Evidence map›Paper›PMID 30823334›Full record

ArticleEnvironmental pollution (Barking, Essex : 1987)2019

Environmental perfluoroalkyl acid exposures are associated with liver disease characterized by apoptosis and altered serum adipocytokines.

John Bassler, Alan Ducatman, Meenal Elliott, Sijin Wen, Banrida Wahlang, John Barnett, Matthew C Cave

Abstract read
In one paragraph

Article in Environmental pollution (Barking, Essex : 1987), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
13.2field-weighted citation impact, top 1% of its field
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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 204 citations in OpenAlex.

  1. Pooled it
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  18. Aloperin improves liver non-alcoholic steatohepatitisArchives of medical science : AMS · 2025
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35 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

John BasslerDepartment of Biostatistics, West Virginia University School of Public Health, Morgantown, WV, 26506, USA.
Alan DucatmanDepartment of Occupational and Environmental Health, West Virginia University School of Public Health, Morgantown, WV, 26506, USA.
Meenal ElliottDepartment of Microbiology, Immunology and Cell Biology, West Virginia University School of Medicine, Morgantown, WV, 26506, USA.
Sijin WenDepartment of Biostatistics, West Virginia University School of Public Health, Morgantown, WV, 26506, USA.
Banrida WahlangDivision of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Louisville School of Medicine, Louisville, KY, 40202, USA.
John BarnettDepartment of Microbiology, Immunology and Cell Biology, West Virginia University School of Medicine, Morgantown, WV, 26506, USA.
Matthew C CaveDivision of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Louisville School of Medicine, Louisville, KY, 40202, USA; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY, 40202, USA; Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, KY, 40202, USA. Electronic address: matt.cave@louisville.edu.
West Virginia University · USUniversity of Louisville · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Sally Lynn Hodder · 2012 to 2026
$81.0M
Role of oxidized linoleic acid metabolites in the pathogenesis of alcoholic liver diseaseP20GM113226 · NIGMS · UNIVERSITY OF LOUISVILLE · PI GHARE, SMITA S · 2016 to 2025
$24.1M
Superfund Training CoreP42ES023716 · NIEHS · UNIVERSITY OF LOUISVILLE · PI FORTNER, JOHN · 2017 to 2025
$18.1M
The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI SHIRISH S BARVE · 2016 to 2026
$17.9M
UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Environmental Liver DiseaseR35ES028373 · NIEHS · UNIVERSITY OF LOUISVILLE · PI CAVE, MATTHEW C · 2017 to 2024
$4.0M
NIAAA NIH HHS P50 AA024337NIEHS NIH HHS P42 ES023716NIEHS NIH HHS R35 ES028373NIEHS NIH HHS T32 ES011564NIGMS NIH HHS P20 GM113226NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

Exposures to perfluoroalkyl substances (PFAS) including perfluoroalkyl acids (PFAAs) are associated with increased liver enzymes in cohort studies including the C8 Health Study. In animal models, PFAAs disrupt hepatic lipid metabolism and induce apoptosis to cause nonalcoholic fatty liver disease (NAFLD). PFAAs are immunotoxic and inhibit pro-inflammatory cytokine release from stimulated leukocytes in vitro. This cross-sectional study tests the hypothesis that environmental PFAAs are associated with increased hepatocyte apoptosis and decreased pro-inflammatory cytokines in serum. Biomarkers previously associated with PFAS exposures and/or NAFLD were evaluated as secondary endpoints. Two hundred adult C8 Health Study participants were included. Measured serum biomarkers included: perfluorohexane sulfonate (PFHxS); perfluorooctanoic acid (PFOA); perfluorooctane sulfonate (PFOS); perfluorononanoic acid (PFNA); cytokeratin 18 M30 (CK18 M30, hepatocyte apoptosis); adipocytokines; insulin; and cleaved complement 3 (C3a). Confounder-adjusted linear regression models determined associations between PFAS and disease biomarkers with cut-offs determined by classification and regression tree analysis. CK18 M30 was positively associated with PFHxS (β = 0.889, p = 0.042); PFOA (β = 2.1, p = 0.005); and PFNA (β = 0.567, p = 0.03). Tumor necrosis factor α (TNFα) was inversely associated with PFHxS (β = -0.799, p = 0.001); PFOA (β = - 1.242, p = 0.001); and PFOS (β = -0.704, p < 0.001). Interleukin 8 was inversely associated with PFOS and PFNA. PFAAs were also associated with sexually dimorphic adipocytokine and C3a responses. Overall, PFAA exposures were associated with the novel combination of increased biomarkers of hepatocyte apoptosis and decreased serum TNFα. These data support previous findings from cohorts and experimental systems that PFAAs may cause liver injury while downregulated some aspects of the immune response. Further studies of PFAAs in NAFLD are warranted and should evaluate sex differences.

Indexed as

AdipokinesAdultAgedAnimalsApoptosisBiomarkersChemical and Drug Induced Liver InjuryCross-Sectional StudiesEnvironmental ExposureFemaleFluorocarbonsHumansLipid MetabolismMaleMiddle AgedAdipokinesBiomarkersFluorocarbonsCytokeratin 18Non-alcoholic fatty liver disease (NAFLD)Perfluoroalkyl acids (PFAAs)Perfluorooctanoic acid (PFOA)Tumor necrosis factor alpha (TNFα)

Identifiers

PMID30823334
PMCPMC6404528
OpenAlexW2910596005

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.