Journal
PEDIATRIC OBESITY
Volume 13, Issue 6, Pages 342-347Publisher
WILEY
DOI: 10.1111/ijpo.12228
Keywords
Air pollution; CK-18; liver; NAFLD; traffic volume
Categories
Funding
- National Institutes of Health [1-F32ES024067, P01ES022845, R21ES024707, P01ES009581, P30ES007048]
- U.S. Environmental Protection Agency [RD083544101]
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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 nonalcoholic 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.
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