Urban Air Pollution Exposure Research Articles

The Urban Factor: Meta-analysis of Air Pollution and Cancer Incidence

Background: Urban air pollution is a significant environmental health concern associated with various adverse health outcomes, including cancer. Understanding the relationship between urban air pollution exposure and cancer incidence is crucial for informing public health interventions and policy decisions. Methods: A systematic review and meta-analysis will be conducted to investigate the association between urban air pollution exposure and cancer incidence. Eligible studies will be identified through comprehensive searches of electronic databases. Inclusion criteria encompassed studies reporting quantitative data on air pollution exposure and cancer outcomes. Data extraction and quality assessment will be performed according to predefined criteria. Results: The systematic search will be yielded X studies meeting the inclusion criteria for the meta-analysis. These studies, representing diverse geographic regions, employed various exposure assessment methods and included cohort, case-control, and cross-sectional designs. The meta-analysis will reveal a statistically significant association between urban air pollution exposure and overall cancer incidence (p < 0.05). The pooled effect will estimate indicated a X% increased risk of cancer per unit increase in air pollution exposure. Conclusion: Our meta-analysis provides robust evidence of a significant association between urban air pollution exposure and cancer incidence. These findings underscore the urgent need for targeted interventions to reduce air pollution levels in urban areas and mitigate cancer risks. Public health policies focusing on environmental quality improvements are crucial for promoting population health and well-being.

Urban Air Pollution Exposure Impact on COVID-19 Transmission in a Few Metropolitan Regions

Based on outdoor air pollution and meteorological daily time series observational and in-situ monitoring data, this study investigated the impacts of environmental factors under different urban climates on COVID-19 transmission in four hotspot European metropolises (Berlin, London, Madrid, and Paris) from March 2020 to March 2022. Through applied statistical methods and cross-correlation tests involving multiple datasets pertaining to the main air pollutants (inhalable particulate matter PM2.5 and PM10, nitrogen dioxide (NO2), and ozone (O3)) and climate parameters (air temperature at 2 m height, relative humidity, wind speed intensity and direction, planetary boundary layer height, and surface solar irradiance), a direct positive impact of aerosol loading (PM2.5, PM10, and aerosol optical depth (AOD)) on COVID-19 spreading and severity was revealed. Despite some urban differences existing between the selected cities, particularly for the spring–summer periods, we have observed negative correlations between daily new COVID-19 cases and deaths and daily average ground-level ozone concentration, air temperature at 2 m height, planetary boundary layer height, and surface solar irradiance. Air relative humidity and urban population density have a direct impact on COVID-19 diffusion in large metropolitan areas, and the findings of this study highlight the crucial role of air pollution, in synergy with climate variability, in viral pathogens dispersion in COVID-19 transmission in large urban areas. This information can be used by decision-makers to develop targeted interventions during epidemic periods to reduce the potential risks associated with air pollution exposure and to promote the sustainable development of urban economies.

A Preliminary Case Study on the Compounding Effects of Local Emissions and Upstream Wildfires on Urban Air Pollution

Interactions between urban and wildfire pollution emissions are active areas of research, with numerous aircraft field campaigns and satellite analyses of wildfire pollution being conducted in recent years. Several studies have found that elevated ozone and particulate pollution levels are both generally associated with wildfire smoke in urban areas. We measured pollutant concentrations at two Utah Division of Air Quality regulatory air quality observation sites and a local hot spot (a COVID-19 testing site) within a 48 h period of increasing wildfire smoke impacts that occurred in Salt Lake City, UT (USA) between 20 and 22 August 2020. The wildfire plume, which passed through the study area during an elevated ozone period during the summer, resulted in increased criteria pollutant and greenhouse gas concentrations. Methane (CH4) and fine particulate matter (PM2.5) increased at comparable rates, and increased NOx led to more ozone. The nitrogen oxide/ozone (NOx/O3) cycle was clearly demonstrated throughout the study period, with NOx titration reducing nighttime ozone. These findings help to illustrate how the compounding effects of urban emissions and exceptional pollution events, such as wildfires, may pose substantial health risks. This preliminary case study supports conducting an expanded, longer-term study on the interactions of variable intensity wildfire smoke plumes on urban air pollution exposure, in addition to the subsequent need to inform health and risk policy in these complex systems.

Chronic exposure to polluted urban air aggravates myocardial infarction by impaired cardiac mitochondrial function and dynamics

Air pollution exposure positively correlates with increased cardiovascular morbidity and mortality rates, mainly due to myocardial infarction (MI). Herein, we aimed to study the metabolic mechanisms underlying this association, focusing on the evaluation of cardiac mitochondrial function and dynamics, together with its impact over MI progression. An initial time course study was performed in BALB/c mice breathing filtered air (FA) or urban air (UA) in whole-body exposure chambers located in Buenos Aires City downtown for up to 16 weeks (n = 8 per group and time point). After 12 weeks, lung inflammatory cell recruitment was evident in UA-exposed mice. Interestingly, impaired redox metabolism, characterized by decreased lung SOD activity and increased GSSG levels and NOX activity, precede local inflammation in this group. At this selected time point, additional mice were exposed to FA or UA (n = 12 per group) and alveolar macrophage PM uptake and nitric oxide (NO) production was observed in UA-exposed mice, together with increased pro-inflammatory cytokine levels (TNF-α and IL-6) in BAL and plasma. Consequently, impaired heart tissue oxygen metabolism and altered mitochondrial ultrastructure and function were observed in UA-exposed mice after 12 weeks, characterized by decreased active state respiration and ATP production rates, and enhanced mitochondrial H2O2 production. Moreover, disturbed cardiac mitochondrial dynamics was detected in this group. This scenario led to a significant increase in the area of infarcted tissue following myocardial ischemia reperfusion injury in vivo, from 43 ± 3% of the area at risk in mice breathing FA to 66 ± 4% in UA-exposed mice (n = 6 per group, p < 0.01), together with a sustained increase in LVEDP during myocardial reperfusion. Taken together, our data unravel cardiac mitochondrial mechanisms that contribute to the understanding of the adverse health effects of urban air pollution exposure, and ultimately highlight the importance of considering environmental factors in the development of cardiovascular diseases.

The Use of Standardized Diesel Exhaust Particles in Alzheimer's Disease Research.

The mechanisms underlying how urban air pollution exposure conveys Alzheimer's disease risk and affects plaque pathology is largely unknown. Because particulate matter, the particle component of urban air pollution, varies across location, pollution source, and time, a single model representative of all ambient particulate matter is unfeasible for research investigating the role of ar pollution in central nervous system diseases. More specifically, the investigation of several models of particulate matter with enrichment of source-specific components are essential to employ, in order to more fully understand what characteristics of particulate matter affects Alzheimer's disease, including standardized diesel exhaust particles.

Diesel exhaust impairs TREM2 to dysregulate neuroinflammation

BackgroundAir pollution has been linked to neurodegenerative diseases, including Alzheimer’s disease (AD), and the underlying neuroimmune mechanisms remain poorly understood. TREM2 is a myeloid cell membrane receptor that is a key regulator of disease-associated microglia (DAM) cells, where loss-of-function TREM2 mutations are associated with an increased risk of AD. At present, the basic function of TREM2 in neuroinflammation is a point of controversy. Further, the impact of air pollution on TREM2 and the DAM phenotype is largely unknown. Using diesel exhaust (DE) as a model of urban air pollution exposure, we sought to address its impact on TREM2 expression, the DAM phenotype, the association of microglia with the neurovasculature, and the role of TREM2 in DE-induced neuroinflammation.MethodsWYK rats were exposed for 4 weeks to DE (0, 50, 150, 500 μg/m3) by inhalation. DE particles (DEP) were administered intratracheally once (600 μg/mouse) or 8 times (100 μg/mouse) across 28 days to male mice (Trem2+/+, Trem2−/−, PHOX+/+, and PHOX−/−).ResultsRats exposed to DE exhibited inverted-U patterns of Trem2 mRNA expression in the hippocampus and frontal cortex, while TREM2 protein was globally diminished, indicating impaired TREM2 expression. Analysis of DAM markers Cx3Cr1, Lyz2, and Lpl in the frontal cortex and hippocampus showed inverted-U patterns of expression as well, supporting dysregulation of the DAM phenotype. Further, microglial-vessel association decreased with DE inhalation in a dose-dependent manner. Mechanistically, intratracheal administration of DEP increased Tnf (TNFα), Ncf1 (p47PHOX), and Ncf2 (p67PHOX) mRNA expression in only Trem2+/+ mice, where Il1b (IL-1β) expression was elevated in only Trem2−/− mice, emphasizing an important role for TREM2 in DEP-induced neuroinflammation.ConclusionsCollectively, these findings reveal a novel role for TREM2 in how air pollution regulates neuroinflammation and provides much needed insight into the potential mechanisms linking urban air pollution to AD.

Chronic neighborhood stressors can modify the effect of nitrogen dioxide on term birthweight in New York City

Urban air pollution exposures are associated with decreased newborn birthweight and developmental impairments, potentially with stronger impacts in communities of lower socioeconomic position (SEP). Here, we examined 28 community stressors - which vary with neighborhood SEP - as potential modifiers of the nitrogen dioxide (NO2)-birthweight association in New York City (NYC). We examined birth records data on 245,345 live births from 2007 to 2010 and administrative data on 28 social stressors aggregated to United Hospital Fund (UHF) areas (n = 34), categorized into quartiles. Residence-specific NO2 exposure concentrations, averaged over each pregnancy, were created using NYC Community Air Survey (NYCCAS) and daily EPA regulatory data. We applied linear mixed-effects modeling using UHF as a clustering variable and tested interactions between social factors and NO2. We observed an averaged 12.6-g (SE = 2.72) decrease in newborn birthweight per IQR increase in NO2 (IQR= 6.24 ppb). We also observed significant decrements in birthweight with higher stressor exposures (main effects), including significant decreases across quartiles for assault rates (p=.02 for trend across quartiles), child abuse (p=.02), murder (p=.007), robbery (p=.03), and perceived lack of safety (p=.02). Interaction analyses revealed weaker NO2-birthweight associations in areas with higher community stressors - including higher assault rates (p=.03), murder (p=.03), robbery (p=.04), or perceived lack of safety (p=.02). We found that birthweights in higher-pollution/higher-violence communities were substantially lower, on average, than in lower-pollution/lower-violence communities. These differences were driven, however, by strong direct associations between violence and birthweight; with very high violence exposures, impacts of pollution were dampened. Non-violent social stressors generally did not confer lower birthweights, nor did they substantially alter NO2 effects. Our results suggest complex interactions among stressors and pollutants, including potential saturation effects at the high end of violence exposures. Research in larger datasets and more flexible methods are needed to characterize non-linear interactions.

Development and Validation of a Crowd-Generated Indicator of Air Pollution Exposures and Health Response using Web Search Log Mining.

Background. Traditional air pollution epidemiologic models use ground-based monitors and/or satellite estimates of ozone and PM2.5 concentrations as surrogates of exposure. It is possible that crowd-sourced or online data may be more effective at reflecting population exposures than these traditional indicators. Here, we constructed models to “nowcast” observed elevated pollution levels, using online search queries to create a Crowd-Generated Air Pollution (CGAP) metric and compared the output to monitoring data. We then used the CGAP metric to examine short-term associations of ED visits for pediatric asthma. Methods. A search term Dictionary Learner-Long-Short Term Memory (DL-LSTM) composite model was developed to combine meteorological data, air pollution measures, and pollution-related search data for Atlanta, and daily CGAP index was generated for ozone and PM2.5 from 2007 to 2008. Daily counts of ED visits for asthma among children aged 5 to 17 were collected as well. Using quasi-Poisson generalized linear models, we assessed short-term associations of measured ambient concentration and modeled CGAP index with ED visits. Results. Both ambient ozone and PM2.5 levels were associated with asthma ED visits. We observed similar patterns for indices from DL-LSTM model trained by meteorological data, air pollution measures, and search data (r = 0.88, p &lt; 0.0001 for ozone; r = 0.71, p &lt; 0.0001). The quasi-Akaike information criterion (AIC) of the modeled CGAP index was similar to or lower than that of ambient levels (3179.399 vs. 3173.754 for ozone; 3177.887 vs. 3198.606 for PM2.5). Conclusion. Our findings provided preliminary validation of the CGAP metric, based on a DL-LSTM algorithm. Results using CGAP were comparable to findings using stationary monitoring data for air pollution. The modeled CGAP index showed promise as a means of potentially providing a sensitive, comprehensive predictor of short-term changes in pediatric asthma ED visits due to urban air pollution exposures.

Inflammation response, oxidative stress and DNA damage caused by urban air pollution exposure increase in the lack of DNA repair XPC protein

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 (PM2.5) 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 PM2.5 exposure. To address these important questions, XPC knockout and wild type mice were exposed to PM2.5 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 PM2.5 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 PM2.5.

Putting Co-Exposures on Equal Footing: An Ecological Analysis of Same-Scale Measures of Air Pollution and Social Factors on Cardiovascular Disease in New York City.

Epidemiologic evidence consistently links urban air pollution exposures to health, even after adjustment for potential spatial confounding by socioeconomic position (SEP), given concerns that air pollution sources may be clustered in and around lower-SEP communities. SEP, however, is often measured with less spatial and temporal resolution than are air pollution exposures (i.e., census-tract socio-demographics vs. fine-scale spatio-temporal air pollution models). Although many questions remain regarding the most appropriate, meaningful scales for the measurement and evaluation of each type of exposure, we aimed to compare associations for multiple air pollutants and social factors against cardiovascular disease (CVD) event rates, with each exposure measured at equal spatial and temporal resolution. We found that, in multivariable census-tract-level models including both types of exposures, most pollutant–CVD associations were non-significant, while most social factors retained significance. Similarly, the magnitude of association was higher for an IQR-range difference in the social factors than in pollutant concentrations. We found that when offered equal spatial and temporal resolution, CVD was more strongly associated with social factors than with air pollutant exposures in census-tract-level analyses in New York City.

THE NEUROINFLAMMATION HYPOTHESIS OF URBAN AIR POLLUTION EFFECTS IN THE BRAIN

Urban air pollution exposure has recently been linked to increased risk of several central nervous system diseases and conditions, including cognitive decline and Alzheimer’s disease. The mechanisms mediating these effects are poorly understood. The neuroinflammation hypothesis holds that the resident brain innate immune cells (microglia), cytokines, and reactive oxygen species responses drive the deleterious neuropathology linked to exposure to air pollution. Here, we will discuss several pathways through which air pollution may trigger neuroinflammation, including the Lung-Brain Axis, and the implications of aging and disease in these processes. These findings provide insight into the mechanisms underlying how air pollution may activate microglia and deleteriously impact central nervous system health.

Particulate and gaseous pollutants on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease

This study examined effects of short-term urban air pollution exposures on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease (CVD). We enrolled 61 patients with multiple CVD risk factors and measured high sensitive C-reactive protein (hs-CRP), fibrinogen, D-dimer, and heart rate variability (HRV) indices. Two health examinations for each participant were performed during December 2002 through September 2003. Changes in inflammation and thrombotic markers and HRV indices with exposures to PM2.5, organic carbon (OC), elemental carbon (EC), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) at 1- to 3-day lags were analyzed using mixed models. The results showed inflammatory and thrombotic markers increased with 1- to 3-day lagged PM2.5 components and gaseous pollutants exposures. hs-CRP maximally increased 0.19 [95% confidence interval (CI): 0.07–0.31] and 0.15 (95% CI: 0.05–0.24) mg/L for an interquartile range (IQR) of 1-day lagged SO2 (2.3 ppb) and CO (0.5 ppm), respectively. D-dimer maximally increased 1.05 (95% CI: 0.13–1.75), 0.72 (95% CI: 0.09–1.21), 0.92 (95% CI: 0.13–1.50), and 0.90 (95% CI: 0.07–1.61) mg/dL for an IQR of 1-day lagged OC (3.9 μg/m3), EC (2.0 μg/m3), SO2, and NO2 (13.4 ppb), respectively. The HRV indices, including low frequency, very low frequency, and the ratio of low frequency to high frequency decreased 19.8 (95% CI: 4.4–32.7), 12.9 (95% CI: 0.8–23.4), and 17.6 (95% CI: 5.4–28.2)% for an IQR of 1-day lagged PM2.5 (20.2 μg/m3), respectively. Our findings demonstrated PM2.5 components and gaseous pollutants exert prolonged inflammatory and thrombotic reactions, while PM2.5 exert an immediate autonomic imbalance.

Urban air pollution affects structural and functional processes of brain maturation in children

Introduction From conception to young adulthood, the human brain undergoes dynamic changes in both its structural and functional organization. This period of life is particularly vulnerable to environmental insults that may interfere with the cascade of neurodevelopmental processes. Exposure to urban air pollution has been associated with poorer cognitive performance, which is thought to be a result of direct interference with brain maturation. We aimed to assess the extent of such potential effects of urban pollution exposure during the prenatal period and the childhood. Methods A group of 263 children, aged 8 to 12 years, underwent magnetic resonance imaging to quantify regional brain volumes and functional connectivity in major neural networks and activation / deactivation dynamics during a sensory task. Prenatal NO2 exposure was estimated using both the mothers address during pregnancy and the data from an urban background monitoring station. A combined measurement of elemental carbon and NO2 in the school environment was used to assess urban air pollution exposure during the childhood period. Results While the children exposed to low prenatal NO2 levels showed an increase in white matter volume (WMV) with advancing age, no WMV progression was observed in the children exposed to higher prenatal levels. Similarly, in the opposite effect to that of age, a higher content of pollutants in the school environment was associated with lower functional integration and segregation in key brain networks relevant to both inner mental processes (the default mode network) and stimulus-driven mental operations. Conclusion Both prenatal and postnatal air pollution exposure appear to adversely affect the structural and functional brain maturation. Further research is needed to determine to what extent these disruptions in the brain maturation process are involved in the poor cognitive performance previously observed in children exposed to air pollution.

Long-term urban air pollution exposures and chronic kidney disease in the elderly population in Taiwan

Long-term urban air pollution exposures and chronic kidney disease in the elderly population in Taiwan

Decreases in Short Term Memory, IQ, and Altered Brain Metabolic Ratios in Urban Apolipoprotein ε4 Children Exposed to Air Pollution.

Children's urban air pollution exposures result in systemic and brain inflammation and the early hallmarks of Alzheimer's disease (AD). The apolipoprotein E (APOE) ε4 allele is the most prevalent genetic risk for AD. We assessed whether APOE in healthy children modulates cognition, olfaction, and metabolic brain indices. The Wechsler Intelligence Scale for Children (WISC-R) and the University of Pennsylvania Smell Identification Test were administered to 50 Mexico City Metropolitan Area children (13.4 ± 4.8 years, 28 APOE ε3 and 22 APOE ε4). N-acetylaspartate (NAA)/creatine (Cr), choline (Cho)/Cr, myo-inositol (mI)/Cr, and NAA/mI were calculated using proton magnetic resonance spectroscopy in the white matter of the frontal and parietal lobes, hippocampus, and pons. APOE ε4 versus ε3 children had a reduced NAA/Cr ratio in the right frontal white matter and decrements on attention, short-term memory, and below-average scores in Verbal and Full Scale IQ (>10 points). APOE modulated the group effects between WISC-R and left frontal and parietal white matter, and hippocampus metabolites. Soap was the predominantly failed odor in urban children and, in APOE ε4 versus ε3 carriers, strongly correlated with left hippocampus mI/Cr ratio. APOE modulates responses to air pollution in the developing brain. APOE ε4 carriers could have a higher risk of developing early AD if they reside in a polluted environment. APOE, cognition, and olfaction testing and targeted magnetic resonance spectroscopy may contribute to the assessment of urban children and their results could provide new paths toward the unprecedented opportunity for early neuroprotection and AD prevention.

Comet assay in salivary leukocytes: evaluation of early effects of air pollution exposure in pre-school children.

Comet assay in salivary leukocytes: evaluation of early effects of air pollution exposure in pre-school children.

Ambient Fine Particulate Matter, Nitrogen Dioxide, and Term Birth Weight in New York, New York

Building on a unique exposure assessment project in New York, New York, we examined the relationship of particulate matter with aerodynamic diameter less than 2.5 μm and nitrogen dioxide with birth weight, restricting the population to term births to nonsmokers, along with other restrictions, to isolate the potential impact of air pollution on growth. We included 252,967 births in 2008-2010 identified in vital records, and we assigned exposure at the residential location by using validated models that accounted for spatial and temporal factors. Estimates of association were adjusted for individual and contextual sociodemographic characteristics and season, using linear mixed models to quantify the predicted change in birth weight in grams related to increasing pollution levels. Adjusted estimates for particulate matter with aerodynamic diameter less than 2.5 μm indicated that for each 10-µg/m(3) increase in exposure, birth weights declined by 18.4, 10.5, 29.7, and 48.4 g for exposures in the first, second, and third trimesters and for the total pregnancy, respectively. Adjusted estimates for nitrogen dioxide indicated that for each 10-ppb increase in exposure, birth weights declined by 14.2, 15.9, 18.0, and 18.0 g for exposures in the first, second, and third trimesters and for the total pregnancy, respectively. These results strongly support the association of urban air pollution exposure with reduced fetal growth.

NO(2) and cancer incidence in Saudi Arabia.

Air pollution exposure has been shown to be associated with an increased risk of specific cancers. This study investigated whether the number and incidence of the most common cancers in Saudi Arabia were associated with urban air pollution exposure, specifically NO2. Overall, high model goodness of fit (GOF) was observed in the Eastern, Riyadh and Makkah regions. The significant coefficients of determination (r2) were higher at the regional level (r2 = 0.32–0.71), weaker at the governorate level (r2 = 0.03–0.43), and declined slightly at the city level (r2 = 0.17–0.33), suggesting that an increased aggregated spatial level increased the explained variability and the model GOF. However, the low GOF at the lowest spatial level suggests that additional variation remains unexplained. At different spatial levels, associations between NO2 concentration and the most common cancers were marginally improved in geographically weighted regression (GWR) analysis, which explained both global and local heterogeneity and variations in cancer incidence. High coefficients of determination were observed between NO2 concentration and lung and breast cancer incidences, followed by prostate, bladder, cervical and ovarian cancers, confirming results from other studies. These results could be improved using individual explanatory variables such as environmental, demographic, behavioral, socio-economic, and genetic risk factors.

A framework for emissions source apportionment in industrial areas: MM5/CALPUFF in a near-field application

This paper examines the relative source contribution to ground-level concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), and PM10 (particulate matter with an aerodynamic diameter <10 μm) in a coastal urban area due to emissions from an industrial complex with multiple stacks, quarrying activities, and a nearby highway. For this purpose, an inventory of CO, oxide of nitrogen (NOx), and PM10 emissions was coupled with the non-steady-state Mesoscale Model 5/California Puff Dispersion Modeling system to simulate individual source contributions under several spatial and temporal scales. As the contribution of a particular source to ground-level concentrations can be evaluated by simulating this single-source emissions or otherwise total emissions except that source, a set of emission sensitivity simulations was designed to examine if CALPUFF maintains a linear relationship between emission rates and predicted concentrations in cases where emitted plumes overlap and chemical transformations are simulated. Source apportionment revealed that ground-level releases (i.e., highway and quarries) extended over large areas dominated the contribution to exposure levels over elevated point sources, despite the fact that cumulative emissions from point sources are higher. Sensitivity analysis indicated that chemical transformations of NOx are insignificant, possibly due to short-range plume transport, with CALPUFF exhibiting a linear response to changes in emission rate. The current paper points to the significance of ground-level emissions in contributing to urban air pollution exposure and questions the viability of the prevailing paradigm of point-source emission reduction, especially that the incremental improvement in air quality associated with this common abatement strategy may not accomplish the desirable benefit in terms of lower exposure with costly emissions capping. Implications: The application of atmospheric dispersion models for source apportionment helps in identifying major contributors to regional air pollution. In industrial urban areas where multiple sources with different geometry contribute to emissions, ground-level releases extended over large areas such as roads and quarries often dominate the contribution to ground-level air pollution. Industrial emissions released at elevated stack heights may experience significant dilution, resulting in minor contribution to exposure at ground level. In such contexts, emission reduction, which is invariably the abatement strategy targeting industries at a significant investment in control equipment or process change, may result in minimal return on investment in terms of improvement in air quality at sensitive receptors.

The impact of urban air pollution exposure on the development of alterations on oxidative stress and behavioral parameters in adult mice

Materials and methods Swiss male mice were daily exposed to the urban polluted air (pollution group) or filtered air (control group) for 3 months inside a special chamber, which reproduced a real exposure condition. We performed activity box and elevated plus-maze (EPM) as behavioral tests; and erythrocyte antioxidant defense parameters, including catalase, superoxide dismutase, glutathione peroxidase activities and total glutathione concentration. Statistical analysis were performed by student t test (p<0.05).