Identifying Environmental Factors Associated with Significant Fibrosis in Metabolic Dysfunction-Associated Steatotic Liver Disease/Steatohepatitis.

Abstract

Background and aim: The role of specific environmental and socioeconomic factors associated with significant liver fibrosis in a diverse, multi-ethnic population is underexplored. We leveraged the Mount Sinai Metabolic dysfunction-associated steatotic liver disease/steatohepatitis (MASLD/MASH) Center of Excellence Longitudinal Registry and publicly available data to explore this association.

Methods: Four hundred sixty-three New York City residents (aged 5-90) who were enrolled in the Mount Sinai MASLD/MASH Center of Excellence Longitudinal Registry were stratified for fibrosis stages using Vibration-controlled transient elastography (F0/1: < 8 kPa, F2: 8-10 kPa, F3: 10-14, F4: > 14 kPa). Using both univariable and multivariable logistic regression analyses, the association was evaluated between health disparities/environmental factors as defined by NYC.gov data (income, air quality, high school graduation rate, and access to parks and education per community district tabulation area) and significant fibrosis (kPa > 8).

Results: Of the 422 adult and 41 pediatric eligible patients, 38% had significant fibrosis (kPa > 8), with the highest mean liver stiffness score found in Staten Island (15.8 kPa) and the lowest in Manhattan (8.9 kPa). The intersection of air pollution and obesity was evident in patients with a BMI over 30 kg/m² living in high-air-pollution areas (> 7 PM_2.5), having nearly double the odds of significant fibrosis (OR 1.85, 95% CI (1.11, 3.09)). No association between lower income and increased fibrosis was observed. Among non-Hispanics, education access was linked to significantly lower odds of fibrosis (OR 0.96, 95% CI (0.927, 1.00)). In adults, alcohol (AUDIT-C score) was associated with lower risk of significant fibrosis (OR 0.75, 95% CI (0.61, 0.92)).

Conclusion: Understanding the interaction of health disparities, environmental risk factors, and liver fibrosis in MASLD informs both mechanistic translational studies as well as targeted population screening strategies.