Exposure to Per- and Polyfluoroalkyl Substances and Liver Cancer: A Systematic Review of Animal and Epidemiological Studies

Abstract

Background and Aims:

The global incidence and mortality rates of liver cancer are rising, necessitating research into environmental and lifestyle risk factors. Early-onset liver cancer, diagnosed before the age of 50, is becoming prevalent, suggesting the potential influence of emerging environmental exposures. Per- and polyfluoroalkyl substances (PFAS) are ubiquitous environmental contaminants that have been linked to liver toxicity in humans and shown to cause hepatotoxic effects in animals, but their role in liver cancer remains unclear. This systematic review synthesizes evidence from animal and epidemiological studies to evaluate associations between PFAS exposure and liver cancer risk.

Methods:

PubMed and Embase were searched through November 2025 for studies on PFAS and liver cancer. Data were independently extracted by two reviewers, and quality was assessed using the U.S. Environmental Protection Agency (EPA) guidelines.

Results:

Twenty-three studies (seven animal, sixteen human) met inclusion criteria. Most studies focused on legacy PFAS, primarily perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS). Animal studies demonstrated increased liver tumor incidence with high-dose PFAS exposure. Human epidemiological findings were mixed: three studies reported positive associations between PFAS and liver cancer, while others showed null associations.

Implications:

While animal studies strongly suggest hepatocarcinogenic effects of PFAS, epidemiological evidence remains inconsistent. Large, prospective studies with robust exposure assessment are needed to clarify these associations and inform public health policy.

Graphical Abstract

Introduction

Liver cancer is a major public health challenge and ranks among the leading causes of cancer-related deaths globally, with a 5-year survival rate of less than 20%.¹ In the United States, the incidence of liver cancer has more than tripled since 1980, while mortality rates have more than doubled.² Hepatocellular carcinoma (HCC), the most prevalent type of liver cancer, accounts for approximately 80% of all liver cancer cases³ and exhibits one of the fastest-growing incidence and mortality trends worldwide.⁴ The incidence of HCC has declined due to vaccination and antiviral therapies, however, cases related to metabolic dysfunction-associated steatotic liver disease (MASLD) are expected to increase and are projected to become the leading cause of HCC by 2030.⁵ Additionally, early-onset liver cancer is an emerging concern with increasing incidence among individuals aged 45 to 49, potentially driven by rising rates of metabolic disorders and other exogenous risk factors.⁶ Environmental exposures, including synthetic chemicals such as PFAS, are emerging as significant risk factors for liver toxicity,^7–15 but their specific role in liver carcinogenesis remains unclear.

PFAS are widely used in industrial applications and consumer products, including non-stick cookware, firefighting foams, and food packaging.^16,17 PFAS comprise of a large class of synthetic chemicals that are highly persistent in the environment leading to their accumulation in water, soil, wildlife, and human tissues. Biomonitoring studies reveal that over 98% of U.S. adults have detectable levels of PFAS in their blood, demonstrating the ubiquity of exposure.^18–20 Although PFAS compounds share resistance to degradation, individual chemicals differ in functional group, chain length, bioaccumulation, and possible toxicological effects. This diversity is important to consider when interpreting evidence on specific compounds.^21,22 Perfluoroalkyl acids (PFAAs) are a well-studied subgroup of PFAS that comprise of perfluoroalkyl carboxylic acids (PFCAs) and perfluoroalkyl sulfonic acids (PFSAs). These subgroups contain both short-chain and long-chain compounds. Long-chain PFAAs such as PFOA and PFOS are often referred to as legacy PFAS. Legacy PFAS refers to older long-chain compounds that have been largely phased out of production due to their potential to cause adverse health effects while emerging PFAS compounds are newer and mostly short-chain, proposed as alternatives to legacy PFAS. The length of the carbon backbone of these compounds determines their classification, long-chain PFAS are defined as PFSAs with 6 or more continuously linked carbon atoms in their molecular structure and PFCAs with 7 or more carbon atoms.²³ Short-chain PFAS compounds have less than 6 carbons for PFSAs and less than 7 carbons for PFCAs.²⁴ Long-chain PFAS are detected in almost all U.S. adults as they are slowly excreted from the body while short-chain PFAS are less commonly detected due to their rapid excretion.^21,22 However, not all short-chain PFAS exhibit rapid excretion, illustrating the complexity of these classification and the hazard the assuming that short-chain PFAS are always excreted rapidly. In the United States, manufacturers have phased out legacy long-chain PFAAs from production voluntarily following negotiations with federal authorities, whereas Europe has initiated formal measures to all PFAS compounds.^25,26 Further, PFOA and perfluorohexane sulfonic (PFHxS) are two legacy PFAS compounds listed under the Stockholm Convention for global elimination while PFOS was listed for restriction.²⁷ The International Agency for Research on Cancer (IARC) has classified PFOA as carcinogenic to humans (Group 1) based on sufficient animal and mechanistic evidence while PFOS has been classified as possibly carcinogenic to humans (Group 2B) based on strong mechanistic evidence.²⁸ As regulations on legacy PFAS have expanded, industries have shifted toward production and use of short-chain and emerging PFAS, many of which have not been characterized in terms of human health impacts. These newer emerging PFAS compounds are also of concern because they are highly persistent in the environment and have demonstrated biological activity, despite being categorized as safer alternatives to long-chain PFAS.²⁹

PFAS preferentially accumulate in the liver due to their strong protein-binding affinity and interaction with bile acid transport mechanisms.^30,31 This bioaccumulation underscores the liver as a primary target of PFAS toxicity. Animal studies have linked exposure of specific PFAS such as PFOA and PFOS with liver enlargement, hepatocellular hypertrophy, and liver tumors.^32–34 A comprehensive review on the risk assessment of PFAS mixtures report that exposure to PFAS in animal models results in necrosis, increased liver weight and other histopathological changes.³⁵ Epidemiological studies have linked PFAS exposure to MASLD in both adults^8,9,13,36,37 and children.^11,38,39 This association is supported by liver biopsy studies,^11,37,39 while a review of human and animal data showed a consistent association between PFAS exposure and biomarkers of liver injury, such as elevated alanine aminotransferase (ALT).⁷ However, the epidemiological evidence linking PFAS exposure to liver cancer remains limited and inconsistent.

Given PFAS’s preferential accumulation in the liver and their known hepatotoxic effects, their potential role in liver carcinogenesis warrants systematic investigation. This review consolidates current knowledge from animal and epidemiological studies aiming to address gaps and guide future research on the relationship between PFAS exposure and liver cancer.

Materials and Methods

Protocol and Registration

This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines.⁴⁰ The protocol is accessible on the USC Center for Translational Exposomics Research website. ⁴¹

Search Strategy

We performed a comprehensive literature search of PubMed and Embase databases for human and animal studies up to November 2025. The following keywords were inputted in the search engines: (“liver” OR “Hepatocellular”) AND (“cancer” OR “malignancy” OR “neoplasia” or “hepatic” OR “carcinogen” OR “carcinogenic” OR “carcinogenicity” OR “tumor”) AND (“PFAS” OR “perfluoroalkyl substances” OR “polyfluoroalkyl substances” OR “per and polyfluoroalkyl substances” OR “per- and polyfluoroalkyl substances” OR perfluorinated OR polyfluorinated OR perfluoro* OR polyfluoro* OR PFAS* OR “perfluorobutanoic acid” OR “perfluorobutanoate” OR “PFBA” OR “perfluorobutane sulfonic acid” OR “perfluorobutanesulfonate” OR “PFBS” OR “perfluorodecanoic acid” OR “perfluorodecanoate” OR “PFDA” OR “perfluorododecanoic acid” OR “PFDoA” OR “perfluorodecane sulfonic acid” OR “perfluorodecane sulfonate” OR “PFDS” OR “perfluoroheptanoic acid” OR “perfluoroenanthic acid” OR “PFHpA” OR “perfluorohexanoic acid” OR “perfluorocaproic acid” OR “PFHxA” OR “perfluorohexylphosphonic acid” OR “PFHxPA” OR “perfluorohexane sulfonic acid” OR “perfluorohexanesulfonate” OR “PFHxS” OR “perfluorononanoic acid” OR “PFNA” OR “perfluorooctanoic acid” OR “PFOA” OR “perfluorooctane sulfonic acid” OR “PFOS” OR “Perfluorooctanoate” OR “perfluorooctanesulfonate” OR “perfluorooctane sulfonamide” OR “PFOSA” OR “perfluoropentanoic acid” OR “PFPeA” OR “perfluoroundecanoic acid” OR “PFUnDA” OR “GenX” OR “HFPO-DA” OR “Hexafluoropropylene Oxide Dimer Acid” OR “HFPO-DoDA” OR “HFPO-TA”).

Our search strategy includes PFAS compounds both widely studied in human biomonitoring programs (e.g. CDC National Biomonitoring Program),⁴² and emerging compounds that have growing toxicological data (e.g., PFHxA and GenX). For each compound, we incorporated commonly used synonyms and alternative chemical names to ensure comprehensive identification of relevant studies.

Eligibility criteria

The citations of all studies identified by the search were downloaded and imported into Covidence systematic review software with duplicate studies between the two databases being automatically removed.⁴³ Eligible studies met the following inclusion criteria: 1) original observational or experimental research studies published in English, excluding abstracts, reviews, meta-analyses, or commentaries; 2) conducted in humans or non-human animal species; 3) reported data on liver cancer; and 4) assessed associations of liver cancer with PFAS exposure. Titles, abstracts, and full texts were screened independently by two reviewers (R.T. and E.B.), with any discrepancies resolved by a third reviewer (L.C.). Non-relevant studies were excluded. Eligible studies underwent a full-text review and were evaluated using the same inclusion criteria.

Data Extraction

Two independent reviewers (R.T. and E.B.) extracted the following data from each included study: study design, sample size, population characteristics including geographic location, PFAS types, exposure and outcome assessment methods, statistical analysis approach, covariates adjusted for and effect estimates with 95% confidence intervals including odds ratios (ORs) and hazard ratios (HRs) (for human studies). For animal studies, they extracted information on species, exposure duration, dose, and outcomes were collected. Discrepancies in data extraction were resolved through discussion with a third reviewer (L.C.).

Quality Assessment

Study quality was evaluated using the U.S. Environmental Protection Agency’s Integrated Risk Information System (IRIS) Handbook.⁴⁴ Two reviewers (R.T. and E.B.) independently evaluated each study, with any discrepancies resolved through discussion. Human studies were evaluated for the following domains: exposure measurement, outcome ascertainment, participant selection, confounding, analysis, selective reporting, and sensitivity. Animal studies were evaluated for: reporting quality, allocation, observational bias/blinding, confounding, selective reporting and attrition, chemical administration and characterization, exposure information (timing, frequency, and duration), endpoint sensitivity and specificity, and results presentation.

As described in the IRIS Handbook, each domain for each study received a rating [good, adequate, deficient (or “not reported”), or critically deficient].

Data Synthesis and Visualization

The current review was unable to directly pool estimates into a meta-analysis due to the heterogenous methodologies for measuring PFAS exposure and liver cancer outcomes. Instead, we synthesized data qualitatively, summarizing study characteristics and findings in narrative and tabular formats. Where possible, forest plots were used to illustrate the range of effect estimates and confidence intervals reported by individual studies. When possible, we additionally assessed potential evidence of a dose-response relationship. When multiple results were reported in a single study, including assessment of relationships by quartile or exposure group, we extracted and visualized all findings. The raw data from included studies were not available for re-expression of results. Figures were created using R Studio Version 4.4.

Results

Study Characteristics and quality

Our search identified 1,498 studies for evaluation after removal of duplicates. After screening titles and abstracts, 1,439 studies were excluded for failing to meet inclusion criteria (e.g., were conference abstracts; lack of relevance to PFAS or liver cancer). The remaining 59 studies were eligible for full-text review, with 23 studies ultimately meeting the inclusion criteria (7 animal studies and 16 human observational studies; Figure 1). Details regarding the studies included and their findings are presented in Tables 1 and 2.

Figure 1.

Inclusion flow chart for 1,498 studies identified by the search strategy.

Table 1.

Summary of the Animal Studies Examining PFAS and Liver Cancer

Study	Country	Species	Exposure	Concentrations	Primary Findings	Limitations
Benninghoff, 2012b	USA	Mount Shasta rainbow trout	Dietary PFOS, PFOA, PFNA, PFDA, and 8:2FtOH	PFOS: 100 ppm (~2.5 mg/kg/day) PFOA: 2000 ppm (~50 mg/kg/day) PFNA: 1000 ppm (~25 mg/kg/day)a PFDA: 200 ppm (~5 mg/kg/day)a 8:2FtOH: 2000 ppm	•↑ Liver tumor incidence in PFDA group •↑ Liver tumor multiplicity and size in PFOA, PFNA, and PFDA groups •↑ Liver cancer rate in PFOS group • No changes in liver tumor incidence, burden or size after dietary exposure to 8:2FtOH	• Did not provide information on blinding • Failed to control for confounding factors
Butenhoff, 2012	USA	Male and Female, Crl:CD®(SD) IGS BR rats	Dietary PFOS	PFOS: 0, 0.5, 2,5, and 20 ppm	•↑ Hepatocellular Adenoma in males •↑ Hepatocellular Adenoma and Hepatocellular Carcinoma in females	• Did not provide information on blinding
Butenhoff, 2012	USA	Male and Female, Crl:CD®(SD) IGS BR rats	Dietary PFOA	PFOA: 0, 30 (low), 300 (high) ppm	• There were no incidences of Hepatocellular Adenomas in male or female rats. • For male rats, incidences of Hepatocellular Carcinomas were 6% in the control group (0 ppm), 2% in the low treatment group (30 ppm), and 10% in the high treatment group (300 ppm). • For female rats, incidences of Hepatocellular Carcinoma were 0% for both control and low treatment group and 2% incidence in the high treatment group.	• Only two dose levels were investigated • Did not provide information on blinding
Biegel, 2001	USA	Male Crl:CD®(SD) IGS BR rats	Dietary PFOA	PFOA: 0, 300 ppm	•↑ Incidence of Hepatocellular Adenoma. • There was no observation Hepatocellular Carcinoma.	• Did not provide information on blinding • Only male rats were included in the experiment
Caverly-Rae, 2015	USA	Male and Female, Crl:CD®(SD)	Oral gavage of deionized water with GenX	GenX (male rats): 0, 0.1, 1, or 50 mg GenX (female rats): 0, 1, 50, or 500 mg	•↑ Hepatocellular Adenoma and Carcinoma in the 500 mg treatment female rats group • Incidences of hepatocellular tumors were similar across all male rats treatment group.	• Oral gavage as exposure route • High dosage levels • Did not provide information on blinding
Klaunig, 2015	USA	Male and Female, Crl:CD®(SD	Oral gavage of deionized water with PFHxA	PFHxA (male rats): 0, 2.5, 15, 100 mg PFHxA (female rats): 0, 5, 30, 200 mg	• No observation of liver tumor incidence among male and female rats.	• Oral gavage as exposure route • Did not provide information on blinding
Tilton, 2008b	USA	Mount Shasta rainbow trout	Dietary PFOA	PFOA: 200 ppm (5 mg/kg/or 1,800 ppm (50 mg/kg/day)	•↑ Liver tumor multiplicity and incidence in the 1,800 ppm group	• Did not provide information on blinding • Failed to control for confounding factors

Note: PFOA, perfluorooctanoic acid; PFOS: perfluorooctane sulfonate; PFDA: perfluorodecanoic acid; PFNA: perfluorononanoic acid

^aPFNA and PFDA doses began at 2000 ppm but were reduced due to unexpected number of mortalities early in the study period

^bIn rainbow trout studies, chemical initiators (e.g. Aflatoxin B₁) were administered prior to PFAS exposure

Table 2.

Summary of the Human Studies Examining PFAS and Liver Cancer

Study Type	Study	Country	N (Liver cancer cases/deaths)	Exposure	Concentrations	Primary Findings	Limitations
Biomonitoring studies	Cao, 2022	China	406 (203)	PFOS, PFOA, PFNA, PFDA*	Mean (median), ng/mL Controls PFOS: 8.3 (5.5); PFOA: 7.3 (5.4); PFNA: 0.41 (0.32); PFDA: 0.14 (0.11) Cases PFOS: 11.0 (7.2); PFOA: 9.3 (6.6); PFNA: 0.49 (0.35); PFDA: 0.37 (0.26)	•↑ Liver cancer per increase of log-PFOA (OR = 1.036, 95% CI = 1.002–1.070) •↑ Liver cancer per increase of log-PFOS (OR = 2.609, 95% CI = 1.179–4.029)	• Used hospital-based controls • Did not describe which variables were selected as confounders in adjusted analyses
	Dai, 2024	China	227 (197)	PFOS, PFOA, PFNA, PFDA*	Mean (median), ng/mL PFOS: 8.906 (4.825) PFOA: 4.024 (1.638) PFNA: 0.839 (0.626) PFDA: 0.478 (0.350)	• HCC patients had higher total serum PFAS than non-HCC patients • No effect estimates were reported	• Comparison (non-HCC) group had other liver diseases • Performed Mann-Whitney U tests for differences as opposed to adjusted regression models
	Eriksen, 2009	Denmark	2012 (67)	PFOS, PFOA	Median (5–95 percentiles) ng/mL Controls PFOS: 34.3 (16.2–61.8) PFOA: 6.6 (3.0–13.0) Cases PFOS: 31.0 (15.8–62.9); PFOA: 5.4 (2.5–13.7)	• No association between PFOA or PFOS and liver cancer	• No limitations
	Goodrich, 2022	USA	100 (50)	PFOS, PFOA, PFNA, PFDA*	Geometric mean (Geometric SD), µg/L Controls PFOS: 29.1 (1.95); PFOA: 4.78 (1.89); PFNA: 0.827 (1.85) PFDA: 0.278 (2.84) Cases PFOS: 29.2 (2.37); PFOA: 4.21 (2.13); PFNA: 0.844 (2.05); PFDA: 0.27 (2.98)	•↑ Liver cancer in high PFOS group (> 54.9 µg/L) compared to low PFOS group • No association with other PFAS and liver cancer	• No limitations
	Moon, 2024	USA	53,885 (below 10)	PFOA, PFOS, PFHxS, PFNA	Not reported	• No association with PFAS and liver cancer risk.	• Self-reported cancer history. • Small number of liver cancer cases (n=<10). • Cross-sectional study design
	Watling, 2025	USA	1,706 (853)	PFOA, PFOS, PFHxS	Not reported	• Overall PFAS concentrations were not association with liver cancer risk. • When stratified by sex, PFOA concentrations was associated with an increase in liver cancer risk among males (OR per 90th percentile vs. 10th percentile: 1.62, 95% CI: 1.07–2.45)	• No absolute values, only relative concentrations for PFAS.
Occupational or Highly Exposed Populations	Alexander, 2003	USA	2,083 (2)	PFOS	Geometric mean (95% CI) in sub-samples, ppm Chemical plant (n=126) 0.9 (0.8–1.1) Film plant (n=60) 0.1 (0.0.1–0.1)	• No increase in liver cancer mortality when compared to the general Alabama population or when comparing high/low exposure groups to non-exposed group	• Estimated PFOS exposure for all participants based off small sample • Small number of liver cancer deaths (n=2) • Lacked information on potential confounding factors
	Alexander, 2024	USA	4,045 (3)	PFOS	Total PFOS-equivalent exposure for 72 job groups: 0.0001 to 1.3 mg/m3	• Liver cancer mortality is not associated with PFOS exposure among chemical manufacturing workers.	• Small number of liver cancer deaths (n=6) • Estimated PFOS exposure using job exposure matrix
	Barry, 2013	USA	32,254 (18)	PFOA	Median (range) in subsample, ng/mL Community (n=28,541) 24.2 (0.25–4,752) Dupont workers (n=1,881) 112.7 (0.25–22,412)	• No association between estimated cumulative PFOA exposure and liver cancer risk	• Small number of liver cancer cases (n=18) • Nature of “survivor cohort” may bias results, especially in fatal cancers • Estimated cumulative PFOA exposure based on subsample • Used self-reported cancer outcomes
	Girardi, 2019	Italy	3,165 (7)	PFOA	Geometric mean (range) in subsample, ng/mL PFOA: 4048 (19–91,900 ng/mL)	•↑ Liver cancer mortality risk in the chemical plant workers (highly exposed group) compared to non-exposed group (RR = 6.69, 95% CI: 1.71 – 26.2) •↑ Liver cancer mortality in the chemical plant workers compared to the general population (SMR = 2.32, 95% CI 1.11–4.87)	• Small number of liver cancer cases (n=7) • Estimated PFOA concentrations in the sample • Lacked information on potential confounding factors
	Leonard, 2008	USA	6,027 (8)	PFOA	Not reported	• There was no significant excess of liver cancer mortality compared with general population and reference worker population.	• Did not perform any exposure assessment or categorize workers based on their job history • Small number of liver cancer deaths (n=8)
	Li, 2021	Sweden	60,507 (24)	PFOS, PFHxS, PFOA	Geometric mean (range) in subcohort, ng/mL Ronneby “never-high” PFOS: 40 (0.58, 839) PFHxS: 30 (0.14, 974) PFOA: 3.5 (0.04, 49) Ronneby “ever-high” PFOS: 199 (0.68, 1868) PFHxS: 176 (0.23, 1658) PFOA: 11 (0.04, 92) Ronneby “early-high” PFOS: 48 (4.5, 505) PFHxS: 43 (1.6, 508) PFOA: 3.6 (0.5, 39) Ronneby “late-high” PFOS: 239 (0.68, 1868) PFHxS: 210 (0.23, 1658) PFOA: 13 (0.04, 92)	• No association between PFAS-contaminated water and liver cancer incidence	• Small number of liver cancer cases (n=24) • Estimated PFAS levels through drinking water data and • Lacked information on confounding factors
	Lundin, 2009	USA	3,993 (3)	PFOA	Median range of serum PFOA levels, μg/L Jobs with definite exposure: 2.6–5.2 Jobs with probable exposure: 0.3–1.5	• Exposure was not associated with liver cancer mortality.	• Estimated PFOA concentrations in a subsample of participants • Small number of liver cancer deaths (n=3)
	Raleigh, 2014	USA	9,027 (24)	PFOA	Estimated PFOA inhalation exposure range, mg/m3 Chemical workers 1×10−8 to 3×10−5 Reference group workers 1×10−9–1×10−7	• No association between estimated PFOA exposure and liver cancer incidence or mortality	• Used estimated PFOA inhalation as exposure • Small number of incident liver cancer cases (n=9) and deaths from liver cancer (n=15) • Lacked information on potential confounding factors
	Steenland, 2012	USA	5,791 (10)	PFOA	Median (range) in subsample, ng/mL 580 (160–2,880)	• No association between estimated PFOA exposure and liver cancer mortality	• Small number of liver cancer deaths (n=10) • Estimated PFOA concentrations for sample • Lacked information on potential confounding factors
	Viera, 2013	USA	25,107 (23)	PFOA	Median of estimated serum PFOA in each water district, μg/L Little Hocking, OH, 125; Lubeck, WV, 65.8; Tupper Plains, OH, 23.9; Belpre, OH, 18.7; Pomeroy, OH, 10.7; Mason, WV, 5.3	• No association between PFOA exposure and risk of liver cancer	• Small number of liver cancer cases in exposed community (n=23) • Used estimations of PFOA exposure

Note: OH, Ohio; PFOA, perfluorooctanoic acid; PFOS: perfluorooctane sulfonate; PFDA: perfluorodecanoic acid; PFNA: perfluorononanoic acid; WV, West Virginia; USA, United States of America

Study quality evaluation results using the IRIS Handbook are provided in Figure 2. For human studies, there were considerable variation in study rigor. Several studies demonstrated clear strengths relating to participant selection. There were common limitations also identified relating to exposure assessment and outcome ascertainment. One study additionally raised analytical concerns: differences in PFAS between the liver cancer and non-liver cancer groups were evaluated via unadjusted Mann Whitney U tests as opposed to regression models adjusted for potential confounders.⁴⁵ The included animal studies had similar strengths in study rigor, however, a key limitation across animal studies was the lack of blinding in experimental procedures.

Figure 2.

Quality evaluation results for studies selected for inclusion in review.

Animal studies

Seven animal studies were identified from the search with five utilizing dietary exposure to PFAS and two utilizing oral gavage of deionized water. Two studies conducted experiments with Mount Shasta rainbow trout ^34,46 and five studies with Sprague Dawley rats.^33,47–50 One study on trout evaluated associations between liver cancer and PFOA (200 or 1,800 ppm),⁴⁶ while the other included PFOA (2000 ppm), PFOS (100 ppm), PFDA (200 ppm), and PFNA (200 ppm).³⁴ These studies examined tumor incidence and multiplicity between exposure groups following a chemical initiator. The compound 8:2 fluorotelomer alcohol (8:2 FtOH) was also examined in one rainbow trout study but reported negative results.³⁴ Only one study on Sprague Dawley rats evaluated associations between dietary PFOS exposure (dietary exposure: 0, 0.5, 2,5, or 20 ppm) and liver cancer.³³ This study examined rates of liver cancer between exposure groups and additionally explored incidence of hepatocellular adenoma.³³ Two rat studies evaluated dietary PFOA exposure at different doses (30 and 300 ppm),^47,48 and the remaining two studies investigated short-chain PFAS (PFHxA and GenX) administered by oral gavage at a range of dose levels specific to each study.^49,50

Three animal studies demonstrated a dose-dependent increase in liver tumor incidence (Table 1).^33,34,46 Studies on Mount Shasta rainbow trout yielded similar findings. For instance, Benninghoff et al. reported a 13% increase in liver cancer following dietary PFOS exposure at 100 ppm over six months. This study also evaluated other PFAS types, demonstrating that PFOA, PFNA, and PFDA increased tumor incidence, multiplicity, and size compared to controls. Similarly, Tilton et al. found that rainbow trout exposed to 1,800 ppm PFOA exhibited significantly higher liver tumor incidence and multiplicity, further supporting a dose-response relationship. Liver carcinogenesis in trout was independent of peroxisome proliferation, and have been related to the strong correlation with estrogen signaling.⁴⁶ In Sprague Dawley rats, dietary exposure to PFOA studies at 30 and 300 ppm was associated with increased liver weight and elevated hepatic enzyme levels.^47,48 However, liver tumor results were inconsistent, Butenhoff et al. found a significant increase in hepatocellular adenoma incidence whereas Biegel et al. reported no hepatocellular adenomas for either male and female rats. For PFOS, 104 weeks of dietary exposure at 20 ppm significantly increased hepatocellular adenoma incidence in both males and females.³³ This same study additionally detected HCC in the female rats of the highest exposure group (20 ppm) but not in males with the same exposure. ³³ In short-chain PFAS studies, PFHxA exposure at any dose level did not produce liver tumors,⁵⁰ while exposure to GenX at 500 mg/kg was associated with hepatocellular adenoma and HCC.⁴⁹

Across species, the findings for PFOA exposure and liver cancer incidence are mixed. Dietary exposure to PFOA in Sprague Dawley rats did not increase incidence of hepatocellular adenoma or carcinoma but the rainbow trout studies reported a dose-dependent increase in liver tumor incidence (Table 1). Short-chain PFAS Results were consistent for PFOS in both species examined.

Human Epidemiological Studies

Overview

We identified 16 epidemiological studies investigating associations between PFAS exposure and liver cancer (Table 2). These studies utilized various methodologies, including case-control, retrospective cohort mortality, and cross-sectional designs, to explore potential links between PFAS exposure and liver cancer incidence or mortality. Overall, findings were mixed: three studies reported positive associations,^51–53 twelve studies reported null associations,^54–65 and one study did not provide regression model estimates for the association.⁴⁵ Most studies examined PFAS exposure in relation to multiple cancer types, with liver cancer as a secondary outcome.

PFOA and Liver Cancer in Highly Exposed Populations and Occupational Cohorts

Seven studies focused on populations with a wide range of PFOA exposure, including occupational cohorts and residents in contaminated areas or near manufacturing facilities.^{52,56,58,60,62–64} Exposure levels were estimated through various methods, such as subsample measurements,^52,63 residential history combined with job exposure matrices,⁵⁶ work history records,^60,62 and exposure modeling using community data.⁶⁴ PFOA plasma concentrations in these studies ranged widely, from 0.25 to 91,900 ng/mL in occupational settings;^52,56,63 while some studies reported inhalation exposures in mg/m³ or water district-specific median levels in μg/L.^62,64 All occupational studies reported low numbers for liver cancer cases and deaths, with 20 as the highest number of deaths,⁵² and 23 as the maximum number of cases.^52,64 While the majority of these studies focused on PFOA exposure, two studies evaluated associations between PFOS exposure and mortality in workers of perfluorooctanesulphonyl fluoride facilities^54,55 and another study examined associations between PFAS-contaminated drinking water and liver cancer incidence.⁵⁹ Alexander et al. randomly selected a subsample of employees from the perfluorooctanesulphonyl fluoride facility and a film plant (non-exposed group) to provide serum samples for PFOS measurement.⁵⁴ The film plant employees had lower PFOS levels [geometric mean (GM): 0.1 ppm] compared to the perfluorooctanesulphonyl fluoride facility employees (GM: 0.9 ppm).⁵⁴ A second occupational cohort study measured PFOS exposure through time-weighted airborne exposure (TWA) and job-tasked-based exposure data matrix in employees of the Decatur facility.⁵⁵ The total PFOS-equivalent exposure for 72 job groups ranged from 0.0001 to 1.3 mg/m³ (Table 2).⁵⁵ Both occupational studies evaluating PFOS reported null associations.^54,55 In the Li et al. (2022) study, PFAS levels were estimated through drinking water data and validated with serum samples from a subcohort of participants in the Ronneby Registry Cohort.⁵⁹ PFAS levels in residents exposed to PFAS-contaminated drinking water were higher than levels in unexposed residents (Table 2).⁵⁹

Girardi et al. identified a significant positive association between PFOA exposure and liver cancer mortality.⁵² Workers at a PFOA manufacturing facility had an increase in liver cancer mortality compared to the general population (SMR: 2.32, 95% CI: 1.11, 4.87) and to unexposed group of metal workers (RR = 6.69, 95% CI: 1.71 – 26.2; Figure 3).⁵² In contrast, six other studies, Barry, Leonard, Lundin, Raleigh, Steenland, and Vieira, found no significant associations between PFOA exposure and liver cancer incidence or mortality (Figure 3; Table 2).^{56,58,60,62–64}

Figure 3. Effect sizes^a from studies on occupational/highly exposed populations estimating PFAS exposure and liver cancer risk of mortality.

^a Estimates represent hazard ratios (HR), odds ratios (OR), risk ratios (RR), and standardized mortality ratios (SMR). The forest plots represent estimates and 95% confidence intervals. The red dotted line at 1 denotes a null association, where values above it suggests increased risk.

^b Note: LC, liver cancer.

*Li (2021) study did not investigate individual PFAS types.

PFOS and Liver Cancer in General Population Biomonitoring Studies

Six studies investigated PFOS exposure and liver cancer risk in general populations, measuring PFAS levels in blood samples of all participants. PFOS plasma concentrations varied widely, with the lowest levels reported in Cao et al. study (median in controls: 8.3 ng/mL; median in cases: 11.0 ng/mL)⁵¹ and the highest in Goodrich et al study (median in controls 31.9 ng/mL; median in cases: 32.7 ng/mL; Figure S1).⁵³ Liver cancer case numbers ranged from 50 to 203 across these studies.^51,53 Two hospital-based case-control studies in China analyzed PFOS concentrations as continuous variables, while the other two studies examined dose-response relationships.^45,51 The remaining two studies utilized data from the National Health and Nutrition Examination Survey (NHANES) and twelve established prospective cohort studies, these studies did not report the distribution of PFAS exposure.^61,65

Two studies identified significant positive associations between PFOS blood concentrations and liver cancer in the general study population (Table 2; Figure 4).^51,53 Goodrich et al. evaluated 100 HCC cases and controls and found that individuals with PFOS levels above the 85th percentile (85th percentile: >54.9 μg/L) had 4.5 times higher odds of HCC compared to those with lower levels.⁵³ Cao et al. also found elevated odds of liver cancer with increasing PFOS levels, reporting a 2.6-fold increase in risk for each log-transformed unit increase in PFOS (OR = 2.61; 95% CI: 1.18–4.03, Figure 4; Table 2).⁵¹ In sex stratified analysis, Watling et al. observed an increased risk of liver cancer among males in the highest quartile of circulating PFOS concentrations.⁶⁵ Conversely, the studies conducted by Eriksen et al. and Moon et al. reported no association between exposure to PFOS and liver cancer incidence in the general U.S. and Danish populations.^57,61 Dai et al. found significantly higher serum PFOS levels in liver cancer cases compared to controls using Mann-Whitney U tests but did not perform regression modeling.⁴⁵

Figure 4. Effect sizes^a from human biomonitoring studies estimating PFAS exposure and liver cancer risk.

^a Estimates represent odds ratios (OR), and incidence rate ratios (IRR). The forest plots represent estimates and 95% confidence intervals. The red dotted line at 1 denotes a null association, where values above it suggests increased risk.

^b Note: LC, liver cancer; HCC, Hepatocellular Carcinoma

Watling et al. (2025) investigated two additional PFAS compounds, PFOA and PFHxS, in their study and observed no overall association between pre-diagnostic PFAS concentrations and liver cancer.⁶⁵ However, sex stratified analysis revealed circulating PFOA concentrations were positively associated with liver cancer risk among males (OR per 90^th percentile vs. 10^th percentile increase = 1.62, 95% CI: 1.07–2.45), whereas in females, PFOA concentrations were negatively associated (OR per 90^th percentile vs. 10^th percentile increase = 0.68, 95% CI: 0.50–0.92).⁶⁵

Dose-Response Analysis of PFAS Exposure and Liver Cancer

Dose-response relationships between PFAS exposure and liver cancer risk remain unclear (Figure S2). Among the studies that evaluated associations by exposure groups or quantiles, only Girardi et al. identified a significant increase in liver cancer mortality at the highest tertile of estimated PFOA exposure (>16,956 ng/mL-yrs; SMR: 3.94, 95% CI: 1.64–9.47).⁵² However, many studies likely lacked sufficient power to detect associations due to low case numbers. For example, Steenland et al. stratified their analysis into quartiles but had only 10 liver cancer deaths across all groups, limiting interpretability.⁶³ Similarly, Alexander et al. (2024) investigated associations between PFOS exposure and cancer mortality among exposed workers, however, only 6 liver cancer deaths reported across the four quartiles.⁵⁴ Overall, inconsistencies in dose-response findings underscore the need for larger studies with more robust exposure assessment and case ascertainment.

Discussion

This review provides a comprehensive synthesis of evidence from experimental and epidemiological studies on the association between PFAS exposure and liver cancer. Several animal studies have demonstrated dose-dependent increases in liver tumor incidence for specific PFAS types (e.g., PFOA, PFOS, PFNA, and PFDA), underscoring the hepatocarcinogenic potential of these compounds. Moreover, the identified human epidemiological studies presented mixed findings, with some reporting positive associations while others show null results. These inconsistencies emphasize challenges in translating experimental findings to human populations and reflect the complexities of exposure assessment, case ascertainment, and confounding factors.

Consistency and Gaps in Epidemiological Evidence

Epidemiological studies varied widely in design, exposure assessment, and population characteristics, contributing to inconsistent findings. Studies of occupational and highly exposed communities predominantly focused on PFOA and often relied on indirect exposure assessments, such as job exposure matrices or environmental data. While one study reported a significant association between PFOA exposure and liver cancer mortality,⁵² most studies found no associations. Hepatocellular carcinoma has around 21 percent five-year survival, with variations by stage, so cross-sectional studies have important limitations to identifying environmental etiologies.⁶⁶ Small numbers of liver cancer cases and limited statistical power likely contributed to these null findings.

In contrast, studies examining PFOS exposure in general populations provided more direct exposure measurements. Two biomonitoring studies identified significant associations between PFOS and liver cancer, particularly at higher exposure levels.^51,53 These findings suggest a potential role for PFOS in hepatocarcinogenesis. However, conflicting results across other studies highlight the need for standardized exposure methodologies and larger, more representative cohorts to confirm these associations.

Variability in PFAS Exposure Measurement

Methodological differences in measuring PFAS exposure may influence study results. Six of the sixteen epidemiological studies directly measured PFAS concentrations in participants’ blood,^{45,51,53,57,61,65} while the remaining studies estimated exposure levels using indirect methods. These indirect methods, such as public water PFAS concentrations or subsample extrapolations, often lack precision. For example, water-based exposure estimates may not accurately reflect individual-level exposures, as people may consume water from alternative sources. Similarly, using water-based and subsamples to infer PFAS levels for an entire cohort may lead to exposure misclassification. Furthermore, most studies relied on single-time-point measurements, which fail to capture cumulative exposure or changes in PFAS levels over time, adding another layer of uncertainty.

Variability in Study Designs

The heterogeneity in study designs among epidemiological research also poses challenges in synthesizing results. Retrospective cohort studies of high-exposure populations and occupational groups allow for stratification into high- and low-exposure categories but risk exposure misclassification. These cohorts may also be subject to the “healthy worker effect,” wherein workers are generally healthier than the broader population, potentially obscuring associations with liver cancer.⁶⁷

Case-control studies further complicate interpretation due to inconsistencies in control selection. For instance, some studies used hospital patients with other liver diseases or cancer diagnoses as controls,^45,51 which may lead to overestimated associations in the control group due to shared risk factors or exposures. Additionally, most cohort and case-control studies (except Goodrich et al. 2022 and Watling et al. 2025) measured PFAS levels post-diagnosis, raising concerns about reverse causality and limiting causal inference.

Variability in Outcome Ascertainment

Differences in how liver cancer outcomes were defined and recorded contribute to variability in findings. Most studies did not differentiate between liver cancer subtypes, which could obscure specific associations. One occupational cohort study⁵² combined liver cancer and cirrhosis mortality into a single outcome, complicating interpretation due to differing disease etiologies.⁶⁸ Additionally, studies relying on mortality data may underestimate liver cancer cases due to diagnostic delays or incomplete reporting, whereas incidence data, while more accurate, depend on the quality and completeness of cancer registries.⁶⁹

Variability in Sample Sizes

A major limitation of all studies included in this review is the small number of liver cancer cases. While studies of occupational and highly exposed populations included thousands of participants, the number of liver cancer cases and deaths were often small. In the Raleigh et al. (2014) study, the total number of participants included in the study was 9,027 but only 15 liver cancer deaths were identified.⁶² In the Barry et al. (2013) study, 32,254 participants were included and 18 liver cancer cases were identified.⁵⁶ Low numbers of cases or deaths for a specific cancer outcome can limit statistical power for detection of true associations.⁷⁰ The natural history of liver cancer may play a role. The low number of cases in such a large cross-sectional study may reflect survival bias for a cancer with high mortality.

Variability in Adjustment of Confounders

Confounders such as age, sex, smoking status, and race and ethnicity can influence both PFAS concentrations and liver cancer risk, yet their inclusion and adjustment in statistical models vary widely across studies. While some studies rigorously adjusted for key factors, other studies fail to include critical variables in their analysis, potentially leading to residual confounding or biased results.⁷¹

It may also be that diet and body composition will prove to be mediating factors for this outcome. MASLD is one of the underlying risk factors for hepatocellular carcinoma.⁷² Discussed in the introduction, exposure to PFAS may be a cause of MASLD. The susceptible population for MASLD is the obese. Associations of PFAS to adverse liver outcomes are more prominent in the obese, albeit also present less prominently in those of normal weight.^73–75 Considering these associations and risk factors may assist in the choice of future study designs. Case-control studies nested in large, longitudinally followed populations who already have MASLD or at high a priori risk of MASLD (and who have banded serum or plasma at enrollment) are a potential cost-effective approach to interrogating a role of PFAS.

Mechanistic Insights from Experimental Studies

While mechanistic and in-vitro studies were not included in the formal review, we summarize relevant evidence to provide biological context for potential mechanisms linking PFAS exposure with liver cancer. The International Agency for Research and Cancer (IARC) has classified PFOS as “possibly carcinogenic to humans” due to its ability to induce epigenetic alterations and immunosuppression in exposed humans.²⁸ Two animal studies identified in the present review suggest a potential link between PFOS exposure and liver cancer.^33,34 Dietary exposure to PFOS in rats showed increased liver tumor incidence, including HCA. Pathological findings from a rat study included hepatocellular hypertrophy, which alongside liver cancer, may indicate excessive activation of peroxisome proliferator-activated receptor alpha (PPARα).³³ This is consistent with findings of altered gene expression in mice following PFAS exposure, however such effects would likely be less pronounced in species with lower PPARα expression (i.e., humans).⁷⁶ The role of PPARα activation in PFAS hepatotoxicity has been an extensively studied mechanism, however, there is ongoing debate on the human relevance largely due to differences between species. In rodents, PFOA strongly activate PPARα while PFOS is considered a weak PPARα activator, suggesting that hepatotoxic effects of PFOS may involve alternative mechanisms.^77–79 Additionally, PFOA-induced liver toxicity involves both PPARα-dependent and independent mechanisms, underscoring the complexity of hepatic effects of PFOA exposure.^80–83 While PPARα activation is associated with hepatotoxic effects of PFAS, it may not fully account for carcinogenic effects in the liver and alternative mechanisms are involved. The importance of the PPARα discussion can be misunderstood and overgeneralized. Based on abundant human data, the significance of species differences in PPAR-α is fundamental to mechanisms and not to human liver toxicity outcomes, since adverse health effects of long-chain PFAS are repeatedly demonstrated in human liver biomarker and lipid biomarker studies.^84,85 Importantly, PFOS can also act through PPARα-independent pathways, as evidenced by PPARα-null mouse and trout models.^34,76 In these models, constitutive androstane receptor (CAR), estrogen receptor α (ERα), and PPAR gamma (PPARγ) appear to be potential contributors to carcinogenic outcomes. Beyond liver cancer, PFOS are capable of inducing more general liver toxicity.⁷ Chronic exposure to PFOS in rodents has consistently resulted in increased liver weight,^86–90 elevated ALT levels,^{33,86,89,91–95} and histological changes such as liver steatosis.^95–99 Mechanisms of toxicity implicated following PFOS exposure are wide-ranging and multifactorial, including dysregulation of lipid metabolism (largely through enhanced lipid uptake and inhibited mitochondrial beta oxidation),^{86,87,89,90,92,95,98} immunomodulation (such as inflammatory cytokine signaling and Kupffer cell activation),^{88–90,92,97,98} and oxidative stress (potentially via mitochondrial disruption).^89,97,98 Such mechanisms are not only harmful to liver health individually but also demonstrate high potential for crosstalk and mutual signal reinforcement, further enhancing the risk of injury and providing an ideal environment for the formation of liver cancer (Figure 5). The findings from these in vivo experiments provide further understanding into the hepatotoxic and potentially carcinogenic effects of PFOS, offering a foundation for exploring cellular and molecular mechanisms in in vitro studies.

Figure 5. Mechanisms of PFAS-induced hepatotoxicity.

General overview of potential mechanisms of toxicity in liver following PFAS exposure based upon reviewed literature. Arrows indicate directionality and suspected mechanistic interactions that may contribute to liver injury.

*Figure 5 was created on Biorender.com

In vitro studies offer valuable insights into potential mechanisms underlying PFAS-induced liver carcinogenesis.^100–102 PFOS has been shown to alter the expression of genes governing lipid metabolism (i.e., CD36) in rodents,^100,103 increasing lipid synthesis and uptake even as lipid export and oxidation are inhibited. Concurrently, PFOS can disrupt the electron transport chain,^100,104 releasing reactive oxygen species (ROS), further damaging mitochondria, impairing antioxidant defenses, and exacerbating lipid accumulation. Such ROS can damage DNA directly, as well as via the formation of toxic lipid peroxidation products (e.g., malondialdehyde and 4-hydroxynonenal).¹⁰⁵ PFOS has also been found to induce inflammatory signaling in human Hepatitis B virus-infected hepatocellular carcinoma cells (SNU449, HCCLM3, MHCC-97H, and Huh7) and hepatic cell line (HL-7702),^101,106 increasing NF-kB both through IkBα degradation and ROS signaling,¹⁰⁰ which can trigger apoptosis, additional oxidative damage, and promote HCC. Furthermore, there is evidence of PFOS manipulating cell cycle regulation, activating c-Myc^103,106and PI3K/AKT/mTOR pathways in both mouse models and human cell lines,^101,103 contributing to uncontrolled cellular proliferation. As with many of the mechanisms previously discussed, there is evidence of the same response across multiple PFAS compounds. In the rainbow trout study included in this review, Tilton et al. (2008) demonstrated PFOA can promote liver tumor development through pathways involving estrogenic genes. This significant finding indicates that hepatocarcinogenesis can occur through mechanisms independent of peroxisome proliferation, which has been a dominant focus in rodent studies.⁴⁶ Indeed, PFOA exposure results in increased PI3K/AKT/mTOR¹⁰² and c-Myc signaling, as well as the overexpression of tumor invasion indicators within rat liver cell lines (i.e., MMP-2 and MMP-9).¹⁰⁷ PFHxS demonstrated similar outcomes, increasing expression of cell cycle regulating proteins (e.g., Cyclin D1)^106–108 and proliferating cell nuclear antigen across rodent models and rat-derived cell lines. Taken together, these lines of evidence exhibit the high potential for hepatotoxicity and carcinogenicity that is consistent across many PFAS compounds and emphasize the importance of expanding our mechanistic understanding.

Review Limitations

Our formal search utilizing a predefined set of search terms may not have captured all relevant studies including those published in technical reports and studies of emerging PFAS. Additional publications may have been missed and future reviews should incorporate these studies to provide the most up to date synthesis of evidence. This systematic review was limited to peer-reviewed in vivo animal and human studies published in scientific journals. As our search strategy was restricted to peer-reviewed journal articles, we acknowledge that this may have resulted in the omission of certain government reports, such as the National Toxicology Program (NTP) study reports which undergo a formal peer-review process conducted by an expert panel. Meta-analyses were also excluded from our review; however, it is important to note that there have been previous reviews and meta-analyses on PFAS exposure and liver cancer. One previously published meta-analysis reported no significant association between PFAS exposure and liver cancer and this discrepancy may reflect differences in inclusion criteria, exposure metrics and statistical methods.¹⁰⁹ Both the present findings and those from excluded meta-analyses underscores the complexity of this association and the need for future research using standardized PFAS measurement, consistent outcome definitions, and harmonized analytical approaches to clarify the relationship.

Gaps and Future Directions

Despite growing evidence linking PFAS exposure to liver toxicity, significant gaps remain in understanding their role in liver cancer development. Several methodological limitations complicate the interpretation of these findings, including exposure misclassification, small case numbers, and inconsistent adjustments for confounding variables. Differences in outcome ascertainment, such as reliance on mortality data or combining liver cancer with other conditions, further challenge the comparability of results across studies. Future research should prioritize standardized, comprehensive PFAS measurements, including pre-diagnostic biomonitoring samples, to improve comparability across studies. Case-control studies nested in already enrolled, high-risk populations may prove cost-effective. Expanding epidemiological research to include short-chain, emerging PFAS and PFAS mixtures is also crucial, as these compounds are increasingly prevalent in the environment and humans are concurrently exposed to multiple contaminants. Longitudinal cohort studies with baseline and follow-up PFAS measurements can establish temporal relationships and account for cumulative exposure. Additionally, future studies should include larger, more diverse populations to examine the interplay of genetic predispositions, environmental exposures, and lifestyle factors. Addressing these gaps will enhance our understanding of PFAS’ potential role in liver cancer and inform effective public health interventions.

Although the number of newly published studies remains limited, this review advances the field beyond prior reviews¹⁰⁹ by integrating evidence from both epidemiological and experimental animal studies to provide a more comprehensive assessment of PFAS-associated liver carcinogenesis. In addition to identifying a newly published human study, our review critically evaluates study quality, risk of bias, and methodological heterogeneity, factors that were not systematically addressed in the previous meta-analysis.¹⁰⁹ Importantly, we incorporate mechanistic evidence from toxicological studies that elucidate plausible biological pathways linking PFAS exposure to liver cancer. This integrative approach strengthens the interpretation of previous findings, emphasizing the need for continued research and rigorous risk assessment.

This review provides a comprehensive summary of the existing evidence on the association between PFAS exposure and liver cancer. Animal studies consistently indicate a dose-dependent increase in liver tumor incidence, reinforcing the potential hepatocarcinogenic effects of PFAS. However, findings from human epidemiological studies are inconsistent, with variability likely stemming from differences in study design, exposure measurement methodologies, and population characteristics. The most compelling epidemiological evidence links PFOS exposure to liver cancer at higher exposure levels, whereas the evidence for PFOA remains limited and largely null. Despite these uncertainties, the persistent nature of PFAS and their widespread environmental distribution underscore the necessity of regulatory measures to reduce exposure. Expanding our understanding of PFAS’ impact on liver cancer will enhance public health interventions but also broader strategies to understand and mitigate environmental health risks.

Supplementary Material

Supplementary Information

Figure S1. PFAS concentrations from human biomonitoring studies estimating PFAS exposure and liver cancer risk.

Figure S2: Effect sizes from epidemiological studies investigating dose-response relationships between PFAS exposure and liver cancer risk.

Synopsis:

Exposure to PFAS may increase risk of hepatocellular carcinoma

Abbreviations:

PFAS

Per- and polyfluoroalkyl substances

PFOA

Perfluorooctanoic Acid

PFOS

Perfluoroctanesulfonic Acid

HCC

Hepatocellular Carcinoma

PFAA

Perfluoroalkyl Acids

PFCA

Perfluoroalkyl carboxylic acid

PFSA

Perfluoroalkyl sulfonic acid

MASLD

Metabolic dysfunction-associated steatotic liver disease

ALT

Alanine aminotransferase

PFNA

Perfluorononanoic acid

PFDA

Perfluorodecanoic acid

HCA

Hepatocellular Adenoma