Abstract
Background/Aim: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in children. Emerging evidence from animal models suggests that mercury (Hg) might exert hepatotoxic effects. However, human evidence is scarce. We aimed to evaluate the association between prenatal Hg exposure and serum biomarkers of liver injury in childhood and examine the hypothesis that inflammation might play a role in this association. Methods: The study included 872 mothers and their children (mean [SD] age: 7.8 [1.3] years) from six European population-based birth cohorts, as part of Human Early-Life Exposome (HELIX) project. Hg levels were assessed in maternal whole blood. We measured alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma‐glutamyltransferase (GGT) levels in child serum. We also assessed eight inflammatory cytokines and adipokines previously linked to liver injury (TNF-α, IFN-γ, IL-1β, IL-6, IL-8, IL-12, IP-10 and leptin) in child plasma.Results: Median (IQR) maternal Hg concentration was 2.0 (1.1-3.6) μg/L. Eighty-five mothers (9.8%) had high Hg concentration (above the value that corresponds to the current U.S. EPA reference level, 5.8 μg/L). Mean (SD) levels of ALT, AST, and GGT in children were 15.7 (6.4), 31.2 (9.1) and 12.5 (3.5) U/L, respectively. Seventy-two children (8.3%) had elevated ALT based on clinical cutoffs for liver injury (≥22.1 U/L for females and ≥25.8 U/L for males). High maternal Hg concentration was associated with 10.4% increase in ALT (95% CI: 1.9%-19.7%) and a 2-fold increase in the risk for elevated ALT (OR 2.0, 95% CI: 1.0-3.9). Using a novel latent variable analysis, we identified a cluster of children at risk for current liver injury (OR 5.3, 95% CI: 2.7-9.7) that was characterized by high maternal Hg exposure and increased plasma levels of TNF-α, IL-1β, IL-6 and IL-8.Conclusions: Prenatal exposure to mercury may be a risk factor for pediatric liver injury and NAFLD development.
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