Traffic‐related air pollution associations with cytokeratin‐18, a marker of hepatocellular apoptosis, in an overweight and obese paediatric population. Issue 6 (20th July 2017) - Hsieh, S.
Summary: Introduction: Traffic‐related air pollution causes fatty liver, inflammation and fibrosis in animal models, but there have been few studies in humans. Objectives: To test the hypothesis that traffic‐related air pollution causes non‐alcoholic fatty liver disease (NAFLD) and increased markers for non‐alcoholic steatohepatitis (NASH); and that NAFLD increases liver susceptibility to increased NASH risk. Methods: Data collected prospectively from 74 overweight or obese children were obtained from the Yale Pediatric Obesity Clinic. Traffic‐related air pollution was characterized as vehicle traffic volume on major roads within a 1 km residential buffer, and as residential nitrogen dioxide (NO2 ) exposure. Outcomes were hepatic fat fraction (HFF) measured by magnetic resonance imaging, liver enzymes using standard assays and plasma cytokeratin‐18 (CK‐18) by immunosorbent assays. Results: Significant non‐linear relationships with air pollution and CK‐18 were found. Plasma CK‐18 at follow‐up increased from approximately 150 U/L to almost 200 U/L as residential traffic volume increased from 220 000 vehicle‐km to 330 000 vehicle‐km, after adjustment for baseline CK‐18, age and gender. Among patients with NAFLD at baseline, CK‐18 increased from 140 U/L to 200 U/L (a 1.5 standard deviation increase in CK‐18) as NO2 increased from 8 to 10 ppb. Conclusions: Traffic‐related air pollution was associated with CK‐18. Effects were larger in children with pre‐existing NAFLD at study entry.