Abstract
The associations between air pollution exposure and nonalcoholic fatty liver disease (NAFLD) remain unclear. The present study included 313,102 individuals from the UK Biobank. Data on air pollution included PM2.5, PMcoarse, PM10, PM2.5absorbance, nitrogen dioxide (NO2), and nitrogen oxides (NOx). A weighted air pollution score (WAPS) was created using PM10 and NOx to evaluate the comprehensive exposure to the five air contaminants. Using Cox proportional hazard models and restricted cubic spline (RCS) models, the relationship between air pollution exposure and the developing NAFLD risk was examined. We also examined the mediating role of BMI. We found that the increased risk of NAFLD was positively correlated with PM2.5, PMcoarse, PM10, PM2.5absorbance, NO2, NOx, and WAPS (all P-trend <0.05). In comparison to individuals who were in the lowest quartile for air contaminants exposure, the HRs of NAFLD for those exposed to the highest quartile were: PM2.5: 1.33 (95 % CI: 1.22 to 1.45), PMcoarse: 1.12 (95 % CI: 1.03 to 1.22), PM10: 1.15 (95 % CI: 1.05 to 1.25), PM2.5 absorbance: 1.27 (95 % CI: 1.17 to 1.39), NO2: 1.38 (95 % CI:1.26 to 1.50), NOx: 1.33 (95 % CI:1.22 to 1.45), and WAPS: 1.32 (95 % CI:1.21 to 1.44). No correlation was found between WAPS and NAFLD risk in those who were normal weight, but it was strong in overweight and obese people. BMI (mediated proportion: 8.18 % for PM2.5; 2.89 % for PM2.5absorbance; 18.8 % for PMcoarse; 12.32 % for PM10; 4.09 % for NO2; 7.72 % for NOX; 8.44 % for WAPS) significantly mediated a portion of the link between air pollution exposure and NAFLD (all PIE < 0.05). Overall, air pollution exposure can increase the developing NAFLD risk, and BMI significantly modifies and mediates the connection. These findings served as mechanical evidence that air pollution contributes to NAFLD in epidemiological investigations.</p>