Systemic chronic inflammation mediates the effect of per- and polyfluoroalkyl substances exposure on the risk of nonalcoholic fatty liver disease: A cross-sectional study among Chinese government employees.

BACKGROUND

A series of studies have revealed a correlation between per- and polyfluoroalkyl substances (PFAS) exposure and the increased risk of nonalcoholic fatty liver disease (NAFLD), yet the potential mechanism remains uncertain.

OBJECTIVE

This study aimed to examine the impact of exposure to PFAS on the risk of developing NAFLD among government employees in China and to investigate the potential mediating role of systemic inflammation.

METHODS

This study consisted of 2,191 individuals and the concentration of serum PFAS was determined by ultra-high-performance liquid chromatography-tandem mass spectrometry. Systemic inflammation was assessed by white blood cell count, platelet count, lymphocyte count, neutrophil-to-lymphocyte ratio, and systemic immune-inflammation index. Generalized linear models were used to ascertain the impact of PFAS exposure on the risk of NAFLD. Additionally, a mediation model was applied to determine whether systemic inflammation mediated the association between PFAS exposure and NAFLD risk.

RESULTS

The results indicated that concentrations of perfluorodecanoic acid (odds ratio [OR] = 1.025; 95% confidence interval [CI] = 1.004, 1.046) and perfluorooctane sulfonate (PFOS) (OR = 1.037; 95% CI = 1.014, 1.060) in serum were associated with increased NAFLD risk after adjusting the covariates. The mediation analysis indicated that the estimated 3.50% of the association between PFOS exposure and NAFLD risk was mediated by the systemic immune-inflammation index ( = 0.030), which was more prominent among subjects under the age of 40.

CONCLUSION

Exposure to perfluorodecanoic acid and PFOS may elevate the risk of NAFLD among Chinese government employees, with systemic inflammation serving as a potential mechanism.