology and Physiology, College of Medicine, Chicago Center for Health and Environment, University of Illinois Chicago, Chicago, IL 60612, USA
  • Department of Food Science and Human Nutrition, Division of Nutritional Sciences, University of Illinois Urbana-Champaign, Urbana, IL 61801, USA
ORCID
Venue
Cancers
Publisher
MDPI AG
Published
2022-06-14
Volume
14
Issue
12
Pages
2919
ISSN
2072-6694
DOI
10.3390/cancers14122919
PMC
PMC9220899
Cited by
110
References
20
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • NCI (R01CA211875, W81XWH2110903)
  • a DOD PRCRP Impact Award (R01CA211875, W81XWH2110903)

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