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Traffic-related air pollution associations with cytokeratin-18, a marker of hepatocellular apoptosis, in an overweight and obese paediatric population.
Hsieh, S; Leaderer, B P; Feldstein, A E; Santoro, N; McKay, L A; Caprio, S; McConnell, R.
Afiliación
  • Hsieh S; Division of Environmental Health, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • Leaderer BP; Department of Environmental Health Sciences, Center for Perinatal, Pediatric and Environmental Epidemiology, Yale School of Public Health, New Haven, CT, USA.
  • Feldstein AE; Division of Gastroenterology, Hepatology and Nutrition, University of California, San Diego, School of Medicine, La Jolla, CA, USA.
  • Santoro N; Department of Pediatrics, Yale School of Medicine, New Haven, CT, USA.
  • McKay LA; Department of Environmental Health Sciences, Center for Perinatal, Pediatric and Environmental Epidemiology, Yale School of Public Health, New Haven, CT, USA.
  • Caprio S; Department of Pediatrics, Yale School of Medicine, New Haven, CT, USA.
  • McConnell R; Division of Environmental Health, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Pediatr Obes ; 13(6): 342-347, 2018 06.
Article en En | MEDLINE | ID: mdl-28730729
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Contaminación del Aire / Queratina-18 / Obesidad Infantil / Enfermedad del Hígado Graso no Alcohólico / Contaminación por Tráfico Vehicular Tipo de estudio: Etiology_studies / Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Child / Female / Humans / Male Idioma: En Revista: Pediatr Obes Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Contaminación del Aire / Queratina-18 / Obesidad Infantil / Enfermedad del Hígado Graso no Alcohólico / Contaminación por Tráfico Vehicular Tipo de estudio: Etiology_studies / Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Child / Female / Humans / Male Idioma: En Revista: Pediatr Obes Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido