Background: Growing evidence suggest that ethylene oxide (EO) may have deleterious effects on health conditions, but the relationship between EO and adulthood nonalcoholic fatty liver disease (NAFLD) remains vague. Our objective is to evaluate whether EO exposure would influence the risk of NAFLD in a nationally cross-sectional study.
Method: In this cross-sectional study, We analyzed 2709 participants from the National Health and Nutrition Examination Survey (NHANES) 2015-2018. Blood concentrations of EO were measured using high-performance liquid chromatography coupled with tandem mass spectrometry.
Results: Hepatic steatosis index (HSI) were applied to define NAFLD. General linear and logistic regression models were adopted to investigate the relationship of Hemoglobin adducts of EO (HbEO) exposure with inflammation, HSI and NAFLD, respectively. Mediation analysis was adopted to further test the effect of inflammatory markers on the association between EO levels and NAFLD risk. General linear regression models showed that increased quartiles of HbEO were positively associated with hs-CRP (high-sensitivity C-reactive protein) (β: 0.113, 95% CI: 0.068-0.157), WBC (white blood cell) (β: 0.458, 95% CI: 0.358-0.559), Neutrophil (β: 0.295, 95% CI: 0.228-0.362), Lymphocyte (β: 0.128, 95% CI: 0.069-0.187), and HSI (β: 0.122, 95% CI: 0.017-0.228), after adjustment for age, gender, race/ethnicity, education, income, smoking status, drinking status, BMI, CVD, hypertension, diabetes, and TC. In logistic regression models, HbEO in the highest quartile was associated with the increased risk of NAFLD than those in the lowest quartile (OR: 2.23, 95% CI: 1.43-3.48, P-trend = 0.01). In addition, The mediation analysis manifested that the inflammatory markers partially mediated the HbEO-NAFLD associations (hs-CRP: 6.5%, WBC: 8.7%, and Neutrophil: 9.6%).
Conclusions: The significant association between EO and NAFLD among US adults, and the underlying mechanisms were required to be identify in the future study.