Most of the studies on air pollution focus on emissions from fossil fuel burning in urban centers. However, approximately half of the world's population is exposed to air pollution caused by biomass burning emissions. In the Brazilian Amazon population, over 10 million people are directly exposed to high levels of pollutants resulting from deforestation and agricultural fires. This work is the first study to present an integrated view of the effects of inhalable particles present in emissions of biomass burning. Exposing human lung cells to particulate matter smaller than 10 µm (PM10), significantly increased the level of reactive oxygen species (ROS), inflammatory cytokines, autophagy, and DNA damage. Continued PM10 exposure activated apoptosis and necrosis. Interestingly, retene, a polycyclic aromatic hydrocarbon present in PM10, is a potential compound for the effects of PM10, causing DNA damage and cell death. The PM10 concentrations observed during Amazon biomass burning were sufficient to induce severe adverse effects in human lung cells. Our study provides new data that will help elucidate the mechanism of PM10-mediated lung cancer development. In addition, the results of this study support the establishment of new guidelines for human health protection in regions strongly impacted by biomass burning.

24The Brazilian Amazon represents about 40% of the world's remaining tropical rainforest. 25However, human activities have become important drivers of disturbance in that region. The 26 majority of forest fire hotspots in the Amazon arc due to deforestation are impacting the health 27 of the local population of over 10 million inhabitants. In this study we characterize western 28Amazonia biomass burning emissions through the quantification of 14 Polycyclic Aromatic 29Hydrocarbons (PAHs), Organic Carbon, Elemental Carbon and unique tracers of biomass 30 burning such as levoglucosan. From the PAHs dataset a toxic equivalence factor is calculated 31 estimating the carcinogenic and mutagenic potential of biomass burning emissions during the 32 studied period. Peak concentration of PM 10 during the dry seasons was observed to reach 60 33 µg.m -3 on the 24h average. Conversely, PM 10 was relatively constant throughout the wet season 34indicating an overall stable balance between aerosol sources and sinks within the filter sampling 35 resolution. Similar behavior is identified for OC and EC components. Levoglucosan was found 36 in significant concentrations (up to 4 µg. m -3 ) during the dry season. Correspondingly, the 37 estimated lung cancer risk calculated during the dry seasons largely exceeded the WHO health-38 based guideline. A source apportionment study was carried out through the use of Absolute 39Principal Factor Analysis (APFA), identifying a three-factor solution. The biomass burning 40 factor is found to be the dominating aerosol source, having 75.4% of PM 10 loading. The second 41 factor depicts an important contribution of several PAHs without a single source class and 42 therefore was considered as mixed sources factor, contributing to 6.3 % of PM 10 . The third factor 43 was mainly associated with fossil fuel combustion emissions, contributing to 18.4 % of PM 10 . 44This work enhances the knowledge of aerosol sources and its impact on climate variability and 45 local population, on a site representative of the deforestation which occupies a significant 46 fraction of the Amazon basin. 47

Particulate matter (PM) exposure is a leading global human health risk. In this study, water-soluble oxidative potential (OP) and intracellular reactive oxygen and nitrogen species (ROS/RNS) production were measured for open biomass burning aerosol collected from the Brazilian Amazon. Compared to ambient samples collected from Atlanta and laboratory-generated secondary organic aerosol (SOA), biomass burning aerosol had comparable OP and induced higher levels of ROS/RNS. Compared to regressed OP ranges for biomass burning factors resolved using source apportionment in prior studies, the samples investigated in this study spanned a wider OP range, suggesting that concentration addition may not be applicable for OP measurements. The discrepancy between ROS/RNS estimated using laboratory polycyclic aromatic hydrocarbons (PAHs) solution mixtures and ROS/RNS measured for the water-soluble hydrophobic fraction of Amazon filter samples further supports this conclusion. These results have important implications as many previous studies are based on linear regressions that assume concentration addition. Finally, a significant correlation was observed between ROS/RNS and levoglucosan concentrations although exposure to pure solutions of levoglucosan induced negligible ROS/RNS. These results demonstrate that levoglucosan may be considered as a predictor for ROS/RNS even though concentration addition may not be an applicable mixture effect model.

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Various environmental contaminants are known to impair the growth trajectories of major organs, indirectly (gestational exposure) or directly (postnatal exposure). Evidence associates pre-gestational and gestational exposure to air pollutants with adverse birth outcomes (e.g., low birth weight, prematurity) and with a wide range of diseases in childhood and later in life. In this review, we explore the way that pre-gestational and gestational exposure to air pollution affects lung development. We present results in topics underlining epidemiological and toxicological evidence. We also provide a summary of the biological mechanisms by which air pollution exposure possibly leads to adverse respiratory outcomes. We conclude that gestational and early life exposure to air pollutants are linked to alterations in lung development and function and to other negative respiratory conditions in childhood (wheezing, asthma) that may last into adulthood. Plausible mechanisms encompass changes in maternal physiology (e.g., hypoxia, oxidative stress and inflammation) and DNA alterations in the fetus. Evidence for pre-gestational and gestational effects on the lung is scarce compared with that on early life exposure and further studies are needed. However, the suggested mechanisms are credible and the evidence of pre-gestational and gestational air pollution exposure is robust for adverse birth outcomes. Air pollutants might change lung developmental trajectories of the unborn child predisposing it to diseases later in life highlighting the urgent need for controls on urban air pollution levels worldwide.

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The Sao Paulo Metropolitan Area is a unique case worldwide due to the extensive use of biofuel, particularly ethanol, by its large fleet of nearly 8 million cars. Based on source apportionment analysis of Organic Aerosols in downtown Sao Paulo, and using ethanol as tracer of passenger vehicles, we have identified primary emissions from light-duty-vehicles (LDV) and heavy-duty-vehicles (HDV), as well as secondary process component. Each of those factors mirror a relevant primary source or secondary process in this densely occupied area. Using those factors as predictors in a multiple linear regression analysis of a wide range of pollutants, we have quantified the role of primary LDV or HDV emissions, as well as atmospheric secondary processes, on air quality degradation. Results show a significant contribution of HDV emissions, despite contributing only about 5% of vehicles number in the region. The latter is responsible, for example, of 40% and 47% of benzene and black carbon atmospheric concentration, respectively. This work describes an innovative use of biofuel as a tracer of passenger vehicle emissions, allowing to better understand the role of vehicular sources on air quality degradation in one of most populated megacities worldwide.

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