Traffic-related air pollution associations with cytokeratin-18, a marker of hepatocellular apoptosis, in an overweight and obese paediatric population

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 (NO 2 ) 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 NO 2 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.