The surface reactivity and implied toxicity of ash produced from sugarcane burning.

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.

Carbon in intimate contact with quartz reduces the biological activity of crystalline silica dusts.

To evaluate the effect of carbonaceous materials on the pathogenic activity of quartz dusts, mixtures of carbon soot (1 and 10%) and quartz (Min-U-Sil) were prepared and then milled so to attain an intimate association of carbon and the quartz surface. Both cellular and cell-free tests show that carbon associated to quartz completely inhibits the typical free radical generation of quartz dusts (through Fenton activity and homolytic cleavage of a C-H bond) and suppresses the oxidative stress and inflammation induced by quartz alone on MH-S murine macrophage cells (lipid peroxidation, nitric oxide release, and tumor necrosis factor-α synthesis). The cytotoxic response to quartz is also largely reduced. An extremely pure quartz milled with 10% of soot showed inactivating effects on the adverse reactions to quartz similar to Min-U-Sil quartz. None of these effects takes place when the same experiments are carried out with mechanically mixed samples, which suggests that carbon acts not just as a radical quencher but because of its association to the quartz surface.

Surface iron inhibits quartz-induced cytotoxic and inflammatory responses in alveolar macrophages.

The mechanism of enhancement/inhibition of quartz toxicity induced by iron is still unclear. Here the amount of iron on a fibrogenic quartz (Qz) was increased by wet impregnation (Fe(NO(3))(3) 0.67 and 6.7 wt %). X-ray diffraction (XRD), XRF diffuse reflectance, UV-vis, and infrared (IR) spectroscopies revealed dispersed ferric ions, and hematite aggregates at the higher loading. Surface features relevant to pathogenicity and cell responses were compared not only to the original quartz but also to reference quartz DQ12. Surface charge (ζ-potential) was more negative on the original and low-loaded specimen than on the high-loaded one. DQ12 had a less negative ζ-potential than Qz, ascribed to the absence of aluminium present in Qz (1.7 wt %). All quartz specimens were able to generate HO(•) radicals, iron-loaded samples being more reactive than original quartz. Iron deposition inhibited the rupture of a C-H bond. All quartzes were phagocytized by alveolar macrophages (AMΦ cell line NR8383) to the same extent, irrespective of their surface state. Conversely, iron loading increased AMΦ viability (evaluated by cytotoxicity and induction of apoptosis). Qz was found to be much less cytotoxic than DQ12. The induction of oxidative stress and inflammatory responses (evaluated by HO-1 mRNA expression and TNF-α mRNA and protein expression) revealed a reduction in inflammogenicity upon iron loading and a more inflammogenic potency of DQ12 ascribed to undissociated SiOH interacting via H-bonding with cell membrane components. The results suggest that besides aluminium also iron at the quartz surface may have an inhibitory effect on adverse health responses.