Talita Dias da Silva1, Viviani Barnabé2, Ana Laura Ricci-Vitor3, Vasileios Papapostolou4, Matias Tagle5, Andres Henriquez6, Joy Lawrence4, Stephen Ferguson4, J Mikhail Wolfson4, Petros Koutrakis4, Pedro Oyola5, Celso Ferreira7, Luiz Carlos de Abreu8, Carlos Bandeira de Mello Monteiro9, John J Godleski4. 1. Harvard T. H. Chan School of Public Health, Harvard University, Boston, MA, USA; Paulista School of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. Electronic address: ft.talitadias@gmail.com. 2. Harvard T. H. Chan School of Public Health, Harvard University, Boston, MA, USA; Medical School, University City of São Paulo, São Paulo, SP, Brazil. 3. Harvard T. H. Chan School of Public Health, Harvard University, Boston, MA, USA; Paulista School of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. 4. Harvard T. H. Chan School of Public Health, Harvard University, Boston, MA, USA. 5. Mario Molina Center for Strategic Studies in Energy and Environment, Santiago, Chile. 6. Oak Ridge Institute for Science and Education, Research Triangle Park, NC, United States. 7. Paulista School of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil. 8. School of Public Health, University of São Paulo, São Paulo, SP, Brazil. 9. School of Arts, Sciences and Humanities, University of São Paulo, São Paulo, SP, Brazil.
Abstract
BACKGROUND: Ethanol vehicles release exhaust gases that contribute to the formation of secondary organic aerosols (SOA). OBJECTIVE: To determine in vivo toxicity resulting from exposure to SOA derived from vehicles using different ethanol-gasoline blends (E0, E10, E22, E85W, E85S, E100). METHODS: Exhaust emissions from vehicles using ethanol blends were delivered to a photochemical chamber and reacted to produce SOA. The aerosol samples were collected on filters, extracted, and dispersed in an aqueous solutions and intratracheally instilled into Sprague Dawley rats in doses of 700 μg/0.2 ml. After 45 min and 4 h pulmonary and cardiac chemiluminescence (CL) was measured to estimate the amount of reactive oxygen species (ROS) produced in the lungs and heart. Inflammation was measured by differential cell count in bronchoalveolar lavages (BAL). RESULTS: Statistically and biologically significant differences in response to secondary particles from the different fuel formulations were detected. Compared to the control group, animals exposed to SOA from gasoline (E0) showed a significantly higher average CL in the lungs at 45 min. The highest CL averages in the heart were observed in the groups exposed to SOA from E10 and pure ethanol (E100) at 45 min. BAL of animals exposed to SOA from E0 and E85S had a significant increased number of macrophages at 45 min. BAL neutrophil count was increased in the groups exposed to E85S (45 min) and E0 (4 h). Animals exposed to E0 and E85W had increased BAL lymphocyte count compared to the control and the other exposed groups. DISCUSSION: Our results suggest that SOA generated by gasoline (E0), followed by ethanol blends E85S and E85W, substantially induce oxidative stress measured by ROS generation and pulmonary inflammation measured by the recruitment of white blood cells in BAL.
BACKGROUND:Ethanol vehicles release exhaust gases that contribute to the formation of secondary organic aerosols (SOA). OBJECTIVE: To determine in vivo toxicity resulting from exposure to SOA derived from vehicles using different ethanol-gasoline blends (E0, E10, E22, E85W, E85S, E100). METHODS: Exhaust emissions from vehicles using ethanol blends were delivered to a photochemical chamber and reacted to produce SOA. The aerosol samples were collected on filters, extracted, and dispersed in an aqueous solutions and intratracheally instilled into Sprague Dawley rats in doses of 700 μg/0.2 ml. After 45 min and 4 h pulmonary and cardiac chemiluminescence (CL) was measured to estimate the amount of reactive oxygen species (ROS) produced in the lungs and heart. Inflammation was measured by differential cell count in bronchoalveolar lavages (BAL). RESULTS: Statistically and biologically significant differences in response to secondary particles from the different fuel formulations were detected. Compared to the control group, animals exposed to SOA from gasoline (E0) showed a significantly higher average CL in the lungs at 45 min. The highest CL averages in the heart were observed in the groups exposed to SOA from E10 and pure ethanol (E100) at 45 min. BAL of animals exposed to SOA from E0 and E85S had a significant increased number of macrophages at 45 min. BAL neutrophil count was increased in the groups exposed to E85S (45 min) and E0 (4 h). Animals exposed to E0 and E85W had increased BAL lymphocyte count compared to the control and the other exposed groups. DISCUSSION: Our results suggest that SOA generated by gasoline (E0), followed by ethanol blends E85S and E85W, substantially induce oxidative stress measured by ROS generation and pulmonary inflammation measured by the recruitment of white blood cells in BAL.