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Air pollution represents a considerable threat to health worldwide. The São Paulo Metropolitan area, in Brazil, has a unique composition of atmospheric pollutants with a population of nearly 20 million people and 9 million passenger cars. It is long known that exposure to particulate matter less than 2.5 µm (PM 2.5 ) can cause various health effects such as DNA damage. One of the most versatile defense mechanisms against the accumulation of DNA damage is the nucleotide excision repair (NER), which includes XPC protein. However, the mechanisms by which NER protects against adverse health effects related to air pollution are largely unknown. We hypothesized that reduction of XPC activity may contribute to inflammation response, oxidative stress and DNA damage after PM 2.5 exposure. To address these important questions, XPC knockout and wild type mice were exposed to PM 2.5 using the Harvard Ambient Particle concentrator. Results from one-single exposure have shown a significant increase in the levels of anti-ICAM, IL-1β, and TNF-α in the polluted group when compared to the filtered air group. Continued chronic PM 2.5 exposure increased levels of carbonylated proteins, especially in the lung of XPC mice, probably as a consequence of oxidative stress. As a response to DNA damage, XPC mice lungs exhibit increased γ-H2AX, followed by severe atypical hyperplasia. Emissions from vehicles are composed of hazardous substances, with polycyclic aromatic hydrocarbons (PAHs) and metals being most frequently cited as the major contributors to negative health impacts. This analysis showed that benzo[b]fluoranthene, 2-nitrofluorene and 9,10-anthraquinone were the most abundant PAHs and derivatives. Taken together, these findings demonstrate the participation of XPC protein, and NER pathway, in the protection of mice against the carcinogenic potential of air pollution. This implicates that DNA is damaged directly (forming adducts) or indirectly (Reactive Oxygen Species) by the various compounds detected in urban PM 2.5 ., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Colorimetric methods are still important for determining nitrate and nitrite. A critical step in the use of these methods to determine nitrate in low concentrations is the reaction time required to totally reduce nitrate to nitrite, i.e., 24h in the dark. This work involved a study of the influence of ultrasonic irradiation on the nitrate reduction reaction by hydrazine. Our findings indicated that ultrasonic irradiation, associated with copper(II) ion as a catalyst, increased the redox reaction rate, decreasing the reaction time to about 10min when the power of the ultrasonic irradiation was set in 14.0357W. The strong influence of the ultrasonic irradiation in the reduction reaction rates can be sustained by an excellent linear correlation (R(2)=0.9993) between the kinetic constants and ultrasonic powers. Nitrate conversion also increased from 68% to 98% at the latter conditions. It thus become clear that high intensity ultrasound is very beneficial for this reduction reaction to proceed in good yield and in short reaction time in comparison to its silent reaction.