The Metropolitan Area of São Paulo has a unique composition of atmospheric pollutants, and positive correlations between exposure and the risk of diseases and mortality have been observed. Here we assessed the effects of ambient fine particulate matter (PM2.5) on genotoxic and global DNA methylation and hydroxymethylation changes, as well as the activities of antioxidant enzymes, in tissues of AJ mice exposed whole body to ambient air enriched in PM2.5, which was concentrated in a chamber near an avenue of intense traffic in São Paulo City, Brazil. Mice exposed to concentrated ambient PM2.5 (1 h daily, 3 months) were compared to in situ ambient air exposed mice as the study control. The concentrated PM2.5 exposed group presented increased levels of the oxidized nucleoside 8-oxo-7,8-dihydro-2′-deoxyguanosine in lung and kidney DNA and increased levels of the etheno adducts 1,N6-etheno-2′-deoxyadenosine and 1,N2-etheno-2′-deoxyguanosine in kidney and liver DNA, respectively. Apart from the genotoxic effects, the exposure to PM2.5 led to decreased levels of the epigenetic mark 5-hydroxymethylcytosine (5-hmC) in lung and liver DNA. Changes in lung, liver, and erythrocyte antioxidant enzyme activities were also observed. Decreased glutathione reductase and increased superoxide dismutase (SOD) activities were observed in the lungs, while the liver presented increased glutathione S-transferase and decreased SOD activities. An increase in SOD activity was also observed in erythrocytes. These changes are consistent with the induction of local and systemic oxidative stress. Mice exposed daily to PM2.5 at a concentration that mimics 24-h exposure to the mean concentration found in ambient air presented, after 3 months, increased levels of DNA lesions related to the occurrence of oxidative stress in the lungs, liver, and kidney, in parallel to decreased global levels of 5-hmC in lung and liver DNA. Genetic and epigenetic alterations induced by pollutants may affect the genes committed to cell cycle control, apoptosis, and cell differentiation, increasing the chance of cancer development, which merits further investigation.

For the first time, cobalt ferrite spinel (CoFe₂O₄) was used as a catalyst in the Fenton process for Remazol Red RR dye degradation in water. CoFe₂O₄ was synthesized via gel combustion using tris(hydroxymethyl)aminomethane as an alternative fuel in one step with a ratio of Ψ = 0.8. Its structural, surface optics, magnetic properties, and the optimal conditions of the Fenton reagents for dye degradation were evaluated. The saturation magnetization and remanence (Ms and Mr, respectively) for the as-prepared powder were 65.7 emu/g and 30.4 emu/g, respectively, and the coercivity (Hc) was 1243 Oe, indicating its ferromagnetic nature and suitability as a magnetic catalyst. Red Remazol RR dye degradation tests were performed using the Fenton process to evaluate the influence of the catalyst dosage and H₂O₂ concentration. The tests were performed in a batch reactor in the dark with constant agitation for 24 h. The best result was obtained using 1 g/L of catalyst with a dye degradation of 80.6%. The optimal concentration of H₂O₂ (1.0 M) resulted in 96.5% dye degradation. Nanoparticle recyclability testing indicated that the material could be satisfactorily reused as a catalyst for at least three cycles. The potential use of the CoFe₂O₄ synthesized in this study as a catalyst for dye degradation by the Fenton process was demonstrated.