Carbonaceous fraction in PM2.5 of six Latin American cities: Seasonal variations, sources and secondary organic carbon contribution.

Latin American (LatAm) cities are grappling with elevated levels of gaseous and particulate pollutants, which are having detrimental effects on both the local ecosystem and human health. Of particular concern are aerosols with smaller diameters (lower or equal to 2.5 µm, PM2.5), known for their ability to penetrate deep into the respiratory system. While measurements in the region are increasing, they remain limited. This study addresses this gap by presenting the results of a comprehensive, year-long PM2.5 monitoring campaign conducted in six LatAm cities: Buenos Aires, São Paulo, Medellín, San José, Quito and Ciudad de México. Despite all six monitoring sites being urban, they exhibited significant variations in PM2.5 levels, as well as in the content and seasonal behavior of elemental carbon (EC) and organic carbon (OC). Estimations of secondary organic carbon (SOC) using the EC-tracer method revealed a notable SOC relevance across all cities: secondary organic aerosols (SOA) accounted in average for between 19 % to 48 % of the total carbonaceous matter. Source attribution, conducted through the Positive Matrix Factorization (PMF) model, highlights substantial contributions from gasoline and diesel traffic emissions (29 % to 49 % of total carbon, TC), regional biomass burning (21 % to 27 %), and SOA (20 % to 38 %) in all cities, with similar chemical signatures. Additionally, industrial emissions were significant in two cities (Medellín and San José), while two others experienced minor impacts from construction machinery at nearby sites (Buenos Aires and Quito). This comparative analysis underscores the importance of considering not only the thermal optical EC/OC fractions as tracers of sources but also the OC/EC ratio of the PMF factors. This dual approach not only adds depth to the research but also suggests varied methodologies for addressing this crucial environmental concern. This study lays the groundwork for future investigations into the factors influencing the content and seasonality of SOA in the region.

Urban PM2.5 induces ROS generation and RBC damage in COPD patients.

Particulate matters (PM) produce adverse effects on the respiratory system and cause COPD. These effects are thought to involve intrinsic generation of ROS which are present in ambient PM (transition metals and aromatic organic compounds). Here, we examined the chemical composition and ultra-microscopic structure of PM2.5. The effect of this PM was studied in red blood cell (RBC) membranes (ghosts) from healthy volunteers (n = 11) and COPD patients (n = 43). These effects were compared with that produced by a Fenton metal-catalytic ROS generator. Oxidative biomarkers and cell damage were singificantly increased in presence of PM2.5 or ROS generator in RBC of COPD patients as compared with those in cells from healthy volunteers. In contrast, total SH groups, band 3 phospho-tyrosine phosphatase (PTPase) and glucose-6 phosphate dehydrogenase (G6PD) activities were all diminished in cells from COPD patients. In conclusion, PM2.5 increases damage to RBCs from COPD patients, decreases the activity of PTPase and G6PD, and alters the function of the anionic exchanger (AE1) and the antioxidant response by decreasing SH groups.

Airborne particulate matter PM2.5 from Mexico City affects the generation of reactive oxygen species by blood neutrophils from asthmatics: an in vitro approach.

BACKGROUND: The Mexico City Metropolitan Area is densely populated, and toxic air pollutants are generated and concentrated at a higher rate because of its geographic characteristics. It is well known that exposure to particulate matter, especially to fine and ultra-fine particles, enhances the risk of cardio-respiratory diseases, especially in populations susceptible to oxidative stress. The aim of this study was to evaluate the effect of fine particles on the respiratory burst of circulating neutrophils from asthmatic patients living in Mexico City. METHODS: In total, 6 subjects diagnosed with mild asthma and 11 healthy volunteers were asked to participate. Neutrophils were isolated from peripheral venous blood and incubated with fine particles, and the generation of reactive oxygen species was recorded by chemiluminescence. We also measured plasma lipoperoxidation susceptibility and plasma myeloperoxidase and paraoxonase activities by spectrophotometry. RESULTS: Asthmatic patients showed significantly lower plasma paraoxonase activity, higher susceptibility to plasma lipoperoxidation and an increase in myeloperoxidase activity that differed significantly from the control group. In the presence of fine particles, neutrophils from asthmatic patients showed an increased tendency to generate reactive oxygen species after stimulation with fine particles (PM2.5). CONCLUSION: These findings suggest that asthmatic patients have higher oxidation of plasmatic lipids due to reduced antioxidant defense. Furthermore, fine particles tended to increase the respiratory burst of blood human neutrophils from the asthmatic group.On the whole, increased myeloperoxidase activity and susceptibility to lipoperoxidation with a concomitant decrease in paraoxonase activity in asthmatic patients could favor lung infection and hence disrupt the control of asthmatic crises.