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Atopic eczema is a common and complex disease. Missing genetic hereditability and increasing prevalence in industrializing nations point toward an environmental driver. We investigated the temporal association of weather and pollution parameters with eczema severity. This cross-sectional clinical study was performed between May 2018 and March 2020 and is part of the Tower Hamlets Eczema Assessment. All participants had a diagnosis of eczema, lived in East London, were of Bangladeshi ethnicity, and were aged 10 after previous ambient exposure to commonly studied meteorological variables and pollutants. There were 430 participants in the groups with Eczema Area and Severity Index ≤ 10 and 149 in those with Eczema Area and Severity Index > 10. Using logistic generalized additive models and a model selection process, we found that tropospheric ozone averaged over the preceding 270 days was strongly associated with eczema severity alongside the exposure to fine particles with diameters of 2.5 μm or less (fine particulate matter) averaged over the preceding 120 days. In our models and analyses, fine particulate matter appeared to largely act in a supporting role to ozone. We show that long-term exposure to ground-level ozone at high levels has the strongest association with eczema severity.

The risk factors for severe COVID-19 beyond older age and certain underlying health conditions are largely unknown. Recent studies suggested that long-term environmental exposures may be important determinants of severe COVID-19. However, very few environmental factors have been studied, often separately, without considering the totality of the external environment (i.e., the external exposome). We conducted an external exposome-wide association study (ExWAS) using the nationwide county-level COVID-19 mortality data in the contiguous US. A total of 337 variables characterizing the external exposome from 8 data sources were integrated, harmonized, and spatiotemporally linked to each county. A two-phase procedure was used: (1) in Phase 1, a random 50:50 split divided the data into a discovery set and a replication set, and associations between COVID-19 mortality and individual factors were examined using mixed-effect negative binomial regression models, with multiple comparisons addressed, and (2) in Phase 2, a multivariable regression model including all variables that are significant from both the discovery and replication sets in Phase 1 was fitted. A total of 13 and 22 variables were significant in the discovery and replication sets in Phase 1, respectively. All the 4 variables that were significant in both sets in Phase 1 remained statistically significant in Phase 2, including two air toxicants (i.e., nitrogen dioxide or NO2, and benzidine), one vacant land measure, and one food environment measure. This is the first external exposome study of COVID-19 mortality. It confirmed some of the previously reported environmental factors associated with COVID-19 mortality, but also generated unexpected predictors that may warrant more focused evaluation., Graphical abstract Unlabelled Image, Highlights • The first external exposome study of COVID-19 mortality • Confirmed some previously reported associations • Generated unexpected predictors that may warrant more focused evaluation

Highlights • The effects of air pollution on the placental iodine load are scarcely studied. • PPM2.5 in the third trimester of pregnancy was inversely associated with the placental iodine load. • DLNMs estimated the week-specific associations between PM2.5 and the placental iodine load. • Iodine mediates the effect of gestational PM2.5 exposure on cord blood FT4., Background Adequate intake of iodine is required for the production of thyroid hormones and contributes in pregnant women to a healthy brain development and growth in their offspring. To date, some evidence exists that fine particulate air pollution is linked with the fetal thyroid hormone homeostasis. However, possible effects of air pollutants on the placental iodine storage have not been investigated so far. Objectives We investigated the association between air pollution exposure to particulate matter with a diameter less than 2.5 µm (PM2.5), NO2, and black carbon and the placental iodine load. Methods The current study is part of the ENVIRONAGE birth cohort and included 470 mother-newborn pairs. Iodine concentrations were measured in placental tissue. A high-resolution air pollution model was used to estimate the daily exposure to PM2.5, NO2, and black carbon over the entire pregnancy based on the maternal residential addresses. Distributed lag nonlinear models (DLNMs) were used to estimate gestational week-specific associations between placental iodine concentrations and the air pollutants to understand the impact of specific exposure windows. Results PM2.5 showed a positive association with placental iodine concentration between the 16th and 22nd week of gestation. In contrast, a significant inverse association between PM2.5 and placental iodine concentration was observed in gestational weeks 29–35. The effect estimate, for a 5 µg/m3 increment in PM2.5 concentration, was the strongest at week 32 (β −0.11 µg/kg; 95%CI: −0.18 to −0.03). No associations were observed between placental iodine concentrations and NO2 or black carbon. Assuming causality, we estimated that placental iodine mediated 26% (−0.33 pmol/L; 95%CI: −0.70 to 0.04 pmol/L) of the estimated effect of a 5 µg/m3 increment in PM2.5 exposure on cord blood free thyroxine (FT4) concentrations. Conclusion In utero exposure to particulate matter during the third trimester of pregnancy is linked with a lower placental iodine load. Furthermore, the effect of air pollution on cord blood FT4 levels was partially mediated by the placental iodine load.

International audience; Indoor environments contribute significantly to total human exposure to air pollutants, as people spend most of their time indoors. Household air pollution (HAP) resulting from cooking with polluting ("dirty") fuels, which include coal, kerosene, and biomass (wood, charcoal, crop residues, and animal manure) is a global environmental health problem. Indoor pollutants are gases, particulates, toxins, and microorganisms among others, that can have an impact especially on the health of children and adults through a combination of different mechanisms on oxidative stress and gene activation, epigenetic, cellular, and immunological systems. Air pollution is a major risk factor and contributor to morbidity and mortality from major chronic diseases. Children are significantly affected by the impact of the environment due to biological immaturity, prenatal and postnatal lung development. Poor air quality has been related to an increased prevalence of clinical manifestations of allergic asthma and rhinitis. Health professionals should increase their role in managing the exposure of children and adults to air pollution with better methods of care, prevention, and collective action. Interventions to reduce household pollutants may promote health and can be achieved with education, community, and health professional involvement.

In present study, the variation in concentration of key air pollutants such as PM2.5, PM10, NO2, SO2 and O3 during the pre-lockdown and post-lockdown phase has been investigated. In addition, the monthly concentration of air pollutants in March, April and May of 2020 is also compared with that of 2019 to unfold the effect of restricted emissions under similar meteorological conditions. To evaluate the global impact of COVID-19 on the air quality, ground-based data from 162 monitoring stations from 12 cities across the globe are analysed for the first time. The concentration of PM2.5, PM10 and NO2 were reduced by 20–34%, 24–47% and 32–64%, respectively, due to restriction on anthropogenic emission sources during lockdown. However, a lower reduction in SO2 was observed due to functional power plants. O3 concentration was found to be increased due to the declined emission of NO. Nevertheless, the achieved improvements were temporary as the pollution level has gone up again in cities where lockdown was lifted. The study might assist the environmentalist, government and policymakers to curb down the air pollution in future by implementing the strategic lockdowns at the pollution hotspots with minimal economic loss., Graphical abstract Unlabelled Image, Highlights • Positive impacts of COVID-19 on environment are demonstrated. • Air quality data of 162 monitoring stations from 12 cities across the globe are assessed. • PM2.5, PM10 and NO2 have shown a significant reduction in lockdown phase as compared to pre-lockdown phase. • A notable improvement in air quality is observed during lockdown across the globe. • Achieved improvement in air quality is temporary as pollution level increased in cities where lockdown was lifted.

We have reviewed a considerable amount of recent scientific papers relating inflammation caused by air pollution with chronic and severe medical conditions. Furthermore, there are evidences relating organ inflammation caused by not only outdoor long-term but also short-term inhaled radioisotopes contained in high polluted air or in household natural radioactive background aerosols, in addition to SARS-COV-2 attached to bioaerosols, which are related with a worst evolution of severe acute respiratory syndrome patients. Reactive oxygen species (ROS) production induced by the interaction with environmental ionizing radiation contained in pollution is pointed out as a critical mechanism that predispose mainly to elder population, but not excluding young subjects, presenting previous chronic conditions of lung inflammation or neuroinflammation, which can lead to the most serious consequences.

In order to control the spread of COVID-19, social distancing measures were implemented in many countries. This study investigated changes in air pollution during the social distancing after the COVID-19 outbreak in Korea. Ambient PM2.5, PM10, NO2, and CO that are particularly related to industrial activities and traffic were reduced during the social distancing in response to the COVID-19 outbreak. In March 2020, immediately after social distancing, mean levels of PM2.5, PM10, NO2, and CO decreased nationwide from last year's mean levels by 16.98 μg/m3, 21.61 μg/m3, 4.16 ppb, and 0.09 ppm, respectively (p-value for the year-to-year difference, Graphical abstract Unlabelled Image, Highlights • Social distancing was implemented in order to control the spread of COVID-19. • Social distancing may have a certain positive effect in levels of air pollution. • Ambient PM2.5, PM10, NO2, and CO are related to industrial activities and traffic. • All PM2.5, PM10, NO2, and CO levels were reduced during social distancing. • We point toward reducing air pollution in a sustainable post-COVID-19 world.

The coronavirus disease 2019 (COVID-19) pandemic has caused an unprecedented global health crisis, with several countries imposing lockdowns to control the coronavirus spread. Important research efforts are focused on evaluating the association of environmental factors with the survival and spread of the virus and different works have been published, with contradictory results in some cases. Data with spatial and temporal information is a key factor to get reliable results and, although there are some data repositories for monitoring the disease both globally and locally, an application that integrates and aggregates data from meteorological and air quality variables with COVID-19 information has not been described so far to the best of our knowledge. Here, we present DatAC (Data Against COVID-19), a data fusion project with an interactive web frontend that integrates COVID-19 and environmental data in Spain. DatAC is provided with powerful data analysis and statistical capabilities that allow users to explore and analyze individual trends and associations among the provided data. Using the application, we have evaluated the impact of the Spanish lockdown on the air quality, observing that NO2, CO, PM2.5, PM10 and SO2 levels decreased drastically in the entire territory, while O3 levels increased. We observed similar trends in urban and rural areas, although the impact has been more important in the former. Moreover, the application allowed us to analyze correlations among climate factors, such as ambient temperature, and the incidence of COVID-19 in Spain. Our results indicate that temperature is not the driving factor and without effective control actions, outbreaks will appear and warm weather will not substantially limit the growth of the pandemic. DatAC is available at https://covid19.genyo.es., Graphical abstract Unlabelled Image, Highlights • DatAC integrates spatio-temporal data of weather, air quality and COVID-19. • NO2, CO, SO2, PM2.5 and PM10 declined after lockdown, while O3 levels rose. • The lockdown impact on rural air quality is smaller than in urban environments. • Current data does not support climatic factors as driving factors of the pandemic.

Being heavily dependent to oil products (mainly gasoline and diesel), the French transport sector is the main emitter of Particulate Matter (PMs) whose critical levels induce harmful health effects for urban inhabitants. We selected three major French cities (Paris, Lyon, and Marseille) to investigate the relationship between the Coronavirus Disease 19 (COVID-19) outbreak and air pollution. Using Artificial Neural Networks (ANNs) experiments, we have determined the concentration of PM2.5and PM10linked to COVID-19-related deaths. Our focus is on the potential effects of Particulate Matter (PM) in spreading the epidemic. The underlying hypothesis is that a pre-determined particulate concentration can foster COVID-19 and make the respiratory system more susceptible to this infection. The empirical strategy used an innovative Machine Learning (ML) methodology. In particular, through the so-called cutting technique in ANNs, we found new threshold levels of PM2.5and PM10connected to COVID-19: 17.4µg/m3(PM2.5) and 29.6µg/m3(PM10) for Paris; 15.6µg/m3(PM2.5) and 20.6µg/m3(PM10) for Lyon; 14.3µg/m3(PM2.5) and 22.04µg/m3(PM10) for Marseille. Interestingly, all the threshold values identified by the ANNs are higher than the limits imposed by the European Parliament. Finally, a Causal Direction from Dependency (D2C) algorithm is applied to check the consistency of our findings.

Allergic rhinitis affects the quality of life of millions of people worldwide. Air pollution not only causes morbidity, but nearly 3 million people per year die from unhealthy indoor air exposure. Furthermore, allergic rhinitis and air pollution interact. This report summarizes the discussion of an International Expert Consensus on the management of allergic rhinitis aggravated by air pollution. The report begins with a review of indoor and outdoor air pollutants followed by epidemiologic evidence showing the impact of air pollution and climate change on the upper airway and allergic rhinitis. Mechanisms, particularly oxidative stress, potentially explaining the interactions between air pollution and allergic rhinitis are discussed. Treatment for the management of allergic rhinitis aggravated by air pollution primarily involves treating allergic rhinitis by guidelines and reducing exposure to pollutants. Fexofenadine a non-sedating oral antihistamine improves AR symptoms aggravated by air pollution. However, more efficacy studies on other pharmacological therapy of coexisting AR and air pollution are currently lacking. Keywords: Allergic rhinitis, Occupational rhinitis, Air pollution, Climate change, Air pollutants, Indoor air quality, Oxidative stress, Antioxidant enzymes

Angiotensin-converting enzyme-2 (ACE2) is one of the major components of the renin-angiotensin system (RAS) and participates in the physiological functions of the cardiovascular system and lungs. Recent studies identified ACE2 as the receptor for the S-protein of the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and thus acts as the gateway for viral entry into the human body. Virus infection causes an imbalance in the RAS axis and induces acute lungs injury and fibrosis. Various factors regulate ACE2 expression patterns as well as control its epigenetic status at both transcription and translational levels. This review is mainly focused on the impact of environmental toxicants, drugs, endocrine disruptors, and hypoxia as controlling parameters for ACE2 expression and its possible modulation by epigenetic changes which are marked by DNA methylation, histone modifications, and micro-RNAs (miRNAs) profile. Furthermore, we have emphasized on interventions of various phytochemicals and bioactive compounds as epidrugs that regulate ACE2-S-protein interaction and thereby curb viral infection. Since ACE2 is an important component of the RAAS axis and a crucial entry point of SARS-CoV-2, the dynamics of ACE2 expression in response to various extrinsic and intrinsic factors are of contemporary relevance. We have collated updated information on ACE2 expression modulated by epidrugs, and urge to take over further studies on these important physiological regulators to unravel many more systemic linkages related to both metabolic and infectious diseases, in general and SARS-CoV-2 in particular for further development of targeted interventions.

Soil-transmitted helminths infect billions of people globally, particularly those residing in low- and middle-income regions with poor environmental sanitation and high levels of air and water pollution. Helminths display potent immunomodulatory activity by activating T helper type 2 (Th2) anti-inflammatory and Th3 regulatory immune responses. The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the virus that causes Coronavirus disease 2019 (COVID-19), can exacerbate Th1/Th17 pro-inflammatory cytokine production in humans, leading to a cytokine storm. Air pollutants (particulate matter, oxygen radicals, hydrocarbons and volatile organic compounds) and water pollutants (metals and organic chemicals) can also intensify Th1/Th17 immune response and could exacerbate SARS-CoV-2 related respiratory distress and failure. The present review focused on the epidemiology of SARS-CoV-2, helminths and fine particulate matter 2.5 µm or less in diameter (PM2.5) air pollution exposure in helminth endemic regions, the possible immunomodulatory activity of helminths against SARS-CoV-2 hyper-inflammatory immune response, and whether air and water pollutants can further exacerbate SARS-CoV-2 related cytokine storm and in the process hinder helminths immunomodulatory functionality. Helminth Th2/Th3 immune response is associated with reductions in lung inflammation and damage, and decreased expression levels of angiotensin-converting enzyme 2 (ACE2) receptors (SARS-CoV-2 uses the ACE2 receptors to infect cells and associated with extensive lung damage). However, air pollutants are associated with overexpression of ACE2 receptors in the epithelial cell surface of the respiratory tract and exhaustion of Th2 immune response. Helminth-induced immunosuppression activity reduces vaccination efficacy, and diminishes vital Th1 cytokine production immune responses that are crucial for combating early stage infections. This could be reversed by continuous air pollution exposure which is known to intensify Th1 pro-inflammatory cytokine production to a point where the immunosuppressive activities of helminths could be hindered. Again, suppressed activities of helminths can also be disadvantageous against SARS-CoV-2 inflammatory response. This “yin and yang” approach seems complex and requires more understanding. Further studies are warranted in a cohort of SARS-CoV-2 infected individuals residing in helminths and air pollution endemic regions to offer more insights, and to impact mass periodic deworming programmes and environmental health policies.

Background Exposure to ambient air pollution is related to 4.2 million premature deaths per year worldwide and is associated with a variety of adverse health outcomes, such as respiratory and cardiovascular morbidity. Furthermore, exposure to air pollution can increase human sensitivity to respiratory pathogens via damage to the respiratory tract or via airborne transmission on the surface of particulate matter, and might be an additional factor influencing COVID-19 morbidity and mortality rates. The aim of this study was to examine the association between populations' exposure to air pollution and the morbidity and mortality rates from COVID-19. Methods We examined the association between population-weighted long-term exposure to PM2.5 and NOx, and the morbidity and mortality over time following the detection of the first COVID-19 positive case in 36 OECD countries. Pearson and Spearman correlations between daily COVID-19 morbidity and mortality (Jan–Jun 2020) on the 10th, 20th, 40th, 60th and 80th days since first confirmed case in the country, and demographic, health, economic, and environmental data were calculated. Multivariate linear regression were used to examine the associations between demographic, health, economic and air pollution features and the rate of confirmed cases and deaths on the 60th and 80th days following the first confirmed case. Results PM2.5 concentrations in 2015–2017 were positively correlated with COVID-19 morbidity and mortality on the 10th, 20th, 40th and 60th days since the first confirmed case in all countries. NOx concentrations in 2015–2017 and country's density (population/Km2) were positively correlated with COVID-19 morbidity and mortality on the 60th day. All multivariate linear regressions consisting PM2.5 concentrations models were statistically significant. Our models also emphasize the importance of the relative number of hospital beds in decreasing the morbidity and mortality of COVID-19. Conclusions The adverse health outcomes stemming from long-term exposure to various air pollutants has long been known to the scientific community. According to our results and previously published studies, it appears that long-term exposure to air pollutants concentrations exceeding WHO guidelines, such as PM2.5 and NOx, might exacerbate morbidity and mortality rates from COVID-19. These results should raise a red flag globally among decision makers about the urgent need to reduce air pollution and its harmful effects., Highlights • The link between PM2.5 & NOx chronic exposure to COVID-19 morbidity was examined. • Data from 36 OECD countries was analyzed and modeled. • Chronic exposure to air pollution is associated with COVID-19 morbidity & mortality. • The results emphasize the urgent need to reduce air pollution and its harmful effects.

Background Atopic dermatitis (AD) is a chronic, inflammatory skin disorder characterised by intense itch and eczematous lesions. Rising prevalence of AD has been observed worldwide including in Asia. Understanding the risk factors associated with AD may explain its pathogenicity and identify new preventive strategies and treatments. However, AD-associated risk factors and comorbidities specific to Asia have not been systematically reviewed. Methods We performed a systematic review in accordance with the Preferred Reporting Item for Systematic Review and Meta-Analyses (PRISMA) guidelines and summarised epidemiological studies investigating personal, family, and environmental factors and comorbidities associated with AD in Asia. Significant factors were assessed if they can be altered through lifestyle practices and further classified into non-modifiable and modifiable factors. Meta-analysis using the random-effect model was also conducted to provide an overall estimate for several significant factors. Results We identified a total of 162 epidemiological studies conducted in Asia. Among non-modifiable factors, a family history of atopic diseases was the most reported, suggesting the involvement of genetics in AD pathogenesis. Among modifiable factors, the results of meta-analyses revealed maternal smoking as the strongest risk factor with a pooled odds ratio (OR) of 2.95 (95% CI, 2.43–3.60), followed by active smoking (pooled OR, 1.91, 95% CI, 1.41–2.59). Conclusion While a family history may aid clinicians in identifying high-risk individuals, literature has long suggested the importance of gene-environment interaction. This review identified several modifiable factors including medical treatments, indoor and outdoor environmental exposure, and personal and family lifestyle specific to Asia. Based on the meta-analyses performed, prevention strategies against AD may start from changing personal and family lifestyle choices, especially smoking habits.

While accumulating evidence shows that air pollution exposure is an important risk factor to influenza prevalence, their association has been inadequately investigated in mountainous regions with dense populations and high humidity. We aim to estimate the association and exposure-outcome effects between exposure to nitrogen dioxide (NO2) and influenza prevalence in a mountainous region with a dense population and high humidity. We investigated 14,993 patients with confirmed influenza cases from January 2013 to December 2017 in Chongqing, a mountainous city in southwest China. We developed distributed lag non-linear models with quasi-Poisson link to take into account the lag and non-linear effects of NO2 exposure on influenza prevalence. We estimated that the cumulative effect of a 10 μg/m3 increase in NO2 with seven-day lag (i.e., summing all the contributions up to seven days) corresponded to relative risk of 1.24 (95% CI: 1.17–1.31) in daily influenza prevalence. Comparing to annual mean of the World Health Organization air quality guidelines of 40 μg/m3 for NO2, we estimated that 14.01% (95% CI: 10.69–17.08%) of the influenza cases were attributable to excessive NO2 exposure. Our results suggest that NO2 exposure could worsen the risk of influenza infection in this mountainous city, filling the gap of relevant researches in densely populated and mountainous cities. Our findings provide evidence for developing influenza surveillance and early warning systems., Graphical abstract Image 1, Highlights • Influenza prevalence is associated with NO2 exposure in a mountainous city. • Exposure-response effect is delineated with distributed lag nonlinear regression. • Distributed lag nonlinear effects over seven-day lag are modeled. • Cumulative effect of a 10 μg/m3 NO2 increase corresponds to relative risk of 1.24 • Attributable fraction due to NO2 exposure exceeding WHO AQG is 14.01%.

Background Endogenous nitric oxide (NO) may contribute to ischemic and anesthetic preconditioning while exogenous NO protects against ischemia-reperfusion (I/R) injury in the heart and other organs. Why those beneficial effects observed in animal models do not always translate into clinical effectiveness remains unclear. To mitigate reperfusion damage a source of NO is required. NO inhalation is known to increase tissue NO metabolites, but little information exists about the lifetime of these species. We therefore sought to investigate the fate of major NO metabolite classes following NO inhalation in mice in vivo. Methods C57BL/6J mice were exposed to 80 ppm NO for 1 h. NO metabolites were measured in blood (plasma and erythrocytes) and tissues (heart, liver, lung, kidney and brain) immediately after NO exposure and up to 48 h thereafter. Concentrations of S-nitrosothiols, N-nitrosamines and NO-heme products as well as nitrite and nitrate were quantified by gas-phase chemiluminescence and ion chromatography. In separate experiments, mice breathed 80 ppm NO for 1 h prior to cardiac I/R injury (induced by coronary arterial ligation for 1 h, followed by recovery). After sacrifice, the size of the myocardial infarction (MI) and the area at risk (AAR) were measured. Results After NO inhalation, elevated nitroso/nitrosyl levels returned to baseline over the next 24 h, with distinct multi-phasic decay profiles in each compartment. S/N-nitroso compounds and NO-hemoglobin in blood decreased exponentially, but remained above baseline for up to 30min, whereas nitrate was elevated for up to 3hrs after discontinuing NO breathing. Hepatic S/N-nitroso species concentrations remained steady for 30min before dropping exponentially. Nitrate only rose in blood, liver and kidney; nitrite tended to be lower in all organs immediately after NO inhalation but fluctuated considerably in concentration thereafter. NO inhalation before myocardial ischemia decreased the ratio of MI/AAR by 30% vs controls (p = 0.002); only cardiac S-nitrosothiols and NO-hemes were elevated at time of reperfusion onset. Conclusions Metabolites in blood do not reflect NO metabolite status of any organ. Although NO is rapidly inactivated by hemoglobin-mediated oxidation in the circulation, long-lived tissue metabolites may account for the myocardial preconditioning effects of inhaled NO. NO inhalation may afford similar protection in other organs., Highlights • Breathing 80 ppm NO for 1 h increases NO metabolite concentrations, except nitrite, in murine blood/tissues. • After NO inhalation, elevated NO metabolites return to baseline in a compartment-specific manner. • Cardiac S-nitrosothiol and NO-heme levels remain elevated for ∼1 h after discontinuation of NO treatment. • Breathing 80 ppm NO for 1 h just before cardiac ischemia reduces reperfusion injury in mice.

The Aim of the study was to reveal if PET-CT analysis of primary and of secondary lung cancer could be related to the onset of lipid peroxidation in cancer and in surrounding non-malignant lung tissue. Methods: Nineteen patients with primary lung cancer and seventeen patients with pulmonary metastasis were involved in the study. Their lungs were analyzed by PET-CT scanning before radical surgical removal of the cancer. Specific immunohistochemistry for the major bioactive marker of lipid peroxidation, 4-hydroxynonenal (HNE), was done for the malignant and surrounding non-malignant lung tissue using genuine monoclonal antibody specific for the HNE-histidine adducts. Results: Both the intensity of the PET-CT analysis and the HNE-immunohistochemistry were in correlation with the size of the tumors analyzed, while primary lung carcinomas were larger than the metastatic tumors. The intensity of the HNE-immunohistochemistry in the surrounding lung tissue was more pronounced in the metastatic than in the primary tumors, but it was negatively correlated with the cancer volume determined by PET-CT. The appearance of HNE was more pronounced in non-malignant surrounding tissue than in cancer or stromal cells, both in case of primary and metastatic tumors. Conclusions: Both PET-CT and HNE-immunohistochemistry reflect the size of the malignant tissue. However, lipid peroxidation of non-malignant lung tissue in the vicinity of cancer is more pronounced in metastatic than in primary malignancies and might represent the mechanism of defense against cancer, as was recently revealed also in case of human liver cancer. Keywords: Lipid peroxidation (LPO), 4-hydroxynonenal (HNE), Positron emission tomography and computed tomography (PET-CT), Cell growth regulation, Inflammation, Immunohistochemistry

Oxidative stress is a common mediator in pathogenicity of established cardiovascular risk factors. Furthermore, it likely mediates effects of emerging, less well-defined variables that contribute to residual risk not explained by traditional factors. Functional oxidative modifications of cellular proteins, both reversible and irreversible, are a causal step in cellular dysfunction. Identifying markers of oxidative stress has been the focus of many researchers as they have the potential to act as an “integrator” of a multitude of processes that drive cardiovascular pathobiology. One of the major challenges is the accurate quantification of reactive oxygen species with very short half-life. Redox-sensitive proteins with important cellular functions are confined to signalling microdomains in cardiovascular cells and are not readily available for quantification. A popular approach is the measurement of stable by-products modified under conditions of oxidative stress that have entered the circulation. However, these may not accurately reflect redox stress at the cell/tissue level. Many of these modifications are “functionally silent”. Functional significance of the oxidative modifications enhances their validity as a proposed biological marker of cardiovascular disease, and is the strength of the redox cysteine modifications such as glutathionylation. We review selected biomarkers of oxidative stress that show promise in cardiovascular medicine, as well as new methodologies for high-throughput measurement in research and clinical settings. Although associated with disease severity, further studies are required to examine the utility of the most promising oxidative biomarkers to predict prognosis or response to treatment., Graphical abstract, Highlights • Oxidative stress is a common mediator in pathobiology of risk factors for CVD. • Oxidative modifications of proteins and lipids alter cellular function. • Some oxidative biomarkers have been associated with severity of CVD. • Pathophysiologically relevant biomarkers may integrate the effect of risk factors. • Utility of oxidative biomarkers to guide prognosis/treatment merits further work.

Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children in the Western world. Despite advances in asthma management, acute exacerbations continue to occur and impose considerable morbidity on patients and constitute a major burden on health care resources. Respiratory tract viruses have emerged as the most frequent triggers for exacerbations in both children and adults; however, the mechanisms underlying these remain poorly understood. More recently, it has become increasingly clear that interactions might exist between viruses and other triggers, increasing the likelihood of an exacerbation. In this article we begin with an overview of the health, economic, and social burden that exacerbations of asthma carry with them. This is followed by a review of the pathogenesis of asthma exacerbations, highlighting the various triggers responsible and multiple interactions that exist between them. The final section first addresses what preventative measures are currently available for asthma exacerbations and subsequently examines which of the new treatments in development might lessen the burden of exacerbations in the future.

A land use regression (LUR) model for the mapping of NO(2) concentrations in Ottawa, Canada was created based on data from 29 passive air quality samplers from the City of Ottawa's National Capital Air Quality Mapping Project and two permanent stations. Model sensitivity was assessed against three spatial representations of population: population at the dissemination area level, population at the dissemination block level and a dasymetrically derived population representation. A spatial database with land use, roads, population, zoning, greenspaces and elevation was created. Polycategorical zoning data were used in dasymetric mapping to spatially focus population data derived from the dissemination blocks to a sub-block level for comparison purposes. Dasymetric population mapping provided no significant LUR model improvement in explained variance when compared to block level population; however, both the former were significantly better than the dissemination area level population representations. However, where block level population is not available or too costly to acquire, our method using polycategorical zoning data provides a viable alternative in LUR modelling endeavours.

Visibility in Hong Kong has deteriorated significantly over 40 years with visibility below 8km in the absence of fog, mist, or precipitation, increasing from 6.6 days in 1968 to 54.1 days in 2007. We assessed the short-term mortality effects of daily loss of visibility. During 1996-2006, we obtained mortality data for non-accidental and cardiorespiratory causes, visibility recorded as visual range in kilometers, temperature, and relative humidity from an urban observatory, and concentrations of four criteria pollutants. A generalized additive Poisson regression model with penalized cubic regression splines was fitted to control for time variant covariates. For non-accidental mortality, an interquartile range (IQR) of 6.5km decrease in visibility at lag0-1 days was associated with an excess risk (ER%) [95% CI] of 1.13 [0.49, 1.76] for all ages and 1.37 [0.65, 2.09] for ages 65 years and over; for cardiovascular mortality of 1.31 [0.13, 2.49] for all ages, and 1.72 [0.44, 3.00] for ages 65 years and over; and for respiratory mortality of 1.92 [0.49, 3.35] for all ages and 1.76 [0.28, 3.25] for ages 65 years and over. The estimated ER% for daily mortality derived from both visibility and air pollutant data were comparable in terms of magnitude, lag pattern, and exposure-response relationships especially when using particulate matter with aerodynamic diameter < or = 10 microm to predict the mortality associated with visibility. Visibility provides a useful proxy for the assessment of environmental health risks from ambient air pollutants and a valid approach for the assessment of the public health impacts of air pollution and the benefits of air quality improvement measures in developing countries where pollutant monitoring data are scarce.