Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2026
Chemical exposure and hepatic steatosis: How environmental factors impact liver health.
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Boullion Jolie A, Agrawal Akshat, Xing Diensn, Bhuiyan Md Shenuarin, Rom Oren, Conrad Steven A, Vanchiere John A, Orr A Wayne, Kevil Christopher G, Bhuiyan Mohammad Alfrad Nobel
Аннотация
BACKGROUND: Hepatic steatosis is increasingly prevalent in the U.S., alongside widespread exposure to per- and polyfluoroalkyl substances (PFAS), volatile organic compounds (VOCs), and heavy metals (HMs). While these toxins have individually been linked to hepatic steatosis, few studies assess their combined effects. This study evaluates the association between multi-toxin exposure and hepatic steatosis.
METHODS: NHANES 2017-2020 data were analyzed to identify participants with hepatic steatosis (FibroScan® CAP™ ≥238 dB/m). PFAS, VOCs, and HMs were measured in blood and urine. Hierarchical clustering generated four toxin-combination models, followed by logistic regression unadjusted and adjusted for confounders. Sensitivity analyses included bootstrap resampling and Firth logistic regression.
RESULTS: In Model 4, clusters 1 and 2 had the highest odds of hepatic steatosis (OR 8.62 and 9.37, p < 0.001 vs. cluster 3), with elevated PFAS (cluster 1) and PFAS plus HMs (cluster 2). Higher risk was associated with female sex, Mexican American and Non-Hispanic Asian ethnicity, and higher income. Sensitivity analyses were consistent.
CONCLUSION: Combined exposure to PFAS and HMs is linked to increased hepatic steatosis risk. Targeted public health interventions are needed to reduce these exposures.
METHODS: NHANES 2017-2020 data were analyzed to identify participants with hepatic steatosis (FibroScan® CAP™ ≥238 dB/m). PFAS, VOCs, and HMs were measured in blood and urine. Hierarchical clustering generated four toxin-combination models, followed by logistic regression unadjusted and adjusted for confounders. Sensitivity analyses included bootstrap resampling and Firth logistic regression.
RESULTS: In Model 4, clusters 1 and 2 had the highest odds of hepatic steatosis (OR 8.62 and 9.37, p < 0.001 vs. cluster 3), with elevated PFAS (cluster 1) and PFAS plus HMs (cluster 2). Higher risk was associated with female sex, Mexican American and Non-Hispanic Asian ethnicity, and higher income. Sensitivity analyses were consistent.
CONCLUSION: Combined exposure to PFAS and HMs is linked to increased hepatic steatosis risk. Targeted public health interventions are needed to reduce these exposures.