title: The surface reactivity and implied toxicity of ash produced from sugarcane burning.
abstract: Sugarcane combustion generates fine-grained particulate that has the potential to be a respiratory health hazard because of its grain size and composition. In particular, conversion of amorphous silica to crystalline forms during burning may provide a source of toxic particles. In this study, we investigate and evaluate the toxicity of sugarcane ash and bagasse ash formed from commercial sugarcane burning. Experiments to determine the main physicochemical properties of the particles, known to modulate biological responses, were combined with cellular toxicity assays to gain insight into the potential reactions that could occur at the particle-lung interface following inhalation. The specific surface area of the particles ranged from ∼16 to 90 m(2) g(-1) . The samples did not generate hydroxyl- or carbon-centered radicals in cell-free tests. However, all samples were able to 'scavenge' an external source of hydroxyl radicals, which may be indicative of defects on the particle surfaces that may interfere with cellular processes. The bioavailable iron on the particle surfaces was low (2-3 μmol m(-2) ), indicating a low propensity for iron-catalyzed radical generation. The sample surfaces were all hydrophilic and slightly acidic, which may be due to the presence of oxygenated (functional) groups. The ability to cause oxidative stress and membrane rupture in red blood cells (hemolysis) was found to be low, indicating that the samples are not toxic by the mechanisms tested. Cytotoxicity of sugarcane ash was observed, by measuring lactate dehydrogenase release, after incubation of relatively high concentrations of ash with murine alveolar macrophage cells. All samples induced nitrogen oxide release (although only at very high concentrations) and reactive oxygen species generation (although the bagasse samples were less potent than the sugarcane ash). However, the samples induced significantly lower cytotoxic effects and nitrogen oxide generation when compared with the positive control.
authors.affiliation: Department of Geography, University of Cambridge, Downing Place, Cambridge CB2 3EN, United Kingdom; Department of Mineralogy, Natural History Museum, Cromwell Road, London SW7 5BD, United Kingdom.
authors.forename: Jennifer S
authors.initials: JS
authors.lastname: Le Blond
authors.forename: Maura
authors.initials: M
authors.lastname: Tomatis
authors.forename: Claire J
authors.initials: CJ
authors.lastname: Horwell
authors.forename: Christina
authors.initials: C
authors.lastname: Dunster
authors.forename: Fiona
authors.initials: F
authors.lastname: Murphy
authors.forename: Ingrid
authors.initials: I
authors.lastname: Corazzari
authors.forename: Francesca
authors.initials: F
authors.lastname: Grendene
authors.forename: Francesco
authors.initials: F
authors.lastname: Turci
authors.forename: Elena
authors.initials: E
authors.lastname: Gazzano
authors.forename: Dario
authors.initials: D
authors.lastname: Ghigo
authors.forename: Ben J
authors.initials: BJ
authors.lastname: Williamson
authors.forename: Clive
authors.initials: C
authors.lastname: Oppenheimer
authors.forename: Bice
authors.initials: B
authors.lastname: Fubini
mesh_terms: D000818:Animals; D002244:Carbon / Q000737:chemistry; D002478:Cells, Cultured; D002482:Cellulose / Q000633:toxicity*; D003460:Crystallization; D004912:Erythrocytes / Q000187:drug effects*; D005390:Fires; D017665:Hydroxyl Radical / Q000737:chemistry; D007501:Iron / Q000737:chemistry; D016676:Macrophages, Alveolar / Q000187:drug effects*; D051379:Mice; D018384:Oxidative Stress; D010316:Particle Size; D031786:Saccharum / Q000633:toxicity*; D012822:Silicon Dioxide / Q000633:toxicity*
chemical_list: D017665:Hydroxyl Radical; D002244:Carbon; D012822:Silicon Dioxide; D002482:Cellulose; C027433:bagasse; D007501:Iron