Two long-standing air quality challenges in the United States are the control of tropospheric ozone and particulate matter, both of which are responsible for widespread damage to human health and the environment. This thesis presents three modeling applications in support of policy development and regulatory actions for control of these pollutants in the eastern United States, taking advantage of recent advancements in sensitivity techniques in a regional Eulerian photochemical air quality model. A broad evaluation of regional atmospheric pollution and transboundary air quality management, including the international scale, and an analysis of successful transboundary management efforts are also presented. The first modeling application is an evaluation of local and interstate impacts on ozone and fine particulate matter (PM2.5) from ground-level and elevated nitrogen oxide plus nitrogen dioxide and from sulfur dioxide emissions from individual states. This analysis identifies states responsible for a significant amount of regional secondary pollution, and states which do not have independent control over much of their pollution concentrations. An average of approximately 77% of each state s ozone and PM2.5 concentrations that are sensitive to the emissions evaluated are found to be formed from emissions from other states. The second application is an assessment of impacts from emissions from a single power-plant on resulting regional ozone concentrations. Three sensitivity techniques and two 3D photochemical models are applied. Ozone increases greater than 0.5 ppbv are found over eight states downwind from the power-plant. The third application supports the extension of a body of research aimed at advancing understanding of the ozone formation potential, or reactivity , of VOCs for use in regional-scale, rather than urban-scale, regulations. Air quality impacts of VOCs emissions from solvent use and manufacture are presented, scientific barriers to accounting for reactivity in regulations are discussed, current and upcoming regulatory applications are described, and results from a regional scale evaluation of reactivity quantification are presented.

Engineering directly impacts current and future regulatory policy decisions. The foundation of air pollution control and air pollution dispersion modeling lies in the math, chemistry, and physics of the environment. Therefore, regulatory decision making must rely upon sound science and engineering as the core of appropriate policy making (objective analysis in lieu of subjective opinion). This research evaluated particulate matter and ammonia concentration data as well as two modeling methods, a backward Lagrangian stochastic model and a Gaussian plume dispersion model. This analysis assessed the uncertainty surrounding each sampling procedure in order to gain a better understanding of the uncertainty in the final emission rate calculation (a basis for federal regulation), and it assessed the differences between emission rates generated using two different dispersion models. First, this research evaluated the uncertainty encompassing the gravimetric sampling of particulate matter and the passive ammonia sampling technique at an animal feeding operation. Future research will be to further determine the wind velocity profile as well as determining the vertical temperature gradient during the modeling time period. This information will help quantify the uncertainty of the meteorological model inputs into the dispersion model, which will aid in understanding the propagated uncertainty in the dispersion modeling outputs. Next, an evaluation of the emission rates generated by both the Industrial Source Complex (Gaussian) model and the WindTrax (backward-Lagrangian stochastic) model revealed that the calculated emission concentrations from each model using the average emission rate generated by the model are extremely close in value. However, the average emission rates calculated by the models vary by a factor of 10. This is extremely troubling. In conclusion, current and future sources are regulated based on emission rate data from previous time periods. Emission factors are published for regulation of various sources, and these emission factors are derived based upon back-calculated model emission rates and site management practices. Thus, this factor of 10 ratio in the emission rates could prove troubling in terms of regulation if the model that the emission rate is back-calculated from is not used as the model to predict a future downwind pollutant concentration.

Particulate matters – affected air pollution and air pollution sources in the Northern part of Klaipeda are being analysed in the final work. The first part of the work focuses on the air pollution in Lithuania and worldwide, leteron methods and devices for measuring the concentration of the particulate matters in the air are being analysed. Earlier research works on this subject are being analysed together with various information sources. With the help of modern efficient air polution measurement devices, particulate matters – affected air pollution and air pollution causes in the Northern part of Klaipeda were examined. After collecting data on transport concentration in certain streets of the seaport, it was possible to do the modelling of segments of these streets. the resuls of the modelling are being compared with the results of the pre-existing research. The conclusions and recommendations of the final work are based on the analyses of the particulate matters – affected air pollution and itas spread in Klaipeda. the work consists of 8 parts; the Introduction, the Literature overview, the analyses of the air pollution estimation methods and devices, Particulate matters – affected air pollution analyses in Klaipeda city, the modelling of the particulate matters spread in the seaport, Conclusions, Suggestions and References. The volume of work is 119 p., excluding appendices, 56 illustrations, 17 Figures, 58 reference sources. Articles for publication and publications... [to full text]

Asthma is a chronic respiratory disease with a high prevalence in Western countries, including Canada, and increased exacerbations have been associated with ambient air pollution. The maintenance of airways tone is critically dependent on the endogenous bronchodilator, nitric oxide (NO). The nitric oxide synthase (NOS) isoenzymes produce NO from the amino acid, L-arginine, and competition for substrate with the arginase isoenzymes can limit NO production. Imbalances between these pathways have been implicated in the airways hyperresponsiveness (AHR) of asthma. The overall objective of this work was to determine whether arginase and downstream polyamine metabolites are functionally involved in airways responsiveness in animal models of asthma and the adverse responses of allergic animals to air pollution. To this purpose, the expression profiles of proteins involved in L-arginine metabolism were determined in lung tissues from human asthmatics and murine models of ovalbumin (OVA)-induced airways inflammation. Expression of arginase 1 was increased in human asthma and animal models. Competitive inhibition of arginase attenuated AHR in vivo. The roles of the downstream metabolites of arginase, the polyamines (putrescine, spermidine and spermine) were examined by administering them via inhalation to anaesthetized mice. It was demonstrated that spermine increases methacholine responsiveness in normal and allergic mice. Additionally, inhibition of polyamine synthesis improved AHR in a murine model. Thus, arginase and downstream polyamine metabolites contribute to AHR in asthma. Finally, the potential role of arginase in the exacerbation of asthma by air pollution was investigated. For this purpose, murine sub-acute and chronic murine models of allergic airways inflammation were employed, which exhibit inflammatory cell influx and remodeling/AHR, respectively, to determine the role of arginase in the response to concentrated ambient fine particles plus ozone. Allergic mice that were exposed to air pollution exhibited increased arginase activity and expression, compared to filtered air-exposed controls. Furthermore, inhibition of arginase attenuated the air pollution-induced AHR. Thus, the studies of the arginase pathway and downstream metabolites described in this thesis indicate that arginase inhibition may be a therapeutic target in asthma and may also protect susceptible populations against the adverse health effects of air pollution.

Asthma is a chronic respiratory disease with a high prevalence in Western countries, including Canada, and increased exacerbations have been associated with ambient air pollution. The maintenance of airways tone is critically dependent on the endogenous bronchodilator, nitric oxide (NO). The nitric oxide synthase (NOS) isoenzymes produce NO from the amino acid, L-arginine, and competition for substrate with the arginase isoenzymes can limit NO production. Imbalances between these pathways have been implicated in the airways hyperresponsiveness (AHR) of asthma. The overall objective of this work was to determine whether arginase and downstream polyamine metabolites are functionally involved in airways responsiveness in animal models of asthma and the adverse responses of allergic animals to air pollution. To this purpose, the expression profiles of proteins involved in L-arginine metabolism were determined in lung tissues from human asthmatics and murine models of ovalbumin (OVA)-induced airways inflammation. Expression of arginase 1 was increased in human asthma and animal models. Competitive inhibition of arginase attenuated AHR in vivo. The roles of the downstream metabolites of arginase, the polyamines (putrescine, spermidine and spermine) were examined by administering them via inhalation to anaesthetized mice. It was demonstrated that spermine increases methacholine responsiveness in normal and allergic mice. Additionally, inhibition of polyamine synthesis improved AHR in a murine model. Thus, arginase and downstream polyamine metabolites contribute to AHR in asthma. Finally, the potential role of arginase in the exacerbation of asthma by air pollution was investigated. For this purpose, murine sub-acute and chronic murine models of allergic airways inflammation were employed, which exhibit inflammatory cell influx and remodeling/AHR, respectively, to determine the role of arginase in the response to concentrated ambient fine particles plus ozone. Allergic mice that were exposed to air pollution exhibited increased arginase activity and expression, compared to filtered air-exposed controls. Furthermore, inhibition of arginase attenuated the air pollution-induced AHR. Thus, the studies of the arginase pathway and downstream metabolites described in this thesis indicate that arginase inhibition may be a therapeutic target in asthma and may also protect susceptible populations against the adverse health effects of air pollution.

The amount of organic carbon (OC) present in Siberian Arctic permafrost soils is estimated at twice the amount of carbon currently in the atmosphere. The shelf seas of the Arctic Ocean receive large amounts of this terrestrial OC from Eurasian Arctic rivers and from coastal erosion. Degradation of this land-derived material in the sea would result in the production of dissolved carbon dioxide and may then add to the atmospheric carbon dioxide reservoir. Observations from the Siberian Arctic suggest that transfer of carbon from land to the marine environment is accelerating. However, it is not clear how much of the transported OC is degraded and oxidized, nor how much is removed from the active carbon cycle by burial in marine sediment. Using bulk geochemical parameters, total OC, d13C and D14C isotope composition, and specific molecular markers of plant wax lipids and lignin phenols, the abundance and composition of OC was determined in both dissolved and particulate carrier phases: the colloidal OC (COC; part of the dissolved OC), particulate OC (POC), and sedimentary OC (SOC). Statistical modelling was used to quantify the relative contribution of OC sources to these phases. Terrestrial OC is derived from the seasonally thawing top layer of permafrost soil (topsoil OC) and frozen OC derived from beneath the active layer eroded at the coast, commonly identified as yedoma ice complex deposit OC (yedoma ICD-OC). These carbon pools are transported differently in the aquatic conduits. Topsoil OC was found in young DOC and POC, in the river water, and the shelf water column, suggesting long-distance transport of this fraction. The yedoma ICD-OC was found as old particulate OC that settles out rapidly to the underlying sediment and is laterally transported across the shelf, likely dispersed by bottom nepheloid layer transport or via ice rafting. These two modes of OC transport resulted in different degradation states of topsoil OC and yedoma ICD-OC. Terrestrial CuO oxidation derived biomarkers indicated a highly degraded component in the COC. In contrast, the terrestrial component of the SOC was much less degraded. In line with earlier suggestions the mineral component in yedoma ICD functions as weight and surface protection of the associated OC, which led to burial in the sediment, and limited OC degradation. The degradability of the terrestrial OC in shelf sediment was also addressed in direct incubation studies. Molecular markers indicate marine OC (from primary production) was more readily degraded than terrestrial OC. Degradation was also faster in sediment from the East Siberian Sea, where the marine contribution was higher compared to the Laptev Sea. Although terrestrial carbon in the sediment was degraded slower, the terrestrial component also contributed to carbon dioxide formation in the incubations of marine sediment. These results contribute to our understanding of the marine fate of land-derived OC from the Siberian Arctic. The mobilization of topsoil OC is expected to grow in magnitude with climate warming and associated active layer deepening. This translocated topsoil OC component was found to be highly degraded, which suggests degradation during transport and a possible contribution to atmospheric carbon dioxide. Similarly, the yedoma ICD-OC (and or old mineral soil carbon) may become a stronger source with accelerated warming, but slow degradation may limit its impact on active carbon cycling in the Siberian Shelf Seas. / <p>At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript.</p>

Degalinės yra vienas iš pavojingesnių aplinkos taršos šaltinių, nes jų aplinkoje į atmosferą išsiskiria įvairūs tiek aplinkai, tiek žmogaus sveikatai pavojingi teršalai. Šio tyrimo tikslas – nustatyti oro taršos lygį degalinės aplinkoje bei gretimose jos teritorijose, pasirinkus tipišką priemiesčio degalinę. Tyrime buvo nustatinėjamos azoto dioksido, sieros dioksido, benzeno, formaldehido, bei kietųjų dalelių koncentracijos aplinkos ore. Atlikus tyrimus nustatyta, kad didžiausios lakiųjų organinių junginių bei dujų koncentracijos yra degalinės operatoriaus darbo vietoje, kur azoto dioksido (2,03 ppm), benzeno (1,52 ppm) ir formaldehido (1,43 ppm) koncentracijos ore viršijo didžiausias leidžiamas koncentracijas darbo aplinkoje. Degalinėje, lauke visų tirtų lakiųjų organinių junginių ir dujų koncentracijos viršijo ribines vertes aplinkos ore. Taip pat nustatyta, kad už degalinės teritorijos teršalų koncentracija ore padidėja likus 100 m iki degalinės. Kietųjų dalelių tyrimai parodė, kad degalinės aplinkoje daugiausiai vyrauja 0,3 – 0,5 µm dydžio dalelės. Taip pat degalinės teritorijoje, lauke buvo viršyta didžiausia leidžiama kietųjų dalelių koncentracija aplinkos ore. / A petrol station is one of the most dangerous sources which are known to contribute greatly to the pollution of the environment due to normal pollutants they emit into atmosphere. The aim of the research is to assess the level of the pollution in the surroundings of a particular city petrol station as well as in the territory of the nearly by petrol stations. A research has been carried out to measure the amount of nitrogen dioxide, nitrogen monoxide, sulfur dioxide, benzene, formaldehyde and particulate matters concentrations in the air. After carrying out the research it was found out that the largest concentration of volatile organic compounds and gases was discovered in the working place of the operator of the petrol station where the concentrations of nitrogen dioxide (2,03 ppm), benzene (1,52 ppm) and formaldehyde (1,43 ppm) in the air exceeded all the limits allowed in working places. The concentration of gases and volatile organic compounds in the station and outside it exceeded the marginal value of in the air. Research also proved that the concentrations of pollutants increase in its amount 100 m around the petrol station. The test on particulate matters shoved that the prevailing size of the particulate matters was about 0,3 – 0,5 µm and their concentration highly exceeded the permitted amounts in the territory of the petrol station.

Background: The negative effects of air pollution on morbidity and mortality have been known since the mid 20th century. The two most well known examples are the Meuse Valley disaster in the 1930’ies and the London black fog in December 1952. Whilst there are numerous epidemiological studies, in which associations between morbidity and mortality and high levels of pollutants have been reported, the underlying mechanisms are not clear. Two of the main air pollutants are particulate matter (PM) mostly emanating from diesel exhaust (DE), and ozone, both of which are highly oxidative. Exposure to DE has resulted in adverse effects both in the respiratory tract and in the cardiovascular system. High ozone levels have also been shown to be associated with increased admissions to hospital for respiratory as well as cardiovascular conditions. The main aim of this thesis was to investigate the respiratory and cardiovascular effects of a combination of exposures to ozone and DE. DE generated during the urban part of the standardized European Transient Cycle (ETC) was compared to DE generated by an idling engine. It was also evaluated whether an acute exposure to ozone would have any effects on the cardiovascular system as assessed by venous occlusion forearm plethysmography and heart rate variability (HRV). In addition, fraction of exhaled nitric oxide (FENO) was evaluated as a potential marker for acute exposure to ozone or DE. Methods: Four double-blind randomized cross-over exposure studies were conducted to investigate the effects of ozone and DE on both the respiratory tract and the vascular function in healthy volunteers. All of the exposures were performed in purposely built “walk-in” chambers with strictly controlled exposures. In the first study, the volunteers were exposed to DE (300µg/m3) generated by an idling engine or to air, for one hour in the morning and to ozone (200 ppb) for two hours in the afternoon. A bronchoscopy with bronchial wash (BW) and bronchoalveolar lavage (BAL) was performed 24 hours after the initial exposure. In study II and III, an assessment of vascular function using venous occlusion forearm plethysmography was performed after an exposure to DE (250 µg/m3) generated under transient running conditions, compared to air exposure (study II) and ozone and air exposure (study III). HRV was assessed under a 24 hour period starting before each exposure (study III). In study IV, FENO measurements were conducted after DE and ozone exposures to investigate whether the previously established airway inflammation would be detectable by this non-invasive method. Results: DE exposure enhanced the established ozone-induced airway inflammation in terms of a pronounced neutrophilia in BW. DE generated under transient running conditions, impaired vascular function in healthy volunteers, whereas exposure to ozone did not. HRV were not altered by exposure to ozone. Exposure to DE caused a significant increase in FENO at the 10  (FENO10) and 50 (FENO50) mL/s flow rates at 6 hours post-exposure, but ozone exposure did not affect FENO at any flow rate or time point. Conclusion: We have tried to mimic real-life exposure to air pollutants. In the first study, an exposure to DE followed by an exposure to ozone in the afternoon resulted in an enhanced airway inflammation, suggesting an additive or synergistic effect, supporting the epidemiological findings of unfavorable effects of the combination of these two air pollutants. DE generated by an engine running at the urban part of the standardized European Transient Cycle impaired two important and complementary aspects of vascular function, the regulation of vascular tone and endogenous fibrinolysis. This has previously been shown with DE generated at idling conditions. This suggests that the mechanisms behind the adverse effects can be found in the properties of the particles and not in the gaseous components. In these studies, exposure to ozone did not impair vascular function in healthy subjects, or cause any alterations in HRV. This suggests that the epidemiological evidence for an increased risk of cardiovascular mortality following acute exposure to ozone might not be totally accurate. Previous controlled exposure studies with ozone have not shown an airway inflammation affecting the endothelium, at least not in the same time-frame as following DE exposure. FENO could possibly be a useful tool for assessing airway inflammation caused by DE, whereas the powerful oxidant ozone did not affect FENO. This suggests that the airway inflammatory effects caused by these two pollutants are regulated via different mechanisms.

Air pollution is ranked by the World Health Organisation as one of the top ten contributors to the global burden of disease and injury. Epidemiological studies have shown that exposure to air pollution is associated with cardiorespiratory diseases. However, most of the previous studies have looked at this issue using air pollution data from a single monitoring site or average values from a few monitoring sites in a city. There is increasing concern that the relationships between air pollution and mortality may vary with geographical area, particularly for a big city. This thesis consisted of three interlinked studies that aimed to examine the spatial variation in the relationship between long-term exposure to air pollution and cardiorespiratory mortality in Brisbane, Australia. The first study evaluated the long-term air pollution trends in Brisbane, Australia. Air pollution data used in this study were provided by the Queensland Environmental Protection Agency (QEPA). The data comprised the daily average concentrations of particulate matter less then 10 µm in aerodynamic diameter (PM10), nitrogen dioxide (NO2), ozone (O3) and sulphur dioxide (SO2) between 1 January 1980 and 31 December 2004 in two monitoring sites (i.e. Eagle farm and Rocklea), and in other available monitoring sites between 1 January 1996 and 31 December 2004. Computerised data files of daily mortality between 1 January 1996 and 31 December 2004 in Brisbane city were provided by the Office of Economic and Statistical Research of the Queensland Treasury. Population data and the Socio-Economic Indexes for Areas (SEIFA) data in 2001 were obtained from the Australian Bureau of Statistics (ABS) for each statistical local area (SLA) of the Brisbane city. The long-term air pollution (the daily maximum 1-hour average or daily 24-hour average concentrations of NO2, O3 and PM10) trends were evaluated using a polynomial regression model in two monitoring sites (Eagle Farm and Rocklea) in Brisbane, Australia, between 1980 and 2003. The study found that there were significant up-and-down features for air pollution concentrations in both monitoring sites in Brisbane. Rocklea recorded a substantially higher number of days with concentrations above the relevant daily maximum 1-hour or 24-hour standards than that in Eagle Farm. Additionally, there was a significant spatial variation in air pollution concentrations between these areas. Therefore, the results indicated a need to examine the spatial variation in the relationship between long-term exposure to air pollution and cardiorespiratory mortality in Brisbane. The second study examined the spatial variation of SO2 concentrations and cardiorespiratory mortality in Brisbane between 1999 and 2001. Air pollutant concentrations were estimated using geographical information systems (GIS) techniques at a SLA level. Spatial distribution analysis and a multivariable logistic regression model were employed to investigate the impact of gaseous air pollution on cardiorespiratory mortality after adjusting for potential confounding effects of age, sex, calendar year and SEIFA. The results of this study indicate that for every 1 ppb increase in annual average SO2 concentration, there was an estimated increase of 4.4 % (95 % confidence interval (CI): 1.4 - 7.6 %) and 4.8 % (95 % CI: 2.0 - 7.7 %) in cardiovascular and cardiorespiratory mortality, respectively. We estimated that the excess number of cardiorespiratory deaths attributable to SO2 was 312 (3.4% of total cardiorespiratory deaths) in Brisbane during the study period. Our results suggest that long-term exposure to SO2, even at low levels, is a significant hazard to population health. The final study examined the association of long-term exposure to gaseous air pollution (including NO2, O3 and SO2) with cardiorespiratory mortality in Brisbane, Australia, 1996 - 2004. The pollutant concentrations were estimated using GIS techniques at a SLA level. Logistic regression was used to investigate the impact of NO2, O3 and SO2 on cardiorespiratory mortality after adjusting for potential confounding effects of age, sex, calendar year and SEIFA. The study found that there was an estimated 3.1% (95% CI: 0.4 - 5.8%) and 0.5% (95% CI: -0.03 - 1.3 %) increase in cardiorespiratory mortality for 1 ppb increment in annual average concentration of SO2 and O3, respectively. However there was no significant relationship between NO2 and cardiorespiratory mortality observed in the multiple gaseous pollutants model. The results also indicated that long-term exposure to gaseous air pollutants in Brisbane, even at the levels lower than most cities in the world (especially SO2), were associated with cardiorespiratory mortality. Therefore, spatial patterns of gaseous air pollutants and their impact on health outcomes need to be assessed for an evaluation of long-term effects of air pollution on population health in metropolitan areas. This study examined the relationship between air pollution and health outcomes. GIS and relevant mapping technologies were used to display the spatial patterns of air pollution and cardiorespiratory mortality at a SLA level. The results of this study show that long-term exposure to gaseous air pollution was associated with cardiorespiratory mortality in Brisbane and this association appeared to vary with geographic area. These findings may have important public health implications in the control and prevention of air pollution-related health effects, since now many countries and governments have paid more attention to control wide spread air pollution and to protect our environment and human health.

As nanopartículas atmosféricas podem causar diversos efeitos à saúde já que durante a inalação podem penetrar mais profundamente no sistema respiratório humano, atingindo inclusive os alvéolos e a corrente sanguínea, e, desta forma, aumentar os efeitos toxicológicos prejudiciais. Estas partículas podem ser emitidas diretamente para a atmosfera (partículas primárias) ou ser formadas por conversão gás-partícula (partículas secundárias). Durante a última década, estudos têm sido realizados para uma melhor compreensão sobre as concentrações de nanopartículas, avaliando sua emissão, formação, dispersão, exposição e os efeitos à saúde. No entanto, poucos estudos foram realizados no Brasil e desta forma ainda há pouca informação em relação a esta temática. A Região Metropolitana de Porto Alegre - RMPA (Brasil) possui forte tráfego veicular, cerca de 1,8 milhões de veículos e, apesar das fontes móveis impactarem fortemente a qualidade do ar nesta região e ser a principal fonte de nanopartículas, não há estudos que avaliem em profundidade os níveis deste importante poluente ambiental. Desta forma, no presente estudo foram avaliadas as concentrações de nanopartículas em diferentes pontos da RMPA. Além disso, foram avaliadas as concentrações ambientais de partículas <1 μm (MP1) e metais associados, bem como foram identificadas e quantificadas as contribuições de fontes utilizando o modelo receptor Positive Matrix Factorization (PMF). Em adição, foi realizada uma análise das assinaturas espectrais no infravermelho de nitro-hidrocarbonetos policíclicos aromáticos (nitro-HPAs) associados ao MP1. Este grupo de compostos orgânicos possui uma ampla distribuição no ambiente e, por possuírem propriedades mutagênicas e carcinogênicas, seus riscos ambientais foram calculados. Desta forma, considerando os resultados obtidos, verificou-se uma forte contribuição antropogênica dos poluentes avaliados na RMPA. Esta degradação da qualidade do ar está em geral associada ao tráfego veicular, especialmente no que se refere aos níveis de nanopartículas e nitro-HPAs associados ao MP1. Além disso, as emissões industriais, a queima de carvão, biomassa e óleo combustível, bem como a queima de combustíveis veiculares apresentaram forte influência nos níveis de metais observados em MP1. / Atmospheric nanoparticles can cause health effects, as during inhalation penetrate more deeply into the human respiratory system, including the alveoli and reaching the bloodstream, and thereby increase the damaging toxicological effects. These particles can be emitted directly to the atmosphere (primary particles) or be formed by gas-to-particle conversion (secondary particle). Over the last decade, studies have been conducted for a better understanding of the nanoparticles, assessing the emission, formation, dispersion, exposure and health effects. However, few studies have been conducted in Brazil and thus there is little information regarding this subject. The Metropolitan Area of Porto Alegre - MAPA (Brazil) has a strong vehicular traffic, about 1.8 million vehicles and, despite mobile sources strongly impact the air quality in this region and be the main source of nanoparticles, there are no studies that evaluate in depth the levels of this important environmental pollutant. Thus, considering this knowledge gap, the present study evaluated the nanoparticle concentrations in different sites of the MAPA. In addition, environmental concentrations of particles <1 μm (MP1) and associated metals were evaluated and the sources were identified and quantified using the receptor model Positive Matrix Factorization (PMF). In addition, an analysis of the infrared spectral signatures of nitro polycyclic aromatic hydrocarbons (nitro-PAHs) associated with PM1 was performed. This group of organic compounds has a wide distribution in the environment, and because they have mutagenic and carcinogenic properties, their environmental risks were calculated. Thus, considering the obtained results, a strong anthropogenic contribution of the evaluated pollutants in the MAPA was observed. This degradation of the air quality in general is associated with vehicular traffic, especially regarding the levels of nanoparticles and nitro-PAHs associated with PM1. In addition, industrial emissions, coal, biomass and fuel oil combustion, as well as vehicle fuels combustion had a strong influence on the metal levels observed in PM1.