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Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?
Abstract
This paper investigates the correlation between the high level of Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) lethality and the atmospheric pollution in Northern Italy. Indeed, Lombardy and Emilia Romagna are Italian regions with both the highest level of virus lethality in the world and one of Europe's most polluted area. Based on this correlation, this paper analyzes the possible link between pollution and the development of acute respiratory distress syndrome and eventually death. We provide evidence that people living in an area with high levels of pollutant are more prone to develop chronic respiratory conditions and suitable to any infective agent. Moreover, a prolonged exposure to air pollution leads to a chronic inflammatory stimulus, even in young and healthy subjects. We conclude that the high level of pollution in Northern Italy should be considered an additional co-factor of the high level of lethality recorded in that area.
... Cilia and upper airway defenses could have been weakened by persistent exposure to air pollution, which may have encouraged viral invasion by allowing viruses to invade lower airways, increasing COVID-19 occurrence and lethality [7]. The immune system could be severely compromised by a highly infectious virus, such as the novel SARS-CoV-2. ...
... This scientific study supports the evidence that chronic illnesses are linked to environmental pollution, particularly in urban areas. Air pollution is a well-known contributor to chronic inflammation, resulting in an overactive innate immune system [7]. Long-term air pollution exposure can lead to persistent immune system disturbances [56]. ...
... Long-term air pollution exposure can lead to persistent immune system disturbances [56]. It may result in a weakened circulatory and respiratory viral invasion, thus increasing the risk of the severe outcome of COVID-19 [7]. ...
Emissions from motor vehicles and industrial sources have contributed to air pollution worldwide. The effect of chronic exposure to air pollution is associated with the severity of the COVID-19 infection. This ecological investigation explored the relationship between meteorological parameters, air pollutants, and COVID-19 cases among residents in Selangor and Kuala Lumpur between 18 March and 1 June in the years 2019 and 2020. The air pollutants considered in this study comprised particulate matter (PM2.5, PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and carbon monoxide (CO), whereas wind direction (WD), ambient temperature (AT), relative humidity (RH), solar radiation (SR), and wind speed (WS) were analyzed for meteorological information. On average, air pollutants demonstrated lower concentrations than in 2019 for both locations except PM2.5 in Kuala Lumpur. The cumulative COVID-19 cases were negatively correlated with SR and WS but positively correlated with O3, NO2, RH, PM10, and PM2.5. Overall, RH (r = 0.494; p < 0.001) and PM2.5 (r = −0.396, p < 0.001) were identified as the most significant parameters that correlated positively and negatively with the total cases of COVID-19 in Kuala Lumpur and Selangor, respectively. Boosted Trees (BT) prediction showed that the optimal combination for achieving the lowest Root Mean Squared Error (RMSE), Mean Squared Error (MSE), and Mean Absolute Error (MAE) and a higher R-squared (R2) correlation between actual and predicted COVID-19 cases was achieved with a learning rate of 0.2, a minimum leaf size of 7, and 30 learners. The model yielded an R2 value of 0.81, a RMSE of 0.44, a MSE of 0.19, and a MAE of 0.35. Using the BT predictive model, the number of COVID-19 cases in Selangor was projected with an R2 value of 0.77. This study aligns with the existing notion of connecting meteorological factors and chronic exposure to airborne pollutants with the incidence of COVID-19. Integrated governance for holistic approaches would be needed for air quality management post-COVID-19 in Malaysia.
... It has been suggested that environmental factors such as air pollution, may have played a role in facilitating the spread and transmission of SARS-CoV-2, with a number of mechanisms suggested (Comunian et al., 2020;Conticini et al., 2020). ...
... The capability of PM 2.5 to induce an increase of ACE2 and the capability of SARS-CoV-2 to exploit it support ecological studies, during the first wave of COVID-19, reporting positive correlations between the daily COVID-19 incidence and PM 2.5 concentrations, both in China (Zhu et al., 2020) and northern Italy (Fattorini and Regoli, 2020), two strongly polluted regions. The northern regions of Italy have been more strongly affected by the SARS-CoV-2 pandemic than other areas with similar socio-economic backgrounds (Conticini et al., 2020;Borro et al., 2020;Fattorini and Regoli, 2020). These regions represent one of the most severely polluted area in Europe. ...
COVID-19 pandemic had a significant impact on global public health. The spread of the disease was related to the high transmissibility of SARS-CoV-2 virus but incidence and mortality rate suggested a possible relationship with environmental factors. Air pollution has been hypothesized to play a role in the transmission of the virus and the resulting severity of the disease. Here we report a plausible in vitro toxicological mode of action by which fine particulate matter (PM2.5) could promote a higher infection rate of SARS-CoV-2 and severity of COVID-19 disease. PM2.5 promotes a 1.5 fold over-expression of the angiotensin 2 converting enzyme (ACE2) which is exploited by viral particles to enter human lung alveolar cells (1.5 fold increase in RAB5 protein) and increases their inflammatory state (IL-8 and NF-kB protein expression). Our results provide a basis for further exploring the possible synergy between biological threats and air pollutants and ask for a deeper understanding of how air quality could influence new pandemics in the future.
... Air pollution represents one of the main reasons for extended inflammation, subsequently leading to innate immune system hyper-activation [40]. Air pollution can affect many parts of the human body. ...
... because of its high contagiousness, and it was declared a public health emergency of global concern by the World Health Organization (WHO). The course of the ailment is frequently mild and undistinguishable from common flu, but in a full-size range of cases, it may additionally require hospitalization, eventually leading to ARDS and death [40]. ...
The emission of air pollutants weakens the body’s immune system and can increase the prevalence of coronaviruses. This study examined the effects of six environmental pollutant gases, including Carbon Dioxide (CO2), Methane (CH4), Nitrous Oxide (N2O), Hydrofluorocarbons (HFC), Perfluorocarbons (PFC), and Sulphur Hexafluoride (SF6), on the prevalence of coronaviruses (i.e., coronavirus cases, total deaths, and active cases) in 30 European countries. Due to the benefits of ridge regression, this method was used to investigate the effects of those environmental pollutants on coronavirus cases. The results showed that all six gases had a positive effect on active coronavirus cases in European countries. This study concludes that industrialized European countries could focus on reducing environmental pollutants to decrease the effects of future pandemics.
... Other works have proposed that climatic and pollution variables affect the spread and deaths due to COVID-19 (Anand et al., 2021;Conticini et al., 2020;Lembo et al., 2021;Urrutia-Pereira et al., 2020). Some studies suggest that cities with high pollution levels and specific meteorological conditions can register further spread of the virus (Coccia, 2020a). ...
... Air pollution is one of the causes of prolonged inflammation; prolonged exposure to atmospheric pollution sources leads to chronic inflammation. This explains the high prevalence and mortality of SARS-CoV-2 among the populations that live in highly polluted areas (Conticini et al., 2020). Besides, the Centre for Research on Energy and Clean Air (CREA) final report concluded that high air pollution affects the body's defenses, increasing the potential of contract viral diseases such as COVID-19 (Myllyvirta and Thieriot, 2020). ...
Recent studies show that aerosols are highly linked to the spread of the COVID−19 pandemic. Furthermore, during this pandemic, the largest Saharan dust intrusion event has reached the Caribbean region in the last 20 years, called “Godzilla” African Dust or GAD. This study aims to analyze the correlation between the spread of COVID−19 and the GAD event in the main cities of the Colombian Caribbean region. The results showed a positive correlation between the spread of COVID−19 and the GAD event in most cities. Our findings could serve as input for the development of a strategy in the prevention of COVID−19 and other similar viral diseases during the Saharan dust intrusion events that reach the Caribbean region each year from Africa. Our results may help design strategies to prevent future outbreaks of COVID-19 and reduce the risk of future pandemics of similar viral diseases. Especially during the Saharan dust intrusion events that reach the Caribbean region each year.
... P ortable personal air quality sensors facilitating the monitoring and mitigation of personal pollution exposure are becoming increasingly affordable and available thanks to advances in miniaturization and sensor technology. As exposure to pollutants has been linked with many acute and chronic diseases [1]- [6], several types of cancer [3], [7], [8] and even the occurrence and severity of COVID-19 [9]- [12], these devices provide essential information for mitigating personal health risks and contribute toward improved health. Besides benefits to individuals, portable air quality sensors help to improve the resolution and coverage of air quality information [13], offering policymakers and other stakeholders Submitted for review September 15, 2023. ...
p>We develop a portable and affordable solution for estimating personal exposure to black carbon (BC) using low- cost sensors and machine learning. Our approach uses other pollutants and environmental variables as proxies for estimating the concentrations of BC and combines this with machine learning based sensor calibration to improve the quality of the inputs that are used as proxies in the modeling. We extensively validate the feasibility of our approach and demonstrate its benefits with benchmarks conducted on real world data from two different urban locations with different population densities and characteristics. Our results demonstrate that our approach can accurately estimate BC ( R <sup>2</sup> higher than 0.9) without relying on a dedicated sensor. The results also highlight how calibration is essential for ensuring accurate modeling on low-cost sensor measurements. Our results offer a novel affordable and portable solution that can be used to estimate personal exposure to BC and, more generally, demonstrate how low-cost sensors and proxy modeling can increase the spatiotemporal scale at which information about BC level is available. </p
... P ortable personal air quality sensors facilitating the monitoring and mitigation of personal pollution exposure are becoming increasingly affordable and available thanks to advances in miniaturization and sensor technology. As exposure to pollutants has been linked with many acute and chronic diseases [1]- [6], several types of cancer [3], [7], [8] and even the occurrence and severity of COVID-19 [9]- [12], these devices provide essential information for mitigating personal health risks and contribute toward improved health. Besides benefits to individuals, portable air quality sensors help to improve the resolution and coverage of air quality information [13], offering policymakers and other stakeholders Submitted for review September 15, 2023. ...
p>We develop a portable and affordable solution for estimating personal exposure to black carbon (BC) using low- cost sensors and machine learning. Our approach uses other pollutants and environmental variables as proxies for estimating the concentrations of BC and combines this with machine learning based sensor calibration to improve the quality of the inputs that are used as proxies in the modeling. We extensively validate the feasibility of our approach and demonstrate its benefits with benchmarks conducted on real world data from two different urban locations with different population densities and characteristics. Our results demonstrate that our approach can accurately estimate BC ( R <sup>2</sup> higher than 0.9) without relying on a dedicated sensor. The results also highlight how calibration is essential for ensuring accurate modeling on low-cost sensor measurements. Our results offer a novel affordable and portable solution that can be used to estimate personal exposure to BC and, more generally, demonstrate how low-cost sensors and proxy modeling can increase the spatiotemporal scale at which information about BC level is available. </p
... Air pollution is considered one of the threat factors in spreading COVID-19, where an increase in 8% COVID-19 death rate is observed with an increase of 1 mg m −3 of particulate matter. [21][22][23] The respiratory system is the part most affected by SARS-CoV-2 and the inhaled aerosols deposit in different regions of the respiratory system. Upon exposure to air pollutants, such as ozone (O 3 ) and nitrogen dioxide (NO 2 ), free radicals are produced through heterogeneous and multiphase chemistry on reactive encounters between different air pollutants and atmospheric oxidants. ...
The present study investigates the effects of air pollution and climate factors on the acceleration of SARS-CoV-2 transmission and mortality. In particular, the correlations between O3, NO2, PM2.5, PM10 and SO2 concentrations with daily number of infections and fatalities caused by the second wave of COVID-19 during the time period March–June 2021 in Indian cities with different climate zones are analyzed. The chemical transformations in the atmosphere that translated to dispersion of SARS-CoV-2 aerosols and their deposition in the respiratory system are studied. The results suggested that exposure to a higher level of O3 may weaken the respiratory system, and therefore resistance against COVID-19 is suppressed. The infectious aerosols undergo reactive encounters with atmospheric oxidants, forming secondary aerosols before deposition in the lungs. The pulmonary epithelium is naturally protected against atmospheric O3 and secondary aerosols by lung-lining fluids that contain ascorbic acid, AH2 and other antioxidants. Since O3 and COVID-19 infections showed a positive correlation, AH2 and the underlying tissues will be the most affected. The mechanism for the interaction of O3 with AH2 is studied using quantum chemical methods. During this interaction, a persistent ozonide is formed in lung-lining fluids and this is acidified by the inhaled aerosols. Earlier epidemiological and toxicological studies revealed that this ozonide leads to the formation of cytotoxic free radicals that can cause oxidative stress during breathing. Thus, O3 plays a significant role in the deposition of aerosols in the lungs. The results of this study add to prevailing evidence as well as providing new insights into the role of ambient O3 in the dispersion and deposition of SARS-CoV-2 aerosols.
... Studies have also focused on environmental factors mainly because of "flu" like symptoms and have revealed higher epidemic rates of COVID-19 with lower average temperature (Alvarez-Ramirez and Meraz, 2020; Ficetola and Rubolini, 2020;Pirouz et al., 2020). Moreover, a positive association between atmospheric pollution levels and a high level of COVID-19 lethality has been noted, since high pollutant levels render the population more vulnerable to respiratory diseases (Conticini, et al., 2020;Setti, et al., 2020). In fact, the discourse on incumbent respiratory disorders and COVID-19 necessarily brings into context an in-depth study of how vulnerable groups are affected by COVID-19. ...
Big cities are highly complex spatial units and have diverse subpopulations and neighborhoods with different sociocultural needs and vulnerable groups concerning public health emergencies, such as COVID-19. When these cities face an epidemic that spreads rapidly within the urban community, then human density and the urban setting have proven to be a tremendous liability and a matter of concern. The present study in this context is a preliminary attempt to understand the COVID-19 pandemic in the Indian context. The paper presents a city-level study of 46 million-plus cities in India to identify major determining factors (demographic, economic, environmental, infrastructural, and institutional interventions) of the COVID-19 infection and related deaths in different lockdown and unlock phases. Using the multiple regression model we found that the impact of these factors does significantly explains the variation in the COVID-19 infections and related deaths. However, the role of individual indicators does seem to have a differential impact across phases of the lockdown strategy. Indicators, such as GDP, hospital-doctor ratio, public transport usage, and administrative status of the city have been found to be the most significant factors influencing COVID-19 cases and deaths. On the other hand, co-morbidities do not appear as consistent significant factors, while the much-debated density parameter plays an insignificant role in the Indian big cities. We would like to emphasize that the results are at best indicative in nature, and for an in-depth understanding of each of these factors and spatial complexity, we require further detailed analysis at a more disaggregated level.
... WCR may increase the adverse effects of patients infected by SARs-CoV-2 and exacerbate the severity of COVID [1]. Epidemiological studies have indicated that the coexistence of COVID and environmental pollution, such as particulate matter (PM), increased the severity of the disease [2,3]; these studies have allowed establishment of a model of transmission [4]. In vitro models have indicated a greater toxic effect when non-ionizing radiation and ambient air pollution act together on immune cells exposed to 2.45 GHz, 12W EMF RF for 8, 24, 48 or 72 h [5,6]. ...
Programmed cell death constitutes a fundamental part of the immune response to viral infection. This process forms part of the host defence mechanism and also enables establishment of biomarkers of disease severity. Natural or anthropogenic sources of microwaves emit energy and may alter the ecology of the COVID-19 virus in the environment. Determining the associated effects on the immune system and on the health of hosts with COVID-19 disease is thus important. In this review paper, we consider studies analyzing the influence of electromagnetic fields on innate and acquired immune responses in humans, and above all on preclinical experimental animal models and in vitro models, and we also consider studies analyzing immunity acquired from COVID-19 infections associated with cell death. We focus on the effects of electromagnetic fields and the influence of oxidative stress on stimulation or immunomodulation, the inflammatory response, autoimmunity and the participation of intracellular calcium channels in the immunology of COVID-19 disease. Non-ionizing radiation can activate or reduce the inflammatory response, oxidative stress and the entry of intracellular calcium and can facilitate or reduce cell death. The review of experimental study findings indicates that exposure to non-ionizing radiation can also have a bidirectional effect on the immune system, either slowing down or enhancing the processes that lead to the cell death associated with COVID-19 disease.
... Residents have been exposed to natural and anthropogenic air pollution during the pandemic. The risk of infectious diseases being transmitted through aerosols has been found to be higher than through air pollution owing to urbanization [96]. Globally, the air quality improved significantly during the lockdown. ...
The COVID-19 pandemic has affected smart city operations and planning. Smart cities, where digital technologies are concentrated and implemented, face new challenges in becoming sustainable from social, ecological, and economic perspectives. Using text mining methodologies of topic modeling and network analysis, this study aims to identify keywords in the field of smart cities after the pandemic and provide a future-oriented perspective on the direction of smart cities. A corpus of 1882 papers was collected from the Web of Science and Scopus databases from December 2019 to November 2022. We identified six categories of potential issues in smart cities using topic modeling: “supply chain”, “resilience”, “culture and tourism”, “population density”, “mobility”, and “zero carbon emission”. This study differs from previous research because it is a quantitative study based on text mining analysis and deals with smart cities, given the prevalence of COVID-19. This study also provides insights into the development of smart city policies and strategies to improve urban resilience during the pandemic by anticipating and addressing related issues. The findings of this study will assist researchers, policymakers, and planners in developing smart city strategies and decision-making in socioeconomic, environmental, and technological areas.
... Scientists have established a long-term relationship between population growth, production, air pollution and global warming [7]. The impact of pollution on the air environment and human health is real and growing [8][9][10]. ...
This study analyzes for the first time uniformly and causally the level of pollution and air quality for the NE-Romania Region, one of the poorest region in the European Union. Knowing the level of pollution and air quality in this region, which can be taken as a benchmark due to its positional and economic-geographical attributes, responds to current scientific and practical needs. The study uses an hourly database (for five pollutants and five climate elements), from 2009 to 2020, from 19 air quality monitoring stations in northeastern Romania. Pollutant levels were statistically and graphically/cartographically modeled for the entire 2009–2020 interval on the distributive-spatial and regime, temporal component. Inter-station differences and similarities were analyzed causally. Taking advantage of the emergency measures between March 16 and May 14, 2020, we observed the impact of the event on the regional air quality in northeastern Romania. During the emergency period, the metropolitan area of Suceava (with over 100,000 inhabitants) was quarantined, which allowed us to analyze the impact of the quarantine period on the local air quality. We found that, in this region, air quality falls into class I (for NO2, SO2 and CO), II for O3 and III for PM10. During the lockdown periods NO2 and SO2 decreased for the entire region by 8.6 and 14.3%, respectively, and in Suceava by 13.9 and 40.1%, respectively. The causes of the reduction were anthropogenic in nature.
... The northern regions have been the most affected area by the first wave of the COVID-19 epidemic in Italy. The great speed and intensity with which disease has spread to these regions has led to the hypothesis, in some preliminary studies, that high levels of pollution may play a role in epidemic expansion and in determining the severity of the infection (Coccia 2020;Conticini et al. 2020;Fattorini and Regoli 2020;Martelletti and Martelletti 2020). In fact, Northern Italy is one of the most heavily polluted area in Europe in terms of smog and air pollution (Carugno et al. 2016) because it is characterized by a high concentration of densely populated urban areas, as well as by a strong presence of industrial activities. ...
This paper aims to further investigate the relationship between the concentrations of nitrogen dioxide (NO 2 ) and the severity of COVID-19 by analyzing the data of three Italian Regions (Piedmont, Valle d’Aosta and Liguria) during the first wave of the pandemic (February–May 2020). The analyses were conducted at a local scale using Local Labor Systems of ISTAT. The annual average of NO 2 concentrations, obtained from space satellite Sentinel-5P, was used to assess environmental data. While excess mortality data were used to estimate the severity of the pandemic, calculated as the percentage change in deaths recorded in 2020 compared to the average number of deaths of the previous five years (2015–2019). Using quasi-Poisson multivariate regression models, it was possible to estimate the correlation between the incidence rate of the pandemic and some risk factors, including in particular the concentration of NO 2 .
... The northern regions have been the most affected area by the first wave of the COVID-19 epidemic in Italy. The great speed and intensity with which disease has spread to these regions has led to the hypothesis, in some preliminary studies, that high levels of pollution may play a role in epidemic expansion and in determining the severity of the infection (Coccia 2020;Conticini et al. 2020;Fattorini and Regoli 2020;Martelletti and Martelletti 2020). In fact, Northern Italy is one of the most heavily polluted area in Europe in terms of smog and air pollution (Carugno et al. 2016) because it is characterized by a high concentration of densely populated urban areas, as well as by a strong presence of industrial activities. ...
This final chapter of the book highlights some major results of the Post Un-Lock research project conducted inside the SDG11Lab and the Responsible Risk Resilience Center of the Politecnico di Torino with the collaboration of the Medical Statistics and Epidemiology Department of the University of Turin. In particular, it discusses the concepts of proximity and Local Resilience Units in connection with the well-known “15-city” paradigm. This model requires the adoption of new urban and ecosystem criteria as well as advanced technological support systems for post-pandemic public and private urban space planning and management. The conclusions point out to the need for education and appropriate digital skills in order to be able to integrate ecological principles in the design and management of urban areas with the support of high-tech systems.
... The northern regions have been the most affected area by the first wave of the COVID-19 epidemic in Italy. The great speed and intensity with which disease has spread to these regions has led to the hypothesis, in some preliminary studies, that high levels of pollution may play a role in epidemic expansion and in determining the severity of the infection (Coccia 2020;Conticini et al. 2020;Fattorini and Regoli 2020;Martelletti and Martelletti 2020). In fact, Northern Italy is one of the most heavily polluted area in Europe in terms of smog and air pollution (Carugno et al. 2016) because it is characterized by a high concentration of densely populated urban areas, as well as by a strong presence of industrial activities. ...
During the last century, the close relationship between the Lanzo valleys and the Turin conurbation has declined differently because of the specific local resources, networks, and the dominant development model, starting with the historic holiday resort of the Turin upper class up to the industrialization of the lower valley, linked to Turin industry and currently in crisis. Recent projects, carried out by the local community, however, testify to the desire for a new dynamism through innovative experiences that look beyond the traditional activities, as testified by the selection of this area in the first phase of the National Strategy for Internal Areas (SNAI). These dynamics have accelerated in relation to the COVID-19 pandemic which has further re-evaluated the role and importance of some local assets that have favoured the spread of a different model of living characterized by a temporary residency that positively exploits the qualities of an urban-mountain environment. On the other hand, there was a rediscovery of a different tourism, linked to places, history, and nature. This contribution deepens the evolution of these dynamics, focusing on the entire metropolitan-mountain area and on specific municipalities through qualitative-quantitative analyses to evaluate the effects both in the short and long-term allowing to establish which are, in the near future, the permanent assets on which to focus attention to trigger a leverage effect and which ones can be considered as temporary conditions that run out in a short time.
... The northern regions have been the most affected area by the first wave of the COVID-19 epidemic in Italy. The great speed and intensity with which disease has spread to these regions has led to the hypothesis, in some preliminary studies, that high levels of pollution may play a role in epidemic expansion and in determining the severity of the infection (Coccia 2020;Conticini et al. 2020;Fattorini and Regoli 2020;Martelletti and Martelletti 2020). In fact, Northern Italy is one of the most heavily polluted area in Europe in terms of smog and air pollution (Carugno et al. 2016) because it is characterized by a high concentration of densely populated urban areas, as well as by a strong presence of industrial activities. ...
The chapter illustrates the result of the analysis on the municipality of Mappano, located in northern Turin (Italy). The studies were carried out as part of the collaboration between the Municipality of Mappano and the Inter-University Department of Territorial and Urban Studies and Planning (DIST) of the Politecnico di Torino, for the preparation of the first Municipal Urban Plan. The main goal was to contribute to this local planning tool by introducing innovative analyses, descriptions and elaborations which were useful in structuring planning choices. In particular, various data sources were systematized, integrated and coordinated to represent the territory from the point of view of both environmental phenomena and landscape in order to provide sustainability and resilience.
... The northern regions have been the most affected area by the first wave of the COVID-19 epidemic in Italy. The great speed and intensity with which disease has spread to these regions has led to the hypothesis, in some preliminary studies, that high levels of pollution may play a role in epidemic expansion and in determining the severity of the infection (Coccia 2020;Conticini et al. 2020;Fattorini and Regoli 2020;Martelletti and Martelletti 2020). In fact, Northern Italy is one of the most heavily polluted area in Europe in terms of smog and air pollution (Carugno et al. 2016) because it is characterized by a high concentration of densely populated urban areas, as well as by a strong presence of industrial activities. ...
COVID-19 restrictions have changed the perception of space: travel limitations and diffusion of remote activities have narrowed the spaces of everyday life, leading to a rediscovery of proximity. We are both witnessing a re-appropriation of the domestic environment and re-discovering the neighbourhood and those small portions of the city often neglected. This rediscovery is evident in the use of nearby public spaces and in transport, with the decongestion of many urban areas following the reduction of commuting. Even if this is a contingent situation, it is reasonable to think that part of these changes will persist at the end of the emergency. For these reasons, there is a need to focus on neighbourhoods’ quality, spatial organization and adaptive capacity towards both emergencies such as the pandemic and the great urban challenges towards resilience and sustainability. Essentially, sub-local scale must be rethought to meet not only the ordinary needs of its inhabitants but also health or other issues. In this sense, the potential of spatial units based in the concepts of proximity and walkability is explored, giving an interpretation that starting from the 15-min city and the superilla models explore the perspective of “minimum units of resilience” for facing pandemics.
... The northern regions have been the most affected area by the first wave of the COVID-19 epidemic in Italy. The great speed and intensity with which disease has spread to these regions has led to the hypothesis, in some preliminary studies, that high levels of pollution may play a role in epidemic expansion and in determining the severity of the infection (Coccia 2020;Conticini et al. 2020;Fattorini and Regoli 2020;Martelletti and Martelletti 2020). In fact, Northern Italy is one of the most heavily polluted area in Europe in terms of smog and air pollution (Carugno et al. 2016) because it is characterized by a high concentration of densely populated urban areas, as well as by a strong presence of industrial activities. ...
The COVID-19 pandemic has been studied by many scholars from a wide range of disciplines. Among these investigations, planners and regional scientists have researched the spatial spread of the contagion. Most of these studies tried to explore the spread of the disease in a fixed period, like annually, and analysed the spatial variables that are most influential on the COVID-19 spread over territories. On the same line, the chapter investigates the pattern of virus transmission in the 1.181 municipalities of the Piedmont Region during two years of the pandemic over different periods by providing 24 monthly and two annual hot spot maps using the Spatial Statistics Tools on ArcGIS. Consequently, the chapter analyses the correlation between the spread of contagion with three spatial variables (population density, annual average traffic flow, and the ageing index) by performing a statistical analysis on the municipalities which showed unexpectedly higher or unexpectedly lower numbers of contagion. The results show that the impacts of population density and annual average traffic flow are verified on the transmission rate of the cities with unexpectedly higher or lower exposure to COVID-19 contagion than their neighbours both in the first and the second year of the pandemic. For the ageing index, an association is noticed during the first year while not confirmed for the second. In conclusion, the chapter proposes that studying the disease’s variations—at different times and on a regional scale—uncovers the spatial dimension of the phenomenon and would suggest insights for both scientists and policymakers to enrich preparedness as the preferable approach in future planning policies towards transformative resilience.
... The research into the impact of smog on living organisms revealed that particle pollutants increase the risk of developing asthma and allergy 13 , cause arrhythmia 14 , lung cancer 15 and chronic obstructive lung disease 16 , bronchitis 17 , as well as decrease fertility 18,19 and constitute a risk factor for abnormal fetal development 20 . Recent studies also show the possibility of a link between the high level of mortality caused by the severe acute respiratory syndrome CoronaVirus 2 and particulate contamination of the atmosphere 21,22 . Data that clearly demonstrates the harmfulness of particulates makes one issue more stringent standards and recommendations regarding the concentration of these particles in the air. ...
Heavy metals are one of the components of smog, which is mainly the product of burning fossil fuels in residential buildings. These elements, introduced into the body of cattle by inhalation, may enter the milk. The goal of this study was to assess the impact of particulate pollution in the atmospheric air on the concentration of particulate matter in the air of a dairy cattle barn and on the content of selected heavy metals in milk from cows present in the building. Measurements were taken between November and April (148 measurement days). The calculations carried out showed a high correlation (RS = + 0.95) between the concentrations of particulates measured outside and inside the barn, which is indicative of a significant impact of the atmospheric air on the particulate pollution level of the livestock building. The number of days in excess of the daily standard for PM10 inside was 51. The conducted analysis of the chemical composition of the milk collected under high particulate pollution (February) showed that the permitted lead level had been exceeded—21.93 µg/kg (norm 20.00 µg/kg).
... The possible effect of PM10 and PM2.5 pollution on the Covid-19 (SARS-COV-2) pandemic new cases and mortality was intensively studied from less than a year after the pandemic start, mainly based on the situation in the Lombardy region (Italy) where air pollution levels and the mortality were among the highest in Europe. These studies presented a statistical relation between PM levels and Covid-19 morbidity and mortality during the first phase of the pandemic [10][11][12][13][14][15][16][17]. These conditions first consisted of respiratory and cardiovascular distresses [18] and were indeed related to the immune system [19,20]. ...
Rationale: The possible effect of Particulate Matter (PM10 and PM2.5 of diameter 10 and 2.5 µm respectively) levels on Covid-19 mortality is now well established. However, time-evolution of Covid-19 mortality according to PM2.5 levels has been scarcely investigated. Aim: To understand this relationship at the European level for the period 2020 (beginning) - 2022 (end). Methods: 16 representative locations in Europe (81 million people) with heterogeneous levels of PM2.5 (µg.m-3), from low to high. PM2.5 levels were assessed by various methods, and Covid-19 mortality was reported by Johns Hopkins University. Results: The trend of Covid-19 mortality vs. PM2.5 levels varied among locations. Overall, the estimated mean value was of a 40±20% mortality increase per 1 µg.m-3 PM2.5 increase. The stronger the positive gradient of the PM peak, the stronger the positive gradient of the Covid-19 mortality. Exposure to several PM peaks during about a 2-month period was the main contributor to Covid-19 mortality increases. Conclusion: Our data confirm a temporal relation between PM2.5 exposure and Covid-19 mortality, considering a 2-month integration-time for pollution events. Number-concentrations of PM should be used in the future rather than the PM2.5 mass-concentrations (µg.m-3) with the consideration of PM composition to better explain this finding.
... 22 Conticini ve ark., COVID-19'a bağlı yüksek ölüm oranları ile hastaların yaşadıkları bölgelerdeki hava kirliliği arasında bir ilişki saptamıştır. 23 Wu ve ark., ABD'de havadaki 1 μg/m 3 partiküllük bir madde artışının COVID-19 için %15 daha yüksek ölüm oranına yol açtığını bildirmiştir. 24 Karantina nedeniyle hava kirliliğinin azalmasına bağlı olarak hastalı-ğın yükünün daha az olduğunu bildiren çalışmalar da bulunmaktadır. ...
Küreselleşme, sosyal ilişkilerin evrensel bir şekilde yoğunlaşması ve birbirlerinden kilo-metrelerce uzakta yaşayan insanların kaderlerinin birbirine bağlı hale gelmesi şeklinde tanımlanmaktadır. Bu makalenin amacı, küreselleşmenin toplum sağlığı, ekolojik denge ve enfeksiyon hastalıkları üzerindeki etkilerinin tartışılmasıdır. Küreselleşmenin ekonomik, ticari ve teknolojik faydalarının yanısıra ekolojik denge üzerinde olumsuz etkileri de bulunmaktadır. Ekolojik dengenin bozulması nedeniyle vektör ve rezervuar canlıların dağılımında değişiklikler yaşanmakta, bu durum da yeni enfeksiyon etkenlerinin insanlarda salgınlara yol açma riskini artırmaktadır. Ayrıca, küre-selleşmenin getirdiği seyahat olanaklarının gelişmesiyle birlikte insanlar arasındaki etkileşimler art-mış olup, enfeksiyon etkenlerinin hızla yayılması dolayısıyla pandemilerin oluşumu kolaylaşmıştır. Küreselleşmenin enfeksiyon hastalıklarının yayılmasına olan katkısının engellenmesi, bireysel ön-lemlerin yanısıra ulusal ve uluslararası çaba ve/veya fedakarlıklara bağlıdır. Alınacak önlemler, mikro ve makro düzeydeki tüm canlılar arasındaki ekolojik döngü bağlamında ele alınmalı, doğanın dengesinin korunmasına yönelik oluşturulan politikalar sürdürülmelidir. Sonuç olarak Tek Sağlık Kavramı çerçevesinde insan dışındaki canlı türlerinide bilimsel araştırmalara dahil eden bir yaklaşımın benimsenmesine ihtiyaç bulunmaktadır.
ABSTRACT: Globalization is defined as the universal intensification of social relations and the interdependence of the destinies of people living miles apart. The aim of this article is to discuss the effects of globalization on public health, ecological balance, and infectious diseases. Besides the economic, commercial, and technological benefits of globalization, there are also negative effects on the ecological balance. Due to the deterioration of the ecological balance, the distribution of vectors and reservoir organism changes by uprising the risk of novel infectious agents causing human epidemics. In addition, with the development of travel opportunities brought by globalization, interactions between people have increased and the formation of pandemics has become easier due to the rapid spread of infectious agents. Preventing the contribution of globalization to the spread of infectious diseases depends on national and international efforts and/or sacrifices as well as individual measures. The measures to be taken should be considered in the context of the ecological cycle between all living things at micro and macro levels. Moreover, policies targeting stability in nature should be maintained. As a result, there is a need to adopt approaches within the framework of the One Health Concept by including non-human species in the scientific research.
... Epidemiological studies have previously investigated impacts of particulate matter (PM) and gaseous pollutants such as nitrogen oxides (NO X ) and ozone (O 3 ) on COVID-19 outcomes. In most cases, the results have linked mean air pollution levels to COVID-19 severity and mortality (Martelletti and Martelletti, 2020;Dutheil et al., 2020;Zhu et al., 2020;Frontera et al., 2020aFrontera et al., , 2020bConticini et al., 2020;Wang et al., 2020;Setti et al., 2020;Adhikari and Yin, 2020;Copat et al., 2020;Fattorini and Regoli, 2020;Wu et al., 2020;Zoran et al., 2020;Bourdrel et al., 2021;Andersen et al., 2021;Borro et al., 2020). Among the pollutants studied, COVID-19 mortality appears to be most closely related to PM 2.5 (Copat et al., 2020) and NO 2 (Copat et al., 2020;Fattorini and Regoli, 2020;Ogen, 2020;Guan et al., 2020). ...
The relationship between exposure to air pollution and the severity of coronavirus disease 2019 (COVID-19) pneumonia and other outcomes is poorly understood. Beyond age and comorbidity, risk factors for adverse outcomes including death have been poorly studied. The main objective of our study was to examine the relationship between exposure to outdoor air pollution and the risk of death in patients with COVID-19 pneumonia using individual-level data. The secondary objective was to investigate the impact of air pollutants on gas exchange and systemic inflammation in this disease. This cohort study included 1548 patients hospitalised for COVID-19 pneumonia between February and May 2020 in one of four hospitals. Local agencies supplied daily data on environmental air pollutants (PM10, PM2.5, O3, NO2, NO and NOX) and meteorological conditions (temperature and humidity) in the year before hospital admission (from January 2019 to December 2019). Daily exposure to pollution and meteorological conditions by individual postcode of residence was estimated using geospatial Bayesian generalised additive models. The influence of air pollution on pneumonia severity was studied using generalised additive models which included: age, sex, Charlson comorbidity index, hospital, average income, air temperature and humidity, and exposure to each pollutant. Additionally, generalised additive models were generated for exploring the effect of air pollution on C-reactive protein (CRP) level and SpO2/FiO2 at admission. According to our results, both risk of COVID-19 death and CRP level increased significantly with median exposure to PM10, NO2, NO and NOX, while higher exposure to NO2, NO and NOX was associated with lower SpO2/FiO2 ratios. In conclusion, after controlling for socioeconomic, demographic and health-related variables, we found evidence of a significant positive relationship between air pollution and mortality in patients hospitalised for COVID-19 pneumonia. Additionally, inflammation (CRP) and gas exchange (SpO2/FiO2) in these patients were significantly related to exposure to air pollution.
... Another research that concludes the positive correlation between the COVID-19 mortality and high exposure of PM concentrations are presented in Refs. [48,53]. They analysed that persons living in an areas with high levels of PM2.5 concentrations are more sensitive to developing respiratory and cardiovascular diseases. ...
Low quality of the air is becoming a major concern in urban areas. High values of particulate matter (PM) concentrations and various pollutants may be very dangerous for human health and the global environment. The challenge to overcome the problem with the air quality includes efforts to improve healthy air not only by reducing emissions, but also by modifying the urban morphology to reduce the exposure of the population to air pollution. The aim of this contribution is to analyse the influence of the green zones on air quality mitigation through sensor measurements, and to identify the correlation with the meteorological factors. Actually, the objective focuses on identifying the most significant correlation between PM2.5 and PM10 concentrations and the wind speed, as well as a negative correlation between the PM concentrations and wind speed across different measurement locations. Additionally, the estimation of slight correlation between the PM concentrations and the real feel temperature is detected, while insignificant correlations are found between the PM concentrations and the actual temperature, pressure, and humidity. In this paper the effect of the pandemic restriction rules COVID-19 lockdowns and the period without restriction are investigated. The sensor data collected before the pandemic (summer months in 2018), during the global pandemic (summer months 2020), and after the period with restriction measures (2022) are analysed.
... Neither do they generate the same significant and increasing negative externalities as fossil fuels, which ultimately impair economic performance (Davidson and Andrews, 2013). The consequences of such negative externalities were exemplified clearly during the COVID-19 pandemic, as more stringent lockdown measures, and their associated severe economic impacts, were necessary in locations with higher exposure to air pollution and consequently higher mortality (Conticini et al., 2020;Wu et al., 2020). This has, in turn, brought about calls from expert groups and international organizations such as the World Bank and United Nations Environment Programme for economic recovery plans and investments to be based on renewable energy sources (Sinha, 2020;UNEP, 2020;World Bank, 2020). ...
The human economy is in effect a subsystem of the biosphere. Ecosystems provide natural resources that are fundamental to both societal well-being and economic performance. Here, we show how recovery of national economies from systemic crises can be moderated by the natural resources used to power them. By examining data from 133 systemic economic crisis events in 98 countries over 40 years, we found that countries relying on a broad range of electricity sources experienced extended recovery times from crises, though that effect was tempered somewhat when the relative contribution of those sources was increasingly balanced. However, the best predictor of economic recovery was the extent of reliance on renewable energy-we found that economic recovery tends to be swiftest in countries powered primarily by renewable energy sources. These findings have profound implications for global energy policy and reveal the need to consider both the composition and diversity of energy sources in models of economic resilience.
... It was found that during the breakout of COVID-19 in countries like Italy, Germany, Spain, and France, 78% of the deaths were strongly correlated with the areas with high NO 2 levels (Ogen, 2020). In Northern Italy, deaths due to COVID-19 were tall in regions where the pollution level was most elevated compared to other parts of the nation (Conticini et al., 2020). Many of these studies show that air pollution is the leading cause of the spreading of COVID-19 (Martelletti & Martelletti, 2020). ...
This chapter fundamentally aims at the development of generalized framework encapsulating a wide range of dynamic utility functional and resultant latent choice models. The objectives are served by the application of well cherished exponential family of distributions capable of entertaining numerous probabilistic articulations through a single comprehensive and elegant expression. Moreover, the utility of the proposed scheme is further substantiated by delineating the working pedagogy in accordance with the rapidly embraced Bayesian paradigm. The legitimacy of the devised mechanism in the pursuit of optimal decision-making is advocated with respect to diverse experimental states. We entertained varying extent of worth parameters describing the preference ordering, different sample sizes and distinguished stochastic formations to inject the prior information or historic data in the demonstration of choice behaviors.KeywordsChoice behaviorsLatent choice modelsPrior informationUtility functional
... PM 2.5 is fine inhalable particles with a diameter of 2.5 micrometres or less, which can enter the lungs and permeate the bloodstream. Long-term (months to years) exposure to PM 2.5 may stimulate the immune system, lead to increasing inflammatory response, and cause inflammatory disease, such as asthma, even in those who are young and healthy [4,5]. Chronic respiratory conditions, 2 of 12 like asthma, make sufferers more prone to infection by respiratory viral agents like SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), the causative agent of COVID-19 (coronavirus disease 2019). ...
Evidence suggests an association between air pollutant exposure and worse outcomes for respiratory viral diseases, like COVID-19. However, does breathing polluted air over many years affect the susceptibility to SARS-CoV-2 infection or severity of COVID-19 disease, and how intense are these effects? As climate change intensifies, air pollutant levels may rise, which might further affect the burden of respiratory viral diseases. We assessed the effect of increasing exposure to PM2.5 (particulate matter ≤ 2.5 microns in diameter) on SARS-CoV-2 susceptibility or COVID-19 severity and projected the impact on infections and hospitalisations over two years. Simulations in a hypothetical, representative population show that if exposure affects severity, then hospital admissions are projected to increase by 5–10% for a one-unit exposure increase. However, if exposure affects susceptibility, then infections would increase with the potential for onward transmission and hospital admissions could increase by over 60%. Implications of this study highlight the importance of considering this potential additional health and health system burden as part of strategic planning to mitigate and respond to changing air pollution levels. It is also important to better understand at which point PM2.5 exposure affects SARS-CoV-2 infection through to COVID-19 disease progression, to enable improved protection and better support of those most vulnerable.
... Because the same pattern was observed in China, this co-occurrence of a high number of COVID-19 deaths and high levels of atmospheric pollution contributed to generating the hypothesis that the spread of SARS-CoV-2 and the severity of COVID-19 disease might be enhanced by high atmospheric pollution. [2][3][4] However, most epidemiological studies trying to associate long-term air pollution exposure with SARS-CoV-2 incidence or COVID-19 poor prognosis were based on geographical correlations with low spatial resolution and were not designed to elicit possible causal associations. 5,6 This approach was taken in several large-scale nationwide studies conducted in the United States, England, and Germany that reported associations between average air pollution levels in the years before the pandemic and COVID-19 disease and case fatality. ...
Background:
The role of chronic exposure to ambient air pollutants in increasing COVID-19 fatality is still unclear.
Objectives:
The study aimed to investigate the association between long-term exposure to air pollutants and mortality among 4 million COVID-19 cases in Italy.
Methods:
We obtained individual records of all COVID-19 cases identified in Italy from February 2020 to June 2021. We assigned 2016-2019 mean concentrations of particulate matter (PM) with aerodynamic diameter ≤10μm (PM10), PM with aerodynamic diameter ≤2.5μm (PM2.5), and nitrogen dioxide (NO2) to each municipality (n=7,800) as estimates of chronic exposures. We applied a principal component analysis (PCA) and a generalized propensity score (GPS) approach to an extensive list of area-level covariates to account for major determinants of the spatial distribution of COVID-19 case-fatality rates. Then, we applied generalized negative binomial models matched on GPS, age, sex, province, and month. As additional analyses, we fit separate models by pandemic periods, age, and sex; we quantified the numbers of COVID-19 deaths attributable to exceedances in annual air pollutant concentrations above predefined thresholds; and we explored associations between air pollution and alternative outcomes of COVID-19 severity, namely hospitalizations or accesses to intensive care units.
Results:
We analyzed 3,995,202 COVID-19 cases, which generated 124,346 deaths. Overall, case-fatality rates increased by 0.7% [95% confidence interval (CI): 0.5%, 0.9%], 0.3% (95% CI: 0.2%, 0.5%), and 0.6% (95% CI: 0.5%, 0.8%) per 1 μg/m3 increment in PM2.5, PM10, and NO2, respectively. Associations were higher among elderly subjects and during the first (February 2020-June 2020) and the third (December 2020-June 2021) pandemic waves. We estimated ∼8% COVID-19 deaths were attributable to pollutant levels above the World Health Organization 2021 air quality guidelines.
Discussion:
We found suggestive evidence of an association between long-term exposure to ambient air pollutants with mortality among 4 million COVID-19 cases in Italy. https://doi.org/10.1289/EHP11882.
... This contributed to fuel the hypothesis, which had already arisen after the first cases in China, of an active role of atmospheric pollution in the spread of SARS-CoV-2 infection and the severity of COVID-19 disease. [2][3][4] A large body of evidence on the health impact of air pollution has accumulated over the past few years, documenting that nitrogen dioxide (NO 2 ), particulate matter (PM), ozone, sulphur dioxide (SO 2 ), and carbon monoxide cause irritation, inflammation, and serious infections and diseases to the lungs and airways. 5 Exposure to air pollutants can induce oxidative stress, damaging the respiratory system and reducing the resistance to viral and bacterial infections. ...
Background:
after the outbreak of the SARS-CoV-2 pandemic in 2020, several waves of pandemic cases have occurred in Italy. The role of air pollution has been hypothesized and investigated in several studies. However, to date, the role of chronic exposure to air pollutants in increasing incidence of SARS-CoV-2 infections is still debated.
Objectives:
to investigate the association between long-term exposure to air pollutants and the incidence of SARS-CoV-2 infections in Italy.
Design:
a satellite-based air pollution exposure model with 1-km2 spatial resolution for entire Italy was applied and 2016-2019 mean population-weighted concentrations of particulate matter < 10 micron (PM10), PM <2.5 micron (PM2.5), and nitrogen dioxide (NO2) was calculated to each municipality as estimates of chronic exposures. A principal component analysis (PCA) approach was applied to 50+ area-level covariates (geography and topography, population density, mobility, population health, socioeconomic status) to account for the major determinants of the spatial distribution of incidence rates of SARS-CoV-2 infection. Detailed information was further used on intra- and inter-municipal mobility during the pandemic period. Finally, a mixed longitudinal ecological design with the study units consisting of individual municipalities in Italy was applied. Generalized negative binomial models controlling for age, gender, province, month, PCA variables, and population density were estimated.
Setting and participants:
individual records of diagnosed SARS-2-CoV-2 infections in Italy from February 2020 to June 2021 reported to the Italian Integrated Surveillance of COVID-19 were used.
Main outcome measures:
percentage increases in incidence rate (%IR) and corresponding 95% confidence intervals (95% CI) per unit increase in exposure.
Results:
3,995,202 COVID-19 cases in 7,800 municipalities were analysed (total population: 59,589,357 inhabitants). It was found that long-term exposure to PM2.5, PM10, and NO2 was significantly associated with the incidence rates of SARS-CoV-2 infection. In particular, incidence of COVID-19 increased by 0.3% (95%CI 0.1%-0.4%), 0.3% (0.2%-0.4%), and 0.9% (0.8%-1.0%) per 1 μg/m3 increment in PM2.5, PM10 and NO2, respectively. Associations were higher among elderly subjects and during the second pandemic wave (September 2020-December 2020). Several sensitivity analyses confirmed the main results. The results for NO2 were especially robust to multiple sensitivity analyses.
Conclusions:
evidence of an association between long-term exposure to ambient air pollutants and the incidence of SARS-CoV-2 infections in Italy was found.
... Studies by Chen et al., (2010); ; Peng et al., (2020); Ye et al., (2016) are among them. Some recent research, including studies by Conticini et al., (2020); Nicola et al., (2020); Piazzalunga-Expert, (2020); Wu et al., (2020), focus more on the distribution of COVID-19. ...
The goal of this analysis is to examine in greater detail the effect of the COVID-19 pandemic on economic development and the quality of the atmosphere in Indonesia. This report uses secondary data as the primary source, obtained using a secondary data collection method from many different organizations. Different government policies and measures to discourage the escalation of the transmission of the Coronavirus, one of which is large-scale social restrictions (PSBB). However, before Indonesia suffered a recession, the PSBB actually became a barrier to economic development. As a part of this program, the rise in environmental efficiency is another positive effect because traffic that generates emissions and vast manufacturing sectors that create dirty waste is temporarily halted. Based on the findings of the review, this report notes that there is a detrimental effect of COVID-19 on economic development in Indonesia. However, because of the introduction of PSBB, Indonesia's air quality has improved. This report is intended to serve as a reference and assessment of the effects of COVID-19 on the economy and the atmosphere for stakeholders and the general public. In order to allow the government to consider measures that will deter the spread of the coronavirus and restore the economy without damaging improved air quality.
... Hence, The link between the amount of air pollution and the lethality associated with Covid-19 is positive, indicating that the air pollution is the fundamental and secret factor in escalating the worldwide burden of deaths associated with Covid-19 (Gupta, 2021). Long term exposure to the poor air quality Asian Journal of Research in Education and Social Sciences e- ISSN: 2682-8502 | Vol. 5, No. 1, 21-29, 2023 will increase the risks of Covid-19 infection (Travaglio, 2021) which supported by recent studies conducted in northern Italy (Conticini et al., 2020), Europe (Cole et al., 2020;Ogen, 2020), and the USA (Liang et al., 2020;. ...
With the growth of population and migration, the population density is growing. In high population density area, it found that the air spread virus spread rapidly. Covid-19 cases are actively happening in Malaysia and government is implement movement control to avoid the human traffic and reduce the infected case. In metropolis, such as Petaling district with more strata development, it found that the infected cases are higher than other district. Therefore, to study the relationship between air spread virus and density, this paper employed the regression analysis by collected the infected case and death case of Covid-19 from 25/1/2020 to 31/5/2022 as sample for this paper. From the result, it found that there is significant relationship between air spread virus and density. Thus, it is crucial to re-access the current density ratio for future development to prevent the air spread virus.
While many terms are usually associated with suspended matter in the air, airborne particles or particulate matter (PM) generally refer to solid particles that may be composed of multiple phases (e.g., solids, liquid droplets, etc.). Airborne particles vary extensively in physical and chemical characteristics; their sizes can vary from tens of micrometers, that is, slightly smaller than beach sand or hair, to tens of nanometers. Solid airborne particles have been historically related to a wide range of occupational diseases such as various types of pneumoconioses (e.g., “black lung disease”), as well as less occupationally targeted respiratory illnesses such as acute respiratory irritation, asthma, or lung cancer. This chapter outlines airborne particles, its adverse health effects to workers in ( 1 ) areas with targeted production of particles and ( 2 ) in areas where exposure to ambient pollution is inevitable. This chapter presents metrics, techniques, exposure assessments, and biomarkers used for particulate measurements and routine monitoring. Also summarized in this chapter: its toxicity, mechanisms of attack, and carcinogenicity. Lastly, it tabulates existing standards both for the ambient and workplace and outlined some of the existing removal and control technologies. The ubiquity of airborne particles—from outdoor jobs, such as construction and firefighting, to indoor occupations, such as healthcare and custodial jobs, make it a central issue that is necessary to be addressed in any workplace area.
During the past few decades various symptoms and illnesses have been increasingly attributed to nonindustrial indoor environments. In general, indoor exposure to noxious chemical, physical, and biological hazards occur at low levels, however, such indoors exposition are very common (Seltzer, 1994: pp. 318-326). Symptoms such as drowsiness, headache, fatigue, burning eyes and breathing difficulties are signs that could indicate a high percentage of pollutants in the indoor environment, although we often tend to attribute them to other causes. This phenomenon which causes disease is called - sick building syndrome - (SBS) and it is a growing problem (Carrie A Redlich, 1997: pp. 1013-1016). SBS has been reported with increasing frequency since the 1970s, as older, naturally ventilated buildings have been replaced by more energy efficient, “airtight” buildings. SBS was frequently associated with workplaces, where the employees work together and spend most of their time. However, in this pandemic and post-pandemic situation, the smart working, and the greater crowding of living spaces, could cause this problem to arise even in private homes. Now, in the framework of COVID, it has become even more necessary to look closely at the quality of the air in homes. Indeed we spend more and more time inside enclosed and shared places, where the air can be much more polluted than outside. At home and office, we are surrounded, and we daily breathe dangerous but invisible substances, which penetrate our body without being noticed. In order to propose the best house's construction and rebuilding solutions, this review considers the contamination sources that can cause diseases in the house's environment. The innovative approach, based on the complexity of the problem, it focuses attention about the different factors in order to reduce the indoor air pollutions. Finally, having identified the factors that play a significant role in environmental indoor house's contamination, a clear picture should emerge to draw conclusions and propose the best buildings solutions. Based on the complexity of the problem and the need for interdisciplinary research.
Brazil has experienced one of the highest COVID-19 fatality rates globally. While numerous studies have explored the potential connection between air pollution, specifically fine particulate matter (PM 2.5 ), and the exacerbation of SARS-CoV-2 infection, the majority of this research has been conducted in foreign regions—Europe, the United States, and China—correlating generalized pollution levels with health-related scopes. In this study, we aim to delve into the localized relationship between air pollution exposure and its health implications within a specific Brazilian municipality, focusing on COVID-19 susceptibility. Our investigation involves assessing pollution levels through spatial interpolation of in-situ PM 2.5 measurements. A network of affordable sensors collected data across 9 regions in Curitiba, as well as its metropolitan counterpart, Araucaria. Our findings distinctly unveil a significant positive correlation (r up to 0.36, p-value < 0.01) between more polluted areas, even more pronounced during winter months (r up to 0.40, p-value < 0.05), with both COVID-19 mortality and incidence rates. This correlation gains added significance due to the intricate interplay between urban atmospheric pollution and regional human development indexs. Notably, heightened pollution aligns with industrial hubs and intensified vehicular activity. The spatial analysis performed in this study assumes a pivotal role by identifying priority regions that require targeted action post-COVID. By comprehending the localized dynamics between air pollution and its health repercussions, tailored strategies can be implemented to alleviate these effects and ensure the well-being of the public.
Cet article s’intéresse aux effets de la pollution atmosphérique sur les taux d’incidence et de surmortalité liés à la COVID-19 dans 96 départements français. L’analyse exploratoire montre une certaine hétérogénéité et autocorrélation spatiale du virus et de ses conséquences. Nos résultats indiquent d’une part, que la pollution atmosphérique joue un rôle de catalyseur du taux d’incidence, toutefois, ces particules fines (PM2,5) ne présentent pas d’effets significatifs sur le taux de surmortalité. D’autre part, la taille et la part des résidences principales dans l’offre de logements départementale ainsi que la densité démographique impactent significativement le taux d’incidence. JEL classification: I10, Q53, R11, R12, R15.
Public health is now seriously threatened by the COVID-19 outbreak. COVID-19 infections have spread to most countries, but certain regions have had more infections and casualties than others. It is yet unclear what causes these variances specifically. This motivates us to investigate, the association between air pollutants, metrological indices, and COVID-19 cases and deaths. We collected the daily air pollution, metrological and COVID-19 infected cases data and predicted the respiratory casualty. In this study, we assess the impact of air pollution and the metrological indicators on the respiratory infection casualty. First, we assessed how air pollution and metrological parameters correlate to respiratory infection transmission. Our findings highlight that temperature, wind speed, and particulate matter (PM2.5) positively correlate to respiratory virus transmission. In this study, an Enhanced Regularization Function in the Artificial neural networks (ERF-ANN) model predicts respiratory casualty. The ERF-ANN model was found to have minimal errors when predicting respiratory casualties over the rest. We conclude that respiratory infection transmission prefers low temperatures and polluted air. This system will alert chronic patients early based on their environment, and all disease groups will be notified.
Imposing stricter regulations for PM2.5 has the potential to mitigate damaging health and climate change effects. Recent evidence establishing a link between exposure to air pollution and COVID-19 outcomes is one of many arguments for the need to reduce the National Ambient Air Quality Standards (NAAQS) for PM2.5. However, many studies reporting a relationship between COVID-19 outcomes and PM2.5 have been criticized because they are based on ecological regression analyses, where area-level counts of COVID-19 outcomes are regressed on area-level exposure to air pollution and other covariates. It is well known that regression models solely based on area-level data are subject to ecological bias, i.e., they may provide a biased estimate of the association at the individual-level, due to within-area variability of the data. In this paper, we augment county-level COVID-19 mortality data with a nationally representative sample of individual-level covariate information from the American Community Survey along with high-resolution estimates of PM2.5 concentrations obtained from a validated model and aggregated to the census tract for the contiguous United States. We apply a Bayesian hierarchical modeling approach to combine county-, census tract-, and individual-level data to ultimately draw inference about individual-level associations between long-term exposure to PM2.5 and mortality for COVID-19. By analyzing data prior to the Emergency Use Authorization for the COVID-19 vaccines we found that an increase of 1 μg/m3 in long-term PM2.5 exposure, averaged over the 17-year period 2000-2016, is associated with a 3.3% (95% credible interval, 2.8 to 3.8%) increase in an individual's odds of COVID-19 mortality. Code to reproduce our study is publicly available at https://github.com/NSAPH/PM_COVID_ecoinference. The results confirm previous evidence of an association between long-term exposure to PM2.5 and COVID-19 mortality and strengthen the case for tighter regulations on harmful air pollution and greenhouse gas emissions.
The effect of the ambient air quality on the COVID-19 pandemic is a topic that has attracted much attention and still remains of current interest. The study area of Turkey is one of the countries with high case numbers, but there is no detailed investigation dealing with it in the literature. For this reason, the correlation and nexus between COVID-19 cases and deaths in Turkey with the air pollutants of PM 10 , PM 2.5 , SO 2 , CO, NO 2 and O 3 were determined between 1 April and 31 July 2021 using the statistical methods of correlation and wavelet coherence analysis. According to the findings, for the COVID-19 pandemic parameters, there were positive significant correlations with PM 2.5 , SO 2 , CO, and NO 2 and an inverse significant correlation with O 3 . Wavelet transform coherence revealed that air pollution, which has significant effects on human life, was one of the main determinants of the spread and mortality linked to the pandemic. Additionally, it is notable that the national air quality improved during full lockdown periods in the country. The findings obtained in this study are expected to attract the attention of legislating and enforcing authorities and support more decisive steps being taken to reduce environmental pollutants and to control air pollution.
The viral agent is known as beta-corona virus, a common human-animal virus similar to other coronaviruses (SARS and MERS), and known as Middle East Respiratory Syndrome. COVID-19 causes Acute Respiratory Syndrome (SARS), specifically called SARSCoV-2. Improper coexistence of the human intestinal microbiome has been associated with a variety of diseases, including respiratory tract infections through the intestinal tract and lungs. Some studies show that there is a connection between the gut and the lungs, and to some extent the symptoms may be altered by probiotics, thus altering gastrointestinal symptoms optimally and also protecting the respiratory system. Due to the reported ability of various probiotic strains to improve mucosal immunity against pathogens, possible effects in the prevention and treatment of respiratory infections have been suggested. Increased evidence supports the link between the gut and the lungs, so studies should be performed to investigate the possible role of probiotics in reducing COVID-19, either through immune regulatory measures on systemic inflammation or through direct interaction with the lungs. More to be done.
In urban areas around the world, air pollution introduced by vehicular movement is a key concern. However, restricting vehicular traffic during the COVID-19 shutdown improved air quality to some extent. This study was conducted out in the smart city of Bhubaneswar, which is also the state capital of Odisha, India. The study has tried to map Bhubaneswar by collecting the air quality data before, during, and after the COVID lockdown of six air quality monitoring stations present in Bhubaneswar established under “National Ambient Air Monitoring Program” (NAMP). Furthermore, plants, which are the most vulnerable to air pollution, can show a variety of visible changes depending on their level of sensitivity. Moreover, leaves of Mangifera indica, Monoon longifolium, Azadirachta indica, Millettia pinnata, Aegle marmelos were collected from nearby of six air monitoring stations to assess the “Air Pollution Tolerance Index.” M. indica was found to be intermediately tolerant, and all of the other species were found to be sensitive. The structural equation modeling results also revealed a significant relationship between total chlorophyll content, relative water content, ascorbic acid content, leaf extract pH, APTI with species, air quality index, and PM10.
Cities are widely recognized as environments which can present risks to humans. Risks to health and well-being are measured in three groups of indices: physiological, emotional, and cognitive. The environmental factors discussed in studies include physical factors such as noise, heat load, and air pollution, and social factors include feelings of discomfort, crime, transportation, and access to health services. Some studies even argue that stress and health risks are intrinsic to urban environments and that restoration is intrinsic to green environments. This Topic aims to discuss what spaces can be greened and the effect this has on urban environments. It also discusses the effect of the size and layout of parks, vegetation on the walls and roofs of houses, and the effects of different types of vegetation, building materials, and energy-efficient design. Today’s environment demands new design processes, construction techniques, occupancy practices, and management strategies to increase the resilience of the built environment to extreme, uncontrollable, and unpredictable events while providing healthy and sustainable environments for people. This Topic reflects on what the new concept of sustainability for the built environment should be and how to guide new research directions.
Starting from February 2020, Italy was the first among the European countries, to experience dramatic rises in daily COVID-19 deaths and contagions. An important aspect that distinguished the first COVID-19 wave (Feb-Jun 2020) from the following waves of infection in Italy was the sheer imbalance, in terms of deaths and contagion, between Northern and Southern regions of the country. Despite the fact that the South was far less hit by the disease, a series of narratives that associated the spread of the epidemic with some sort of Southern infector started to appear, conveyed by social media posts, news pieces, talk shows, and even football banners. In this chapter, there is an attempt to identify and critically analyse the discourses that inscribe a characteristic “Southernification” of the pandemic in Italy, that is a partial and symbolic attempt to (1) discursively transfer the infection to the South; and/or (2) hand over the responsibilities that are behind the particularly violent first wave of infections in the country to Southern communities, polities, and cultural practices.
Background: The SARS-CoV-2 pandemic has highlighted the risk of infection in long-term care facilities (LTCF) and the vulnerability of residents to severe outcomes. Environmental surveillance may help detect pathogens early and inform Infection Prevention and Control (IPC) measures in these settings.
Methods: Upon notification of SARS-CoV-2 outbreaks, LTCF within a local authority in South West England were approached to take part in this pilot study. Investigators visited to swab common touch-points and elevated ‘non-touch’ surfaces (>1.5m above ground level) and samples were analysed for presence of SARS-CoV-2 genetic material (RNA). Data were collected regarding LTCF infrastructure, staff behaviours, clinical and epidemiological risk factors for infection (staff and residents), and IPC measures.
Criteria for success were: recruitment of three LTCF; detection of SARS-COV-2 RNA; variation in proportion of SARS-CoV-2 positive surfaces by sampling zone; and collection of clinical and epidemiological data for context.
Results: Three LTCFs were recruited, ranging in size and resident demographics. Outbreaks lasted 63, 50 and 30 days with resident attack rates of 53%, 40% and 8%, respectively. The proportion of sample sites on which SARS-CoV-2 was detected was highest in rooms occupied by infected residents and varied elsewhere in the LTCF, with low levels in a facility implementing enhanced IPC measures. The heterogeneity of settings and difficulty obtaining data made it unfeasible to assess association between environmental contamination and infection. A greater proportion of elevated surfaces tested positive for SARS-CoV-2 RNA than common touch-points.
Conclusions: SARS-CoV-2 RNA can be detected in a variety of LTCF outbreak settings, both on common-touch items and in elevated sites out of reach. This suggests that further work is justified, to assess feasibility and utility of environmental sampling for infection surveillance in LTCF.
Coronavirus is airborne and can spread easily. Air pollution may have an impact on breathing and also keep the virus airborne. The levels of air pollution were impacted by the lockdown measures, restricting the vehicular and industrial pollutants. Therefore, there is a need to understand the relation between air pollution levels and the Coronavirus infection rate. The study aims to find the effect of various pollutants across major cities of India on the R-value. The pollution data was collected from the Government’s official portal. The major pollutants on which the data was collected are “PM2.5, PM10, NO, NO2, NOx, SO2, CO, and Ozone”. The data on air pollution levels were also collected for the selected cities from April 2020 to April 2021. The spread is measured as the reproduction number at time ‘t’ (Rt), which is an estimate of infectious disease transmissibility throughout an outbreak, or it is the rating of Coronavirus or any disease’s ability to spread. The data is analysed using MS Excel and R Programming. Descriptive statistics and regularisation are performed on the data. The study results reveal that some pollutants positively and negatively affect the infection rate. However, the effect is very low, and it concluded that the pollution might not directly affect infection rates.KeywordsAir pollutionCOVID-19Economic activityPopulation densityInfection ratePM2.5PM10NO2NOxSO2CONOOzone
Coronavirus-2 (SARS-CoV-2), which is an infectious coronavirus disease, has become a world of concern since the end of 2019. Emerging studies have found that there are many factors that could impact the transmission of coronavirus. Climate change has been a world of concern over centuries. It is inevitable to discover the connections between COVID-19 transmission and climate factors. Some researchers have conducted studies on the relationship mainly in the Northern Hemisphere during the early COVID19 period. As COVID-19 is evolving all the time, we want to discover the relationship from a relatively long-time range in the Southern Hemisphere – New South Wales in Australia in specific. We used a Linear regression model and generalized additive model (GAM) to estimate the interaction of meteorological, air pollutants variables and COVID-19 cases. We found that Temperature at 9 a.m., PM2.5 and PM10 have a positive relationship with covid whereas Relative humidity at 3 p.m., NO, Temperature at 3 p.m. and NO2 have a negative relationship with Covid case number. A better understanding of the relationship does good to generating better pandemic response initiatives and surveillance and could be a reference to other religions.KeywordsClimate changeCovid-19 transmissionAir emissionsRelative humidityTemperature
United Nations Scientific Committee on the Effects of 2006 report was the first document released by an abandoned the classical paradigm that ionizing suppressive, considering the idea that at low doses enhances the appearance of antiinflammatory biomarkers [UNSCEAR 2006]. It considers energetic an immune modulation agent due to the multitude the innate immune system, depending on various age, health status, co-morbidities, genetic background, co-stressors [Lumniczky et al.]. Natural background radiation is the most hazardous public health, followed by medical imaging as a close Naturally occurring radionuclides attach to particulate ionizing radiation after inhalation and deposition in the in this article that exposure to particle radioactivity of inflammation. With that purpose, we have done an on common anti-inflammatory biomarkers between cases on COVID-19 elderly patients, and those found low-intensity natural ionizing radiation in locations with hypothesize that radioactivity increases biomarkers of strategy involved the use of databases from PubMed, (e.g., dose response, hormesis, J-shaped, NLRP3 LNT model, etc.). Extrapolating these effects to artificial ionizing radiation drawn conclusions on the over use of X-ray computed images in elderly ICU admitted patients with pulmonary oxygen species (ROS) generation by this action seems inflammation of leucine-rich protein 3 (NLRP3) inflammasome, waking up an over cytokine production.
Accurate forecasting of regional electrical grid carbon emissions is an essential part of demand response programs for emissions reduction. Most existing research for short-term (day ahead) forecasting focuses on the use of variations of recurrent neural networks, in particular, the Long–Short Term Memory (LSTM) cells. This research proposes a Particle Swarm Optimised-extremely randomised trees (PSO-ERT) regressor model for day ahead forecasting of the emissions intensity of the Australian National Electricity Market (NEM). The PSO-ERT model is compared with LSTM, another method known as Extreme Learning Machine (ELM), and also with two classic machine learning algorithms, Multi-layer perceptron (MLP) and Decision Tree (DT). Models are trained using 1.5 years of weather, demand and generation data collected from the five NEM regions. Results show that the ERT model performs better than both LSTM and ELM with Root Mean Squared Error (RMSE) of 42.9, 109.8, 165.7, 25.4 and 74.1 for New South Wales, Tasmania, South Australia, Queensland and Victoria, respectively. For all models, forecasting performance was better for regions with less renewable generation and for times when renewable generation was a smaller percentage of demand suggesting that the addition of weather forecasts in the predictor feature set would further improve performance.
The coronavirus disease 2019 (COVID-19) pandemic has resulted in numerous cases of illness and death worldwide. Research has shown that there are associations between transmission, as well as the severity of SARS-CoV‑2 (severe acute respiratory syndrome coronavirus 2) infections, and various environmental factors. For example, air pollution with particulate matter is thought to play a crucial role, and both climatic and geographical aspects must be considered. Furthermore, environmental conditions such as industry and urban lifestyle have a significant impact on air quality and thus on health aspects of the population. In this regard, other factors such as chemicals, microplastics, and diet also critically impact health, including respiratory and cardiovascular diseases. Overall, the COVID-19 pandemic has highlighted how closely health and the environment are linked. This review discusses the impact of environmental factors on the COVID-19 pandemic.
Background:
In December 2019, coronavirus disease 2019 (COVID-19) emerged in Wuhan and rapidly spread throughout China.
Methods:
Demographic and clinical data of all confirmed cases with COVID-19 on admission at Tongji Hospital from January 10 to February 12, 2020, were collected and analyzed. The data of laboratory examinations, including peripheral lymphocyte subsets, were analyzed and compared between severe and non-severe patients.
Results:
Of the 452 patients with COVID-19 recruited, 286 were diagnosed as severe infection. The median age was 58 years and 235 were male. The most common symptoms were fever, shortness of breath, expectoration, fatigue, dry cough and myalgia. Severe cases tend to have lower lymphocytes counts, higher leukocytes counts and neutrophil-lymphocyte-ratio (NLR), as well as lower percentages of monocytes, eosinophils, and basophils. Most of severe cases demonstrated elevated levels of infection-related biomarkers and inflammatory cytokines. The number of T cells significantly decreased, and more hampered in severe cases. Both helper T cells and suppressor T cells in patients with COVID-19 were below normal levels, and lower level of helper T cells in severe group. The percentage of naïve helper T cells increased and memory helper T cells decreased in severe cases. Patients with COVID-19 also have lower level of regulatory T cells, and more obviously damaged in severe cases.
Conclusions:
The novel coronavirus might mainly act on lymphocytes, especially T lymphocytes. Surveillance of NLR and lymphocyte subsets is helpful in the early screening of critical illness, diagnosis and treatment of COVID-19.
Mucociliary epithelium lining the upper and lower respiratory tract constitutes the first line of defense of the airway and lungs against inhaled pollutants and pathogens. The concerted beating of multiciliated cells drives mucociliary clearance. Abnormalities in both the structure and function of airway cilia have been implicated in obstructive lung diseases. Emerging evidence reveals a close correlation between lung diseases and environmental stimuli such as sulfur dioxide and tobacco particles. However, the underlying mechanism remains to be described. In this review, we emphasize the importance of airway cilia in mucociliary clearance and discuss how environmental pollutants affect the structure and function of airway cilia, thus shedding light on the function of airway cilia in preventing obstructive lung diseases and revealing the negative effects of environmental pollutants on human health.
Exposure to particulate matter ≤2.5 µm in diameter (PM2.5) profoundly affects human health. However, the role of PM2.5 on lung injury and cytokine levels in mice is currently unknown. The aim was to examine the effect of PM2.5 pollution on lung injury in mice fed at an underground parking lot. A total of 20 female Kunming mice were randomly divided into control and polluted groups, with 10 rats in each group. The control group was kept in the laboratory, while the pollution group was fed in an underground parking lot. The concentrations of pollutants were measured using ambient air quality monitoring instruments. After 3 months of treatment, the lungs were collected and examined using electron microscopy, and the morphological structures were assessed using hematoxylin and eosin staining. The polarization of macrophages was evaluated by immunofluorescence. The concentration of interleukin (IL)-4, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 in peripheral sera were assessed by ELISA. The mRNA and protein levels of IL-4, TNF-α, and TGF-β1 in lung tissues were assessed by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. In the polluted group, the levels of CO, NOx and PM2.5 were significantly higher compared with the control group. Compared with the controls, intracellular edema, an increased number of microvilli and lamellar bodies, smaller lamellar bodies in type II alveolar epithelial cells, and abundant particles induced by PM2.5 in macrophages were observed in the polluted group. The lung ultrastructure changed in the polluted group, revealing exhaust-induced lung injury: The tissues were damaged, and the number of inflammatory cells, neutrophils, polylymphocytes and eosinophils increased in the polluted group compared with the control group. The authors also observed that the number of M1 and M2 macrophages markedly increased after the exhaust treatment. The levels of IL-4, TNF-α and TGF-β1 in the sera and tissues were significantly increased in the polluted group. PM2.5 pollutants in underground garages can lead to lung injury and have a significant impact on the level of inflammatory cytokines in mice. Therefore, the authors suggest that PM2.5 can activate the inflammatory reaction and induce immune dysfunction, leading to ultrastructural damage.
The effect of particulate matter (PM) on health increases with exposure duration but the change from short to longer term is not well studied. We examined the exposure to PM smaller 10 μm (PM10) from short to longer duration and their associations with levels of inflammatory markers in the population-based CoLaus cohort in Lausanne, Switzerland. Baseline and follow-up CoLaus data were used to study the associations between PM10 exposure and inflammatory markers, including the high-sensitivity C-reactive protein (CRP), as well as interleukin 1-beta (IL-1β), interleukin 6 (IL-6), and tumor-necrosis-factor alpha (TNF-α) using mixed models. Exposure was determined for each participant’s home address from hourly air quality simulations at a 5-m resolution. Short-term exposure intervals were 1 day, 1 week, and 1 month prior to the hospital visit (blood withdrawal); long-term exposure intervals were 3 and 6 months prior to the visit. In most time windows, IL-6, IL-1β, and TNF-α were positively associated with PM10. No significant associations were identified for CRP. Adjusted associations with long-term exposures were stronger and more significant than those for short-term exposures. In stratified models, gender, age, smoking status, and hypertension only led to small modifications in effect estimates, though a few of the estimates for IL-6 and TNF-α became non-significant. In this general adult cohort exposed to relatively low average PM10 levels, clear associations with markers of systemic inflammation were observed. Longer duration of elevated exposure was associated with an exacerbated inflammatory response. This may partially explain the elevated disease risk observed with chronic PM10 exposure. It also suggests that reducing prolonged episodes of high PM exposure may be a strategy to reduce inflammatory risk.
Previous studies have shown that exposure to particulate matter (PM) increased variety of health problems, particularly cardiovascular diseases leading to premature mortality. The cardiac effects of particulate matter containing PM10 include increased infarct size, decreased heart function, and increased arrhythmias in experimental ischemia-reperfusion models in rats. The aim of this study was to evaluate the effects of particles with an aerodynamic diameter smaller than 10 μm (PM10) on isolated-rat heart and also to determine the efficacy of gallic acid (GA) as a preventive agent in oxidative damage. The healthy rats were divided into 8 equal groups which served as, control, GA, PM10 (0.5, 2.5, and 5 mg/kg), and PM10+GA groups. PM10 administered into the lungs via the trachea in two stages with 48-h interval. After all experiments, the electrocardiogram was recorded. Then, the hemodynamic parameters and ventricular arrhythmias in rat isolated-hearts were assessed using Langendorff apparatus and according to the Lambeth conventions. In addition, the inflammation and oxidative stress factors in cardiac tissues were evaluated in all groups. The obtained results showed that the exposure to PM caused to decrease in cardiac hemodynamic and electrocardiogram parameters. Also, in PM10 rat groups, the IL-6, TNF-α, and oxidative stress parameters were increased. Gallic acid preserved the value of cardiac parameters and inflammation in rat hearts. In summary, we added a novel therapeutic effect of gallic acid for cardiac dysfunction induced by particulate matter. These findings could be related to antioxidant and antiinflammation properties and the obtained results suggest that natural antioxidant like gallic acid could be a therapeutic agent in prevention and management of health issues in the polluted areas of the world.
Increased proinflammatory interleukin-6 (IL-6) levels are associated with acquired long QT-syndrome (LQTS) in patients with systemic inflammation, leading to higher risks for life-threatening polymorphic ventricular tachycardia such as Torsades de Pointes. However, the functional and molecular mechanisms of this association are not known. In most cases of acquired LQTS, the target ion channel is the human ether-á-go-go-related gene (hERG) encoding the rapid component of the delayed rectifier K current, IKr, which plays a critical role in cardiac repolarization. Here, we tested the hypothesis that IL-6 may cause QT prolongation by suppressing IKr. Electrophysiological and biochemical assays were used to assess the impact of IL-6 on the functional expression of IKr in HEK293 cells and adult guinea-pig ventricular myocytes (AGPVM). In HEK293 cells, IL-6 alone or in combination with the soluble IL-6 receptor (IL-6R), produced a significant depression of IKr peak and tail current densities. Block of IL-6R or Janus kinase (JAK) reversed the inhibitory effects of IL-6 on IKr. In AGPVM, IL-6 prolonged action potential duration (APD) which was further prolonged in the presence of IL-6R. Similar to heterologous cells, IL-6 reduced endogenous guinea pig ERG channel mRNA and protein expression. The data are first to demonstrate that IL-6 inhibition of IKr and the resulting prolongation of APD is mediated via IL-6R and JAK pathway activation and forms the basis for the observed clinical QT interval prolongation. These novel findings may guide the development of targeted anti-arrhythmic therapeutic interventions in patients with LQTS and inflammatory disorders.
Acute respiratory distress syndrome (ARDS) is the most advanced form of acute lung injury (ALI). This is characterized by bilateral pulmonary infiltrates and severe hypoxemia. According to Berlin definition of ARDS, this is defined based on the timings, radiographic changes, edema formation, and severity on the PaO2/FiO2 ratio. During ARDS, the loss of integrity of the epithelium causes the septic shock. The degree of epithelial injury is the major prognostic marker of ARDS. In addition to this, inflammatory cell migration, fibro-proliferation, and activation of apoptosis also play an important role in the pathophysiology of ARDS. The alveolar epithelial cell is the prime target during injury where this cell either undergo apoptosis or epithelial–mesenchymal transition (EMT). Injury to the AECs triggers the changes in the DNA fragmentation and activation of certain apoptotic markers such as caspases at the same time some cells undergo biochemical changes and loses its epithelial morphology as well epithelial biomarkers and gain mesenchymal biomarkers and morphology. In both the cases, the fibrinolytic system plays an important role in maintaining the integrity of the disease process efficiently. This review highlights the research evidence of apoptosis and EMT in lung development, injury and its prognosis in ARDS thereby to develop an effective strategy for the treatment of ARDS.
Background
Experimental and controlled human exposure studies have demonstrated additive effects of ambient particulate matter and ozone on health. A few epidemiological studies have suggested that ambient particulate matter components are important for the combined effects of ambient particulate matter and ozone on health. However, few studies have examined whether ozone changes the effects of ambient particulate matter on pro-inflammatory cytokine production. In this study, the influence of ozone on pro-inflammatory cytokine production in response to ambient particulate matter was evaluated.
Results
Ambient particulate matter smaller than 1 μm was collected and the suspension of this particulate matter was bubbled through 0.12 ppm and 0.24 ppm ozone. THP1 cells were stimulated by the solution containing the particulate matter with and without bubbling through ozone at 1 μg/mL. The interleukin-8 concentrations in the supernatants of THP1 cells stimulated by collected particulate matter dissolved in solution were 108.3 ± 24.7 pg/mL without ozone exposure, 165.0 ± 26.1 pg/mL for 0.12 ppm ozone bubbling for 1 min, 175.1 ± 33.1 pg/mL for 0.12 ppm for 5 min, 183.3 ± 17.8 pg/mL for 0.12 ppm for 15 min, 167.8 ± 35.9 pg/mL for 0.24 ppm for 1 min, 209.2 ± 8.4 pg/mL for 0.24 ppm for 5 min, and 209.3 ± 14.3 pg/mL for 0.24 ppm for 15 min. Ozone significantly increased interleukin-8 concentrations compared to those for particulate matter dissolved in solution without ozone exposure and the solvent only (8.2 ± 0.9 pg/mL) in an ozone concentration-dependent manner. Collected particulate matter in solutions with or without bubbling through ozone had no effect on interleukin-6 production. The antioxidant N-acetyl-L-cysteine significantly inhibited the increases in interleukin-8 induced by solutions with particulate matter, regardless of ozone exposure. The reactive oxygen species concentration in solutions with collected particulate matter was not associated with ozone bubbling.
Conclusion
Ozone may augment the production of interleukin-8 in response to ambient particulate matter by a mechanism unrelated to reactive oxygen species. These results support the epidemiological evidence for combined effects of ambient particulate matter and ozone on human health.
Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO2) exposure (as a marker of traffic-related air pollution) and pro-inflammatory cytokines, and investigated effect modification and mediation by post-bronchodilator airflow obstruction (post-BD-AO) and cardiovascular risk. Data from middle-aged participants in the Tasmanian Longitudinal Health Study (TAHS, n = 1389) were analyzed by multivariable logistic regression, using serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) as the outcome. Mean annual NO2 exposure was estimated at residential addresses using a validated satellite-based land-use regression model. Post-BD-AO was defined by post-BD forced expiratory ratio (FEV1/FVC) < lower limit of normal, and cardiovascular risk by a history of either cerebrovascular or ischaemic heart disease. We found a positive association with increasing serum IL-6 concentration (geometric mean 1.20 (95% CI: 1.1 to 1.3, p = 0.001) per quartile increase in NO2). This was predominantly a direct relationship, with little evidence for either effect modification or mediation via post-BD-AO, or for the small subgroup who reported cardiovascular events. However, there was some evidence consistent with serum IL-6 being on the causal pathway between NO2 and cardiovascular risk. These findings raise the possibility that the interplay between air pollution and systemic inflammation may differ between post-BD airflow obstruction and cardiovascular diseases.
Background
Patients with severe traumatic brain injury (TBI) are at risk of the development of acute respiratory distress syndrome (ARDS). TBI and ARDS pathophysiologic mechanisms are known to independently involve significant inflammatory responses. The literature on the association between plasma inflammatory cytokines and ARDS in patients with TBI is sparse. Methods
The study was a secondary analysis of the safety of a randomized trial of erythropoietin and transfusion threshold in patients with severe TBI. Inflammatory markers within the first 24 hours after injury were compared in patients who developed ARDS and patients without ARDS, using Cox proportional hazards models. ResultsThere were 200 patients enrolled in the study. The majority of plasma and cerebrospinal fluid (CSF) cytokine levels were obtained within 6 hours. Plasma proinflammatory markers IL-6 and IL-8 and anti-inflammatory marker IL-10 were associated with the development of ARDS (adjusted hazard ratio (HR) = 1.55, confidence interval (CI) = 1.14, 2.11, P = 0.005 for IL-6; adjusted HR = 1.32, CI = 1.10, 1.59, P = 0.003 for IL-8). Conclusion
Plasma markers of IL-6, IL-8, and IL-10 are associated with ARDS in patients with severe TBI. Trial registrationNCT00313716 registered 4/2006
Despite the ongoing spread of MERS, there is limited knowledge of the factors affecting its severity and outcomes. We analyzed clinical data and specimens from fourteen MERS patients treated in a hospital who collectively represent a wide spectrum of disease severity, ranging from mild febrile illness to fatal pneumonia, and classified the patients into four groups based on severity and mortality. Comparative and kinetic analyses revealed that high viral loads, weak antibody responses, and lymphopenia accompanying thrombocytopenia were associated with disease mortality, whereas persistent and gradual increases in lymphocyte responses might be required for effective immunity against MERS-CoV infection. Leukocytosis, primarily due to increased neutrophils and monocytes, was generally observed in more severe and fatal cases. The blood levels of cytokines such as IL-10, IL-15, TGF-β, and EGF were either positively or negatively correlated with disease mortality. Robust induction of various chemokines with differential kinetics was more prominent in patients that recovered from pneumonia than in patients with mild febrile illness or deceased patients. The correlation of the virological and immunological responses with disease severity and mortality, as well as their responses to current antiviral therapy, may have prognostic significance during the early phase of MERS.
Ozone is a common environmental air pollutant leading to respiratory illness. The mechanisms regulating ozone-induced airway inflammation remain poorly understood. We hypothesize that ozone-triggered inflammasome activation and interleukin (IL)-1 production regulate neutrophilic airway inflammation through IL-17A. Pulmonary neutrophilic inflammation was induced by extended (72 h) low-dose (0.7 ppm) exposure to ozone. IL-1 receptor 1 (Il1r1)−/−, Il17a−/− mice and the caspase-1 inhibitor acetyl-YVAD-chloromethylketone (Ac-YVAD-cmk) were used for in vivo studies. Cellular inflammation and protein levels in bronchial alveolar lavage fluid (BALF), cytokines, and IL-17A-producing γδT-cells, as well as mitochondrial reactive oxygen species (ROS), mitochondrial DNA (mtDNA) release, and inflammasome activation in lung macrophages were analyzed. Ozone-induced neutrophilic airway inflammation, accompanied an increased production of IL-1β, IL-18, IL-17A, Granulocyte-colony stimulating factor (G-CSF), Interferon-γ inducible protein 10 (IP-10) and BALF protein in the lung. Ozone-induced IL-17A production was predominantly in γδT-cells, and Il17a-knockout mice exhibited reduced airway inflammation. Lung macrophages from ozone-exposed mice exhibited higher levels of mitochondrial ROS, enhanced cytosolic mtDNA, increased caspase-1 activation, and higher production of IL-1β. Il1r1-knockout mice or treatment with Ac-YVAD-cmk decreased the IL-17A production and subsequent airway inflammation. Taken together, we demonstrate that ozone-induced IL-17A and neutrophilic airway inflammation is orchestrated by the caspase-1-IL-1 cascade.
Severe acute respiratory syndrome (SARS) is a recently emerged infectious disease caused by a novel coronavirus, but its immunopathological mechanisms have not yet been fully elucidated. We investigated changes in plasma T helper (Th) cell cytokines, inflammatory cytokines and chemokines in 20 patients diagnosed with SARS. Cytokine profile of SARS patients showed marked elevation of Th1 cytokine interferon (IFN)-gamma, inflammatory cytokines interleukin (IL)-1, IL-6 and IL-12 for at least 2 weeks after disease onset, but there was no significant elevation of inflammatory cytokine tumour necrosis factor (TNF)-alpha, anti-inflammatory cytokine IL-10, Th1 cytokine IL-2 and Th2 cytokine IL-4. The chemokine profile demonstrated significant elevation of neutrophil chemokine IL-8, monocyte chemoattractant protein-1 (MCP-1), and Th1 chemokine IFN-gamma-inducible protein-10 (IP-10). Corticosteroid reduced significantly IL-8, MCP-1 and IP-10 concentrations from 5 to 8 days after treatment (all P < 0.001). Together, the elevation of Th1 cytokine IFN-gamma, inflammatory cytokines IL-1, IL-6 and IL-12 and chemokines IL-8, MCP-1 and IP-10 confirmed the activation of Th1 cell-mediated immunity and hyperinnate inflammatory response in SARS through the accumulation of monocytes/macrophages and neutrophils.
Alveolar macrophages (AM) play a key role in clearing atmospheric particulates from the lung surface and stimulating epithelial cells to produce proinflammatory mediators. The present study examines the role of "acute response" cytokines TNF-alpha and IL-1 beta released by AM exposed to ambient particulate matter with a diameter of <10 microm (PM(10)) in amplifying the proinflammatory mediator expression by A549 cells and human bronchial epithelial cells (HBEC). The results showed that supernatants from human AM incubated 24 h with PM(10) (100 microg/ml) contained more TNF-alpha, IL-1 beta, granulocyte-macrophage colony stimulating factor, IL-6, and IL-8 than nonexposed AM supernatants. The 3-h treatment of A549 cells with PM(10)-exposed AM supernatants increased TNF-alpha, IL-1 beta, IL-8, regulated on activation normal T-cells expressed and secreted (RANTES), and leukemia inhibitory factor mRNA compared with the treatment with nonexposed AM supernatants and, compared with untreated A549 cells, additionally increased ICAM-1 and monocyte chemotactic protein-1 mRNA. Preincubating PM(10)-exposed AM supernatants with anti-IL-1 beta antibodies reduced all the above mediators as well as VEGF mRNA expression (P < 0.05), while anti-TNF-alpha antibodies were less effective (P > 0.05), and the combination of the two antibodies most effective. When HBEC were treated similarly, anti-TNF-alpha antibodies had the greatest effect. In A549 cells PM(10)-exposed AM supernatants increased NF-kappa B, activator protein (AP)-1 and specificity protein 1 binding, while anti-TNF-alpha and anti-IL-1 beta antibodies reduced NF-kappa B and AP-1 binding. We conclude that AM-derived TNF-alpha and IL-1 beta provide a major stimulus for the production of proinflammatory mediators by lung epithelial cells and that their relative importance may depend on the type of epithelial cell target.
Increasing evidence suggests that tumor necrosis factor (TNF)-alpha plays a key role in pulmonary injury caused by environmental ozone (O(3)) in animal models and human subjects. We previously determined that mice genetically deficient in TNF response are protected from lung inflammation and epithelial injury after O(3) exposure.
The present study was designed to determine the molecular mechanisms of TNF receptor (TNF-R)-mediated lung injury induced by O(3).
TNF-R knockout (Tnfr(-/-)) and wild-type (Tnfr(+/+)) mice were exposed to 0.3 ppm O(3) or air (for 6, 24, or 48 h), and lung RNA and proteins were prepared. Mice deficient in p50 nuclear factor (NF)-kappaB (Nfkb1(-/-)) or c-Jun-NH(2) terminal kinase 1 (Jnk1(-/-)) and wild-type controls (Nfkb1(+/+), Jnk1(+/+)) were exposed to O(3) (48 h), and the role of NF-kappaB and mitogen-activated protein kinase (MAPK) as downstream effectors of lung injury was analyzed by bronchoalveolar lavage analyses.
O(3)-induced early activation of TNF-R adaptor complex formation was attenuated in Tnfr(-/-) mice compared with Tnfr(+/+) mice. O(3) significantly activated lung NF-kappaB in Tnfr(+/+) mice before the development of lung injury. Basal and O(3)-induced NF-kappaB activity was suppressed in Tnfr(-/-) mice. Compared with Tnfr(+/+) mice, MAPKs and activator protein (AP)-1 were lower in Tnfr(-/-) mice basally and after O(3). Furthermore, inflammatory cytokines, including macrophage inflammatory protein-2, were differentially expressed in Tnfr(-/-) and Tnfr(+/+) mice after O(3). O(3)-induced lung injury was significantly reduced in Nfkb1(-/-) and Jnk1(-/-) mice relative to respective control animals.
Results suggest that NF-kappaB and MAPK/AP-1 signaling pathways are essential in TNF-R-mediated pulmonary toxicity induced by O(3).
Background:
In late December, 2019, patients presenting with viral pneumonia due to an unidentified microbial agent were reported in Wuhan, China. A novel coronavirus was subsequently identified as the causative pathogen, provisionally named 2019 novel coronavirus (2019-nCoV). As of Jan 26, 2020, more than 2000 cases of 2019-nCoV infection have been confirmed, most of which involved people living in or visiting Wuhan, and human-to-human transmission has been confirmed.
Methods:
We did next-generation sequencing of samples from bronchoalveolar lavage fluid and cultured isolates from nine inpatients, eight of whom had visited the Huanan seafood market in Wuhan. Complete and partial 2019-nCoV genome sequences were obtained from these individuals. Viral contigs were connected using Sanger sequencing to obtain the full-length genomes, with the terminal regions determined by rapid amplification of cDNA ends. Phylogenetic analysis of these 2019-nCoV genomes and those of other coronaviruses was used to determine the evolutionary history of the virus and help infer its likely origin. Homology modelling was done to explore the likely receptor-binding properties of the virus.
Findings:
The ten genome sequences of 2019-nCoV obtained from the nine patients were extremely similar, exhibiting more than 99·98% sequence identity. Notably, 2019-nCoV was closely related (with 88% identity) to two bat-derived severe acute respiratory syndrome (SARS)-like coronaviruses, bat-SL-CoVZC45 and bat-SL-CoVZXC21, collected in 2018 in Zhoushan, eastern China, but were more distant from SARS-CoV (about 79%) and MERS-CoV (about 50%). Phylogenetic analysis revealed that 2019-nCoV fell within the subgenus Sarbecovirus of the genus Betacoronavirus, with a relatively long branch length to its closest relatives bat-SL-CoVZC45 and bat-SL-CoVZXC21, and was genetically distinct from SARS-CoV. Notably, homology modelling revealed that 2019-nCoV had a similar receptor-binding domain structure to that of SARS-CoV, despite amino acid variation at some key residues.
Interpretation:
2019-nCoV is sufficiently divergent from SARS-CoV to be considered a new human-infecting betacoronavirus. Although our phylogenetic analysis suggests that bats might be the original host of this virus, an animal sold at the seafood market in Wuhan might represent an intermediate host facilitating the emergence of the virus in humans. Importantly, structural analysis suggests that 2019-nCoV might be able to bind to the angiotensin-converting enzyme 2 receptor in humans. The future evolution, adaptation, and spread of this virus warrant urgent investigation.
Funding:
National Key Research and Development Program of China, National Major Project for Control and Prevention of Infectious Disease in China, Chinese Academy of Sciences, Shandong First Medical University.
Inflammatory responses have an important role in the onset of many lung diseases associated with urban airborne particulate matter (PM). Here we investigate effects and mechanisms linked to PM-induced expression and release of two main interleukins, IL-6 and IL-8, in human bronchial epithelial BEAS-2B cells. The cells were exposed to well characterized Milan city PM, winter PM2.5 (wPM2.5) and summer PM10 (sPM10), representing combustion and non-combustion sources, respectively. Both wPM2.5 and sPM10 increased mRNA-synthesis and intracellular protein levels of IL-6 and IL-8. Exposure to sPM10 also resulted in continuous and time-dependent increases in release of IL-6 and IL-8 for up to 48 h. By comparison, in wPM2.5-exposed cells IL-8 release was not significantly augmented, while extracellular IL-6 levels were increased but remained constant beyond 24 h exposure. Moreover, wPM2.5 also reduced the lipopolysaccharide (LPS)-increased release of IL-8. No cytotoxicity or significant adsorption of cytokines to wPM2.5 were observed. Immunofluorescence microscopy revealed an accumulation of IL-8 in intracellular vesicles and alterations in actin filament organization in wPM2.5 exposed cells, suggesting that the trafficking of vesicles carrying interleukins to the plasma membrane might be inhibited. Thus, wPM2.5 appeared to impair cytokine release in BEAS-2B cells, in particular of IL-8, possibly by damaging cytoskeletal function involved in protein secretion.
Pollution has long been incriminated in many cardiovascular and respiratory diseases. More recently, studies evaluated the potential role for particulate pollutants in autoimmune diseases, including rheumatoid arthritis (RA). The incidence of RA was found to be higher in urban areas. Living near air pollution emitters was associated with higher risks of developing RA and of producing RA-specific autoantibodies. Nevertheless, no strong epidemiological evidence exists to link one or more specific air pollution particles to RA. The presence in the bronchi of lymphoid satellite islands (inducible bronchus-associated lymphoid tissue, iBALT) is strongly associated with both inflammatory lung disease and RA-associated lung disease. Diesel exhaust particles can stimulate iBALT formation. The induction by air pollution of an inflammatory environment with high citrullination levels in the lung may induce iBALT formation, thereby causing a transition toward a more specific immune response via the production of anti-citrullinated peptide antibodies. Air pollution not only triggers innate immune responses at the molecular level, increasing the levels of proinflammatory cytokines and reactive oxygen species, but is also involved in adaptive immune responses. Thus, via the aryl hydrocarbon receptor (AHR), diesel exhaust particles can trigger a T-cell switch to the Th17 profile. Finally, in the murine collagen-induced arthritis model, animals whose lymphocytes lack the AHR develop milder arthritis.
Exposure to fine particles may trigger pulmonary inflammation/systemic inflammation. The objective of this study was to investigate the association between daily individual exposure to air pollutants and airway inflammation and disease activity in childhood-onset systemic lupus erythematosus (cSLE) patients. A longitudinal panel study was carried out in 108 consecutive appointments with cSLE patients without respiratory diseases. Over four consecutive weeks, daily individual measures of nitrogen dioxide (NO2), fine particulate matter (PM2.5), ambient temperature, and humidity were obtained. This cycle was repeated every 2.5 months along 1 year, and cytokines of exhaled breath condensate-EBC [interleukins (IL) 6, 8, 17 and tumoral necrose factor-α (TNF-α)], fractional exhaled NO (FeNO), and disease activity parameters were collected weekly. Specific generalized estimation equation models were used to assess the impact of these pollutants on the risk of Systemic Lupus Erythematous Disease Activity Index 2000 (SLEDAI-2K) ≥ 8, EBC cytokines, and FeNO, considering the fixed effects for repetitive measurements. The models were adjusted for inflammatory indicators, body mass index, infections, medication, and weather variables. An IQR increase in PM2.5 4-day moving average (18.12 μg/m³) was associated with an increase of 0.05 pg/ml (95% CI 0.01; 0.09, p = 0.03) and 0.04 pg/ml (95% CI 0.02; 0.06, p = 0.01) in IL-17 and TNF-α EBC levels, respectively. Additionally, a short-term effect on FeNO was observed: the PM2.5 3-day moving average was associated with a 0.75 ppb increase (95% CI 0.38; 1.29, p = 0.03) in FeNO. Also, an increase of 1.47 (95% CI 1.10; 1.84) in the risk of SLEDAI-2K ≥ 8 was associated with PM2.5 7-day moving average. Exposure to inhalable fine particles increases airway inflammation/pulmonary and then systemic inflammation in cSLE patients.
Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect almost any organ in the human body. Despite significant advancements in our understanding of SLE over the recent years, its exact mode of onset and disease progression remains elusive. Low concordance rates among monozygotic twins with SLE (as low as 24%), clustering of disease prevalence around polluted regions and an urban – rural difference in prevalence all highlight the importance of environmental influences in SLE. Experimental data strongly suggests a complex interaction between the exposome (or environmental influences) and genome (genetic material) to produce epigenetic changes (epigenome) that can alter the expression of genetic material and lead to development of disease in the susceptible individual. In this review, we focus on the available literature to explore the role of environmental factors in SLE disease onset and progression and to better understand the role of exposome- epigenome – genome interactions in this dreaded disease.
Background:
Long-term exposure to ambient air pollution can lead to adverse health effects in children; however, underlying biological mechanisms are not fully understood.
Objectives:
We evaluated the effect of air pollution exposure during different time periods on mRNA expression as well as circulating levels of inflammatory cytokines in children.
Methods:
We measured a panel of 10 inflammatory markers in peripheral blood samples from 670 8-y-old children in the Barn/Child, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) birth cohort. Outdoor concentrations of nitrogen dioxide (NO2) and particulate matter (PM) with aerodynamic diameter <10 μm (PM10) from road traffic were estimated for residential, daycare, and school addresses using dispersion modeling. Time-weighted average exposures during infancy and at biosampling were linked to serum cytokine levels using linear regression analysis. Furthermore, gene expression data from 16-year-olds in BAMSE (n=238) were used to evaluate links between air pollution exposure and expression of genes coding for the studied inflammatory markers.
Results:
A 10 μg/m(3) increase of NO2 exposure during infancy was associated with a 13.6% (95% confidence interval (CI): 0.8; 28.1%) increase in interleukin-6 (IL-6) levels, as well as with a 27.8% (95% CI: 4.6, 56.2%) increase in IL-10 levels, the latter limited to children with asthma. However, no clear associations were observed for current exposure. Results were similar using PM10, which showed a high correlation with NO2. The functional analysis identified several differentially expressed genes in response to air pollution exposure during infancy, including IL10 , IL13 , and TNF .
Conclusion:
Our results indicate alterations in systemic inflammatory markers in 8-y-old children in relation to early-life exposure to traffic-related air pollution. https://doi.org/10.1289/EHP460.
Rationale:
Epidemiologic evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.
Objective:
To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.
Methods and results:
Blood was collected from healthy, non-smoking, young adults over three study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with elevated levels of endothelial microparticles (annexin V(+)/CD41-/CD31(+)) including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62(+) These changes were accompanied by suppressed circulating levels of pro-angiogenic growth factors (EGF, sCD40L, PDGF, RANTES, GROα, and VEGF), and an increase in the levels of anti-angiogenic (TNFα, IP-10) and proinflammatory cytokines (MCP-1, MIP-1α/β, IL-6, and IL-1β), and markers of endothelial adhesion (sICAM-1 and sVCAM-1). PM2.5 exposure also was associated with an inflammatory response characterized by elevated levels of circulating CD14(+), CD16(+), CD4(+), and CD8(+), but not CD19(+) cells.
Conclusions:
Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an anti-angiogenic plasma profile, and elevated levels of circulating monocytes, and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.
Context:
-Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are a continuum of lung changes arising from a wide variety of lung injuries, frequently resulting in significant morbidity and frequently in death. Research regarding the molecular pathophysiology of ALI/ARDS is ongoing, with the aim toward developing prognostic molecular biomarkers and molecular-based therapy.
Objective:
-To review the clinical, radiologic, and pathologic features of ALI/ARDS; and the molecular pathophysiology of ALI/ARDS, with consideration of possible predictive/prognostic molecular biomarkers and possible molecular-based therapies.
Data sources:
-Examination of the English-language medical literature regarding ALI and ARDS.
Conclusions:
-ARDS is primarily a clinicoradiologic diagnosis; however, lung biopsy plays an important diagnostic role in certain cases. A significant amount of progress has been made in the elucidation of ARDS pathophysiology and in predicting patient response, however, currently there is no viable predictive molecular biomarkers for predicting the severity of ARDS, or molecular-based ARDS therapies. The proinflammatory cytokines TNF-α (tumor necrosis factor α), interleukin (IL)-1β, IL-6, IL-8, and IL-18 are among the most promising as biomarkers for predicting morbidity and mortality.
Tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and transforming growth factor-beta are cytokines synthesized by alveolar macrophages. We investigated the effect of sulfur dioxide, a major air pollutant, on the production of these cytokines by alveolar macrophages. The cells were layered on a polycarbonate membrane and exposed for 30 min to 0.0, 1.0, 2.5, and 5.0 ppm sulfur dioxide at 37 degrees C and 100% air humidity. The cells were incubated for 24 h after exposure, thus allowing cytokine release. Cytotoxic effects of sulfur dioxide were evaluated by trypan blue exclusion. Cytokines were measured with enzyme-linked immunosorbent assays (i.e., tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) or by use of a specific bioassay (i.e., transforming growth factor-beta). The toxicity of sulfur dioxide for alveolar macrophages ranged from 3.1 % to 9.5 %. A 30-min exposure to sulfur dioxide induced a significant decrease in spontaneous and lipopolysaccharide-stimulated tumor necrosis factor-alpha (p < .001) and lipopolysaccharide-stimulated interleukin-1beta release (p < .05). The release of interleukin-6 and transforming growth factor-beta was not affected significantly by sulfur dioxide exposure. Our results demonstrated a functional impairment of alveolar macrophages after sulfur dioxide exposure (i.e., release of tumor necrosis factor-alpha and interleukin-1beta). Neither spontaneous nor stimulated release of interleukin-6 and transforming growth factors were influenced by exposure to sulfur dioxide.