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As the metaverse expands, understanding how people use virtual reality to learn and connect is increasingly important. We used the Transformed Social Interaction paradigm (Bailenson et al., 2004) to examine different avatar identities and environments over time. In Study 1 (n = 81), entitativity, presence, enjoyment, and realism increased over 8 weeks. Avatars that resembled participants increased synchrony, similarities in moment-to-moment nonverbal behaviors between participants. Moreover, self-avatars increased self-presence and realism, but decreased enjoyment, compared to uniform avatars. In Study 2 (n = 137), participants cycled through 192 unique virtual environments. As visible space increased, so did nonverbal synchrony, perceived restorativeness, entitativity, pleasure, arousal, self- and spatial presence, enjoyment, and realism. Outdoor environments increased perceived restorativeness and enjoyment more than indoor environments. Self-presence and realism increased over time in both studies. We discuss implications of avatar appearance and environmental context on social behavior in classroom contexts over time.

This comprehensive chapter provides tools used for successful communication and how they can be wielded to advocate for public health initiatives and generally elevate the public’s value of public health perspectives. Framing, and how it works within storytelling, is described as a strategic tool for closing critical gaps in understanding between public health experts, leaders in other sectors, and the public. A discussion of metaphors as tools is also included, specifically to align the strategic goals of other sectors and public health initiatives (as well as the public’s personal relationship to health) in order to forge understanding and strong collaboration. Communication tools for building support for public health and collaboration tools for building bridges and partnerships meet the need for sector-specific audiences to see the value of collaboration, as well as general trust-building among the public through strategic storytelling.

The cardiometabolic effects of air pollution in the context of mixtures and the underlying mechanisms remain not fully understood. This study aims to investigate the joint effect of air pollutant mixtures on a broad range of cardiometabolic parameters, examine the susceptibility of obese individuals, and determine the role of circulating fatty acids. In this panel study, metabolically healthy normal-weight (MH-NW, n=49) and obese (MHO, n=39) adults completed three longitudinal visits (257 person-visits in total). Personal exposure levels of PM2.5, PM10, O3, NO2, SO2, CO and BC were estimated based on fixed-site monitoring data, time-activity logs and infiltration factor method. Blood pressure, glycemic homeostasis, lipid profiles, systematic inflammation and coagulation biomarkers were measured. Targeted metabolomics was used to quantify twenty-eight plasma free fatty acids (FFAs). Bayesian kernel machine regression models were applied to establish the exposure-response relationships and identify key pollutants. Significant joint effects of measured air pollutants on systematic inflammation and coagulation biomarkers were observed in the MHO group, instead of the MH-NW group. Lipid profiles showed the most significant changes in both groups and O3 contributed the most to the total effect. Specific FFA patterns were identified, and de novo lipogenesis (DNL)-related pattern was most closely related to blood lipid profiles. In particular, interaction analysis suggested that DNL-related FFA pattern augmented the effects of O3 on triglyceride (TG, Pinteraction=0.040), high-density lipoprotein cholesterol (HDL-C, Pinteraction=0.106) and TG/HDL-C (Pinteraction=0.020) in the MHO group but not MH-NW group. This modification was further confirmed by interaction analysis with estimated activity of SCD1, a key enzyme in the DNL pathway. Therefore, despite being metabolically healthy, obese subjects have a higher cardiometabolic susceptibility to air pollution, especially O3, and the DNL pathway may represent an intrinsic driver of lipid susceptibility. This study provides new insights into the cardiometabolic susceptibility of obese individuals to air pollution.

Funder: National Institute for Health Research (NIHR), Funder: Health Effects Institute, Funder: Trafikverket, Funder: Imperial College London, Funder: UK Health Security Agency, Funder: NordFoU, Implementation of regulatory standards has reduced exhaust emissions of particulate matter from road traffic substantially in the developed world. However, nonexhaust particle emissions arising from the wear of brakes, tires, and the road surface, together with the resuspension of road dust, are unregulated and exceed exhaust emissions in many jurisdictions. While knowledge of the sources of nonexhaust particles is fairly good, source-specific measurements of airborne concentrations are few, and studies of the toxicology and epidemiology do not give a clear picture of the health risk posed. This paper reviews the current state of knowledge, with a strong focus on health-related research, highlighting areas where further research is an essential prerequisite for developing focused policy responses to nonexhaust particles.

Background: Pollution of water sources, largely from wide-scale agricultural fertilizer use has resulted in nitrateand nitrite contamination of drinking water. The effects on human health of raised nitrate and nitrite levels indrinking water are currently unclear.Objectives: We conducted a systematic review of peer-reviewed literature on the association of nitrate and nitritein drinking water with human health with a specific focus on cancer.Methods: We searched eight databases from 1 January 1990 until 28 February 2021. Meta-analyses were con-ducted when studies had the same exposure metric and outcome.Results: Of 9835 studies identified in the literature search, we found 111 studies reporting health outcomes, 60 ofwhich reported cancer outcomes (38 case-control studies; 12 cohort studies; 10 other study designs). Most studieswere set in the USA (24), Europe (20) and Taiwan (14), with only 3 studies from low and middle-incomecountries. Nitrate exposure in water (59 studies) was more commonly investigated than nitrite exposure (4studies). Colorectal (15 studies) and gastric (13 studies) cancers were the most reported. In meta-analyses (4studies) we identified a positive association of nitrate exposure with gastric cancer, OR = 1.91 (95%CI =1.09–3.33) per 10 mg/L increment in nitrate ion. We found no association of nitrate exposure with colorectalcancer (10 studies; OR = 1.02 [95%CI = 0.96–1.08]) or cancers at any other site.Conclusions: We identified an association of nitrate in drinking water with gastric cancer but with no other cancersite. There is currently a paucity of robust studies from settings with high levels nitrate pollution in drinkingwater. Research into this area will be valuable to ascertain the true health burden of nitrate contamination ofwater and the need for public policies to protect human health.

Air pollution is associated with up to 8.8 million excess deaths worldwide each year and is a major contributor to the global burden of disease. Cardiovascular conditions are the predominant cause for air pollution-related deaths and there is an urgent need to address the silent pandemic of air pollution on cardiovascular health. Air pollution exposure is associated with acute events like acute coronary syndrome and stroke, and with chronic conditions, such as atherosclerosis and heart failure. Several potential mechanisms have been proposed that link particle inhalation to cardiovascular disease including oxidative stress and inflammation, changes in autonomic balance and neuroendocrine regulation and the particle translocation into the circulation itself. This, in turn, can cause endothelial, vasomotor and fibrinolytic dysfunction and increased thrombogenicity and blood pressure which are implicated in the mediation of adverse cardiovascular events. Certain interventions can help mitigate these adverse effects. At an individual level, this includes the use of a facemask and indoor air purification systems. At an environmental level, interventions reducing the generation or release of combustion-derived pollutants are key and include public health policies to facilitate active transport, cleaner sources of energy and reductions in vehicular and fossil fuel emissions. In this review, we summarise the key pathways and mechanisms that draw together how air pollution can lead to adverse cardiovascular effects, as well as explore potential interventions to reduce the burden of air pollution-induced cardiovascular morbidity and mortality.

BACKGROUND: Empirical evidence suggests a strong link between exposure to air pollution and heart failure incidence, hospitalizations, and mortality, but the biological basis of this remains unclear. We sought to determine the relationship between differential air pollution levels and changes in cardiac structure and function in patients with dilated cardiomyopathy.METHODS AND RESULTS: We undertook a prospective longitudinal observational cohort study of patients in England with dilated cardiomyopathy (enrollment 2009-2015, n = 716, 66% male, 85% Caucasian) and conducted cross sectional analysis at the time of study enrollment. Annual average air pollution exposure estimates for nitrogen dioxide (NO 2) and particulate matter with diameter of 2.5 µm or less (PM 2.5) at enrolment were assigned to each residential postcode (on average 12 households). The relationship between air pollution and cardiac morphology was assessed using linear regression modelling. Greater ambient exposure to NO 2 was associated with higher indexed left ventricular (LV) mass (4.3 g/m 2 increase per interquartile range increase in NO 2, 95% confidence interval 1.9-7.0 g/m 2) and lower LV ejection fraction (-1.5% decrease per interquartile range increase in NO 2, 95% confidence interval -2.7% to -0.2%), independent of age, sex, socioeconomic status, and clinical covariates. The associations were robust to adjustment for smoking status and geographical clustering by postcode area. The effect of air pollution on LV mass was greatest in women. These effects were specific to NO 2 exposure. CONCLUSIONS: Exposure to air pollution is associated with raised LV mass and lower LV ejection fraction, with the strongest effect in women. Although epidemiological associations between air pollution and heart failure have been established and supported by preclinical studies, our findings provide novel empirical evidence of cardiac remodeling and exposure to air pollution with important clinical and public health implications.

Inconsistent communication about COVID-19 from public officials has created mistrust and confusion about public health recommendations, which has contributed to increased mortality in the United St...

Wearing a respirator is generally the most convenient individual intervention against ambient particulate matter (PM), and therefore there has been considerable research into its effectiveness. However, the effects of respirator intervention under different PM concentration settings have been insufficiently elucidated. We conducted a randomized, blinded, crossover intervention study in four representative cities in China in which 128 healthy university students spent 2 h walking along a busy road wearing either a real or a sham respirator and then spent the next 5 h indoors away from traffic pollution. Lung function, blood pressure, and heart rate variability were continuously measured throughout the visit. Linear mixed-effect models were fitted to evaluate the protective effects of respirator intervention on the cardiopulmonary indicators. Results showed that the beneficial effects of respirator intervention were only occasionally significant at specific time points or in specific cities or in selected parameters. Overall, respirator intervention was associated with reduced SBP (6.2 vs. 11.5 mmHg compared to baseline, p

Air pollution is associated with staggering levels of cardiovascular morbidity and mortality. Airborne particulate matter (PM), in particular, has been associated with a wide range of detrimental cardiovascular effects, including impaired vascular function, raised blood pressure, alterations in cardiac rhythm, blood clotting disorders, coronary artery disease, and stroke. Considerable headway has been made in elucidating the biological processes underlying these associations, revealing a labyrinth of multiple interacting mechanistic pathways. Several studies have used pharmacological agents to prevent or reverse the cardiovascular effects of PM; an approach that not only has the advantages of elucidating mechanisms, but also potentially revealing therapeutic agents that could benefit individuals that are especially susceptible to the effects of air pollution. This review gathers investigations with pharmacological agents, offering insight into the biology of how PM, and other air pollutants, may cause cardiovascular morbidity.

More than twenty percent of all cardiovascular disease (CVD) deaths are caused by air pollution — more than three million deaths every year — and these numbers will continue to rise unless the global community takes action. Nine out of ten people worldwide breathe polluted air, which disproportionately affects those living in low-resource settings. The World Heart Federation (WHF) is committed to reducing the impact of air pollution on people’s health and has made this a priority area of its global advocacy efforts. In pursuit of this goal, WHF has formed an Air Pollution Expert Group to inform action on air pollution for CVD health and recommend changes to public health policy. This policy paper lays out the health impacts of air pollution, examines its position on the global policy agenda, demonstrates its relevance to the cardiovascular community, and proposes actionable policy measures to mitigate this deadly risk factor to health. The paper considers the important roles to be played by the Members of WHF, including scientific societies and the physicians that constitute them, heart health foundations, and patient advocacy groups. The paper concludes with a detailed table of recommendations for the various sub-target groups at the global, national, local, and patient level.

Epidemiological studies have consistently linked exposure to PM2.5 with adverse health effects. The oxidative potential (OP) of aerosol particles has been widely suggested as a measure of their potential toxicity. Several acellular chemical assays are now readily employed to measure OP; however, uncertainty remains regarding the atmospheric conditions and specific chemical components of PM2.5 that drive OP. A limited number of studies have simultaneously utilised multiple OP assays with a wide range of concurrent measurements and investigated the seasonality of PM2.5 OP. In this work, filter samples were collected in winter 2016 and summer 2017 during the atmospheric pollution and human health in a Chinese megacity campaign (APHH-Beijing), and PM2.5 OP was analysed using four acellular methods: ascorbic acid (AA), dithiothreitol (DTT), 2,7-dichlorofluorescin/hydrogen peroxidase (DCFH) and electron paramagnetic resonance spectroscopy (EPR). Each assay reflects different oxidising properties of PM2.5, including particle-bound reactive oxygen species (DCFH), superoxide radical production (EPR) and catalytic redox chemistry (DTT/AA), and a combination of these four assays provided a detailed overall picture of the oxidising properties of PM2.5 at a central site in Beijing. Positive correlations of OP (normalised per volume of air) of all four assays with overall PM2.5 mass were observed, with stronger correlations in winter compared to summer. In contrast, when OP assay values were normalised for particle mass, days with higher PM2.5 mass concentrations (μgm−3) were found to have lower mass-normalised OP values as measured by AA and DTT. This finding supports that total PM2.5 mass concentrations alone may not always be the best indicator for particle toxicity. Univariate analysis of OP values and an extensive range of additional measurements, 107 in total, including PM2.5 composition, gas-phase composition and meteorological data, provided detailed insight into the chemical components and atmospheric processes that determine PM2.5 OP variability. Multivariate statistical analyses highlighted associations of OP assay responses with varying chemical components in PM2.5 for both mass- and volume-normalised data. AA and DTT assays were well predicted by a small set of measurements in multiple linear regression (MLR) models and indicated fossil fuel combustion, vehicle emissions and biogenic secondary organic aerosol (SOA) as influential particle sources in the assay response. Mass MLR models of OP associated with compositional source profiles predicted OP almost as well as volume MLR models, illustrating the influence of mass composition on both particle-level OP and total volume OP. Univariate and multivariate analysis showed that different assays cover different chemical spaces, and through comparison of mass- and volume-normalised data we demonstrate that mass-normalised OP provides a more nuanced picture of compositional drivers and sources of OP compared to volume-normalised analysis. This study constitutes one of the most extensive and comprehensive composition datasets currently available and provides a unique opportunity to explore chemical variations in PM2.5 and how they affect both PM2.5 OP and the concentrations of particle-bound reactive oxygen species.

According to the free energy principle biological agents resist a tendency to disorder in their interactions with a dynamically changing environment by keeping themselves in sensory and physiological states that are expected given their embodiment and the niche they inhabit (Friston in Nat Rev Neurosci 11(2):127–138, 2010. doi: 10.1038/nrn2787 ). Why would a biological agent that aims at minimising uncertainty in its encounters with the world ever be motivated to seek out novelty? Novelty for such an agent would arrive in the form of sensory and physiological states that are unexpected. Such an agent ought therefore to avoid novel and surprising interactions with the world one might think. Yet humans and many other animals find play and other forms of novelty-seeking and exploration hugely rewarding. How can this be understood in frameworks for studying the mind that emphasise prediction error minimisation? This problem has been taken up in recent research concerned with epistemic action—actions an agent engages in to reduce uncertainty. However that work leaves two questions unanswered, which it is the aim of our paper to address. First, no account has been given yet of why it should feel good to the agent to engage the world playfully and with curiosity. Second an appeal is made to precision-estimation to explain epistemic action, yet it remains unclear how precision-weighting works in action more generally, or active inference. We argue that an answer to both questions may lie in the bodily states of an agent that track the rate at which free energy is being reduced. The recent literature on the predictive brain has connected the valence of emotional experiences to the rate of change in the reduction of prediction error (Joffily and Coricelli in PLoS Comput Biol 9(6):e1003094, 2013. doi: 10.1371/journal.pcbi.1003094 ; Van de Cruys, in Metzinger and Wiese (eds) Philosophy and predictive processing, vol 24, MIND Group, Frankfurt am Main, 2017. doi: 10.15502/9783958573253 ). In this literature valenced emotional experiences are hypothesised to be identical with changes in the rate at which prediction error is reduced. Experiences are negatively valenced when overall prediction error increases and are positively valenced when the sum of prediction errors decrease. We offer an ecological-enactive interpretation of the concept of valence and its connection to rate of change of prediction error. We show how rate of change should be understood in terms of embodied states of affordance-related action readiness. We then go on to apply this ecological-enactive account of error dynamics to provide an answer to the first question we have raised: It may explain why it should feel good to an agent to be curious and playful. Our ecological-enactive account also allows us to show how error dynamics may provide an answer to the second question we have raised regarding how precision-weighting works in active inference. An agent that is sensitive to rates of error reduction can tune precision on the fly. We show how this ability to tune precision on the go can allow agents to develop skills for adapting better and better to the unexpected, and search out opportunities for resolving uncertainty and progressing in its learning.

[Image: see text] The hydrophobicity of many chemotherapeutic agents usually results in their nonselective passive distribution into healthy cells and organs causing collateral toxicity. Ligand-targeted drugs (LTDs) are a promising class of targeted anticancer agents. The hydrophilicity of the targeting ligands in LTDs limits its nonselective passive tissue distribution and toxicity to healthy cells. In addition, the small size of LTDs allows for better tumor penetration, especially in the case of solid tumors. However, the short circulation half-life of LTDs, due to their hydrophilicity and small size, remains a significant challenge for achieving their full therapeutic potential. Therefore, extending the circulation half-life of targeted chemotherapeutic agents while maintaining their hydrophilicity and small size will represent a significant advance toward effective and safe cancer treatment. Here, we present a new approach for enhancing the safety and efficacy of targeted chemotherapeutic agents. By endowing hydrophobic chemotherapeutic agents with a targeting moiety and a hydrophilic small molecule that binds reversibly to the serum protein transthyretin, we generated small hydrophilic drug conjugates that displayed enhanced circulation half-life in rodents and selectivity to cancer cells. To the best of our knowledge, this is the first demonstration of a successful approach that maintains the small size and hydrophilicity of targeted anticancer agents containing hydrophobic payloads while at the same time extending their circulation half-life. This was demonstrated by the superior in vivo efficacy and lower toxicity of our conjugates in xenograft mouse models of metastatic prostate cancer.

Background Air pollution derived from combustion is associated with considerable cardiorespiratory morbidity and mortality in addition to environmental effects. Replacing petrodiesel with biodiesel may have ecological benefits, but impacts on human health remain unquantified. The objective was to compare acute cardiovascular effects of blended and pure biodiesel exhaust exposure against known adverse effects of petrodiesel exhaust (PDE) exposure in human subjects. In two randomized controlled double-blind crossover studies, healthy volunteers were exposed to PDE or biodiesel exhaust for one hour. In study one, 16 subjects were exposed, on separate occasions, to PDE and 30% rapeseed methyl ester biodiesel blend (RME30) exhaust, aiming at PM10 300 μg/m3. In study two, 19 male subjects were separately exposed to PDE and exhaust from a 100% RME fuel (RME100) using similar engine load and exhaust dilution. Generated exhaust was analyzed for physicochemical composition and oxidative potential. Following exposure, vascular endothelial function was assessed using forearm venous occlusion plethysmography and ex vivo thrombus formation was assessed using a Badimon chamber model of acute arterial injury. Biomarkers of inflammation, platelet activation and fibrinolysis were measured in the blood. Results In study 1, PDE and RME30 exposures were at comparable PM levels (314 ± 27 μg/m3; (PM10 ± SD) and 309 ± 30 μg/m3 respectively), whereas in study 2, the PDE exposure concentrations remained similar (310 ± 34 μg/m3), but RME100 levels were lower in PM (165 ± 16 μg/m3) and PAHs, but higher in particle number concentration. Compared to PDE, PM from RME had less oxidative potential. Forearm infusion of the vasodilators acetylcholine, bradykinin, sodium nitroprusside and verapamil resulted in dose-dependent increases in blood flow after all exposures. Vasodilatation and ex vivo thrombus formation were similar following exposure to exhaust from petrodiesel and the two biodiesel formulations (RME30 and RME100). There were no significant differences in blood biomarkers or exhaled nitric oxide levels between exposures. Conclusions Despite differences in PM composition and particle reactivity, controlled exposure to biodiesel exhaust was associated with similar cardiovascular effects to PDE. We suggest that the potential adverse health effects of biodiesel fuel emissions should be taken into account when evaluating future fuel policies. Trial registration ClinicalTrials.gov, NCT01337882/NCT01883466. Date of first enrollment March 11, 2011, registered April 19, 2011, i.e. retrospectively registered.

Short-term exposure to fine particulate matter (PM2.5) increases thrombotic risk particularly in obese individuals, but the underlying mechanisms remain unclear. This study aims to compare the effects of PM2.5 on inflammation and platelet activation in obese versus normal-weight adults, and investigate potential causal pathways. We conducted a panel study measuring blood markers in 44 obese and 53 normal-weight adults on 3 separate occasions in 2017-2018. Associations between PM2.5/black carbon (BC) and biomarkers were estimated using mixed-effect models. An interaction analysis compared PM2.5/BC-related effects between subgroups. Biomarker combinations and mediation analysis were performed to elucidate the biological pathways. There was a significant "low-high-low" trend of PM2.5 levels across the 3 study periods. Increases in pro-inflammatory cytokines and changes of platelet activation and aggregation markers were associated with PM2.5/BC in obese subgroup only. Among obese subjects, the combination of pro-inflammatory cytokines and that of platelet markers increased 26.8% (95% CI: 16.0%, 37.9%) and 14.7% (95% CI: 1.9%, 27.0%) per IQR increase in PM2.5 over 5-day and 7-day averages. Inflammation mediated 24.5% of the pathways through which PM2.5 promoted platelet activation. This study suggested obese people are susceptible to pro-thrombotic impacts of PM2.5 exposures. PM2.5 may aggravate thrombosis through obesity-related inflammation.

Summary Background 3 billion people worldwide rely on polluting fuels and technologies for domestic cooking and heating. We estimate the global, regional, and national health burden associated with exposure to household air pollution. Methods For the systematic review and meta-analysis, we systematically searched four databases for studies published from database inception to April 2, 2020, that evaluated the risk of adverse cardiorespiratory, paediatric, and maternal outcomes from exposure to household air pollution, compared with no exposure. We used a random-effects model to calculate disease-specific relative risk (RR) meta-estimates. Household air pollution exposure was defined as use of polluting fuels (coal, wood, charcoal, agricultural wastes, animal dung, or kerosene) for household cooking or heating. Temporal trends in mortality and disease burden associated with household air pollution, as measured by disability-adjusted life-years (DALYs), were estimated from 2000 to 2017 using exposure prevalence data from 183 of 193 UN member states. 95% CIs were estimated by propagating uncertainty from the RR meta-estimates, prevalence of household air pollution exposure, and disease-specific mortality and burden estimates using a simulation-based approach. This study is registered with PROSPERO, CRD42019125060. Findings 476 studies (15·5 million participants) from 123 nations (99 [80%] of which were classified as low-income and middle-income) met the inclusion criteria. Household air pollution was positively associated with asthma (RR 1·23, 95% CI 1·11–1·36), acute respiratory infection in both adults (1·53, 1·22–1·93) and children (1·39, 1·29–1·49), chronic obstructive pulmonary disease (1·70, 1·47–1·97), lung cancer (1·69, 1·44–1·98), and tuberculosis (1·26, 1·08–1·48); cerebrovascular disease (1·09, 1·04–1·14) and ischaemic heart disease (1·10, 1·09–1·11); and low birthweight (1·36, 1·19–1·55) and stillbirth (1·22, 1·06–1·41); as well as with under-5 (1·25, 1·18–1·33), respiratory (1·19, 1·18–1·20), and cardiovascular (1·07, 1·04–1·11) mortality. Household air pollution was associated with 1·8 million (95% CI 1·1–2·7) deaths and 60·9 million (34·6–93·3) DALYs in 2017, with the burden overwhelmingly experienced in low-income and middle-income countries (LMICs; 60·8 million [34·6–92·9] DALYs) compared with high-income countries (0·09 million [0·01–0·40] DALYs). From 2000, mortality associated with household air pollution had reduced by 36% (95% CI 29–43) and disease burden by 30% (25–36), with the greatest reductions observed in higher-income nations. Interpretation The burden of cardiorespiratory, paediatric, and maternal diseases associated with household air pollution has declined worldwide but remains high in the world's poorest regions. Urgent integrated health and energy strategies are needed to reduce the adverse health impact of household air pollution, especially in LMICs. Funding British Heart Foundation, Wellcome Trust.

Epidemiological studies have consistently linked exposure to PM2.5 with adverse health effects. The oxidative potential (OP) of aerosol particles has been widely suggested as a measure of their potential toxicity. Several acellular chemical assays are now readily employed to measure OP, however, uncertainty remains regarding the atmospheric conditions and specific chemical components of PM2.5 that drive OP. A limited number of studies have simultaneously utilised multiple OP assays with a wide range of concurrent measurements and investigated the seasonality of PM2.5 OP. In this work, filter samples were collected in winter 2016 and summer 2017 during the atmospheric pollution and human health in a Chinese megacity (APHH-Beijing) campaign, and PM2.5 OP was analysed using four acellular methods; ascorbic acid (AA), dithiothreitol (DTT), 2-7-dichlorofluoroscin/hydrogen peroxidase (DCFH) and electron paramagnetic resonance spectroscopy (EPR). Positive correlations of OP normalised per volume of air of all four assays with overall PM2.5 mass was observed, with stronger correlations in the winter compared to the summer. In contrast, when OP assay values were normalised for particle mass, days with higher PM2.5 mass concentrations (μg m−3) were found to have lower intrinsic mass-normalised OP values as measured by AA and DTT. This indicates that total PM2.5 mass concentrations alone might not always be the best indicator for particle toxicity. Univariate analysis of OP values and an extensive range of additional measurements, 107 in total, including PM2.5 composition, gas phase composition and meteorological data, provides detailed insight into chemical components or atmospheric processes that determine PM2.5 OP variability. Multivariate statistical analyses highlighted associations of OP assay responses with varying chemical components in PM2.5 for both mass- and volume-normalised data. Variable selection was used to produce subsets of measurements indicative of PM2.5 sources, and used to model OP response; AA and DTT assays were well predicted by small panels of measurements, and indicated fossil fuel combustion processes, vehicle emissions and biogenic SOA as most influential in the assay response. Through comparative analysis of both mass- and volume-normalised data we demonstrate the importance of also considering mass-normalised OP when correlating with particle composition measurements, which provides a more nuanced picture of compositional drivers and sources of OP compared to volume-normalised analysis, and which may be more useful in temporal and site comparative contexts.

With the ever-expanding number of manufactured nanomaterials (MNMs) under development there is a vital need for nanotoxicology studies that test the potential for MNMs to cause harm to health. An extensive body of work in cell cultures and animal models is vital to understanding the physicochemical characteristics of MNMs and the biological mechanisms that underlie any detrimental actions to cells and organs. In human subjects, exposure monitoring is combined with measurement of selected health parameters in small panel studies, especially in occupational settings. However, the availability of further in vivo human data would greatly assist the risk assessment of MNMs. Here, the potential for controlled inhalation exposures of MNMs in human subjects is discussed. Controlled exposures to carbon, gold, aluminum, and zinc nanoparticles in humans have already set a precedence to demonstrate the feasibility of this approach. These studies have provided considerable insight into the potential (or not) of nanoparticles to induce inflammation, alter lung function, affect the vasculature, reach the systemic circulation, and accumulate in other organs. The need for further controlled exposures of MNMs in human volunteers - to establish no-effect limits, biological mechanisms, and provide vital data for the risk assessment of MNMs - is advocated.

This study is part of the “Air Polluion Impacts on Cardiopulmonary disease in Beijing: an integrated study of Exposure Science, Toxicologenomics & Environmental Epidemiology (APIC-ESTEE)” project under the UK-China joint research programme “Atmospheric Pollution and Human Health in a Chinese Megacity (APHH-China)”. The aim is to capture the spatio-temporal variability in people's exposure to fine particles (PM2.5) and black carbon (BC) air pollution in Beijing, China. A total of 120 students were recruited for a panel study from ten universities in Haidian District in northwestern Beijing from December 2017 to June 2018. Real-time personal concentrations of PM2.5 and BC were measured over a 24-h period with two research-grade portable personal exposure monitors. Personal microenvironments (MEs) were determined by applying an algorithm to the handheld GPS unit data. On average, the participants spent the most time indoors (79% in Residence and 16% in Workplace), and much less time travelling by Walking, Cycling, Bus and Metro. Similar patterns were observed across participant gender and body-mass index classifications. The participants were exposed to 33.8 ± 27.8 μg m−3 PM2.5 and to 1.9 ± 1.2 μg m−3 BC over the 24-h monitoring period, on average 24.3 μg m−3 (42%) and 0.8 μg m−3 (28%) lower, respectively, than the concurrent fixed-site ambient measurements. Relative differences between personal and ambient BC concentrations showed greater variability across the MEs, highlighting significant contributions from Dining and travelling by Bus, which involve potential combustion of fuels. This study demonstrates the potential value of personal exposure monitoring in investigating air pollution related health effects, and in evaluating the effectiveness of pollution control and intervention measures.

Background Ozone is a highly oxidative gaseous pollutant associated with adverse health outcomes, but markers for internal exposure to ambient ozone are not well-established. Methods We aimed to evaluate the feasibility and suitability of the markers in oral microbiome for ambient ozone exposure. Between March and May in 2018, 97 healthy adults were examined on 2 or 3 occasions for oral swab sampling. Hourly concentrations of ambient ozone 1–7 days preceding sampling were collected. Mixed-effect models were fitted to examine the associations between ambient ozone and the diversity and taxon abundances of oral microbiome. Receiver operating characteristic (ROC) curves estimated the accuracies of markers to delineate between samples exposed to different concentrations of ambient ozone. The associations between the makers and lung function were further examined by linear mixed effect models. Results The averages of daily mean concentrations of ambient ozone (O3-daily), maximum 8-h means (O3-8hmax) and 1-h maximums (O3-1hmax) were respectively 72 μg/m³, 123 μg/m³ and 144 μg/m³. O3-daily was positively associated with α-diversity of oral microbiome, but the exposure-response curves only yielded positive associations in the range of O3-daily from 60 μg/m³ to 75 μg/m³. Results of O3-8hmax and O3-1hmax were consistent with these of O3-daily. With an interquartile range increase in O3-daily at lag04, the abundance of Proteobacteria decreased by 3.1% (95% CI: −4.0%, −2.2%) and Firmicutes increased by 3.3% (95% CI: 2.3%, 4.3%), whilst the Proteobacteria:Firmicutes ratio (P/F) decreased by 0.9 (95% CI: −1.5, −0.4). The areas under ROC curves for Proteobacteria, Firmicutes and P/F were 0.8535, 0.7569 and 0.8929, respectively. Proteobacteria and P/F were associated with forced expiratory volume in the first second and fractional exhaled nitric oxide significantly. Conclusion Ambient ozone disturbs oral microbial homeostasis. Proteobacteria, Firmicutes and their ratio may be potential markers for short-term ambient ozone exposure, and indicators of airway inflammation or lung function decline.

The negative effects of air pollution on human health has been subject to a number of epidemiological studies that consistently link respiratory and cardiovascular diseases to exposure to particulate matter (PM) (Englert, 2004). It is estimated that up to 0.3 million premature deaths per year in Europe and 2.1 million deaths worldwide are the result of exposure to particles with an aerodynamic diameter less than 2.5 μm (PM2.5) (Andersson, 2009). However, identifying the specific particle properties responsible for these health effects, such as their physical and physicochemical characteristics, as well as their chemical composition, remains a challenge. One of the leading hypotheses for how particles cause harm is by inducing oxidative stress and inflammation, which can subsequently lead to disease (Øvrevik, 2015). In particular, reactive oxygen species (ROS), which typically refer to a range of species including hydrogen peroxide (H2O2) possibly including organic peroxides, the hydroxyl radical (.OH) and superoxide radical (O2.-), may substantially contribute to the oxidative potential (OP) of PM and hence influence their toxicity. An excess of ROS in the lung, introduced or generated via particle exposure, leads to an imbalance of the oxidant-antioxidant ratio in favour of the former, which can subsequently promote oxidative stress. There are a number of acellular methods used routinely to measure aerosol OP, including the dithiothreitol assay (DTT), ascorbic acid assay (AA), 2,7-dichlorofluoroscein/hydrogen peroxidase assay (DCFH/HRP), and electron paramagnetic resonance (EPR) spectroscopy. In this work, the OP of aerosol collected in Beijing, China, in the winter 2016 and summer 2017 during the Atmospheric Pollution and Human Health in a Chinese Megacity (APHH) campaign is quantified, with 30 24-hr aerosol filter samples analysed for each season. We use the four aforementioned methods to measure OPAA, OPDTT, OPDCFH and OPEPR, and to extensively characterise the seasonal variation of aerosol OP in a megacity. All OP measurements show a significantly stronger correlation with PM2.5 mass in the winter compared to summer. Furthermore, the OPAA, OPDTT, OPDCFH and OPEPR were correlated using univariate and multivariate analysis with a variety of other measurements such as meteorological data, trace gas measurements and aerosol composition measurements including organic aerosol components and x-ray fluorescence elemental analysis. These results emphasise that the four OP methods applied in this study capture different aspects of aerosol OP between the seasons. As an example, OPAA normalised to account for aerosol mass show that aerosol OPAA in the winter is higher on average and more variable compared to the summer, whereas OPDCFH is more consistent between the winter and summer seasons. OPAA also showed a strong correlation with PM2.5 mass in the winter (r2 = 0.91) but correlated poorly in the summer months (r2 = 0.09), suggesting different aerosol components affect OPAA in summer and winter. Englert, N. Toxicol. Lett. 149, 235–242 (2004). Andersson, C., et al., Atmos. Environ. 43, 3614–3620 (2009). Øvrevik, J., et al., Biomolecules 5, 1399–1440 (2015).

Background Previous studies suggest an association between short-term exposure to carbon monoxide and myocardial infarction. We performed a systematic review and meta-analysis to assess current evidence on this association to support the update of the World Health Organization (WHO) Global Air Quality Guidelines. Methods We searched Medline, Embase and Cochrane Central Register of Controlled Trials to update the evidence published in a previous systematic review up to 30th September 2018 for studies investigating the association between short-term exposure to ambient carbon monoxide (up to lag of seven days) and emergency department visits or hospital admissions and mortality due to myocardial infarction. Two reviewers assessed potentially eligible studies and performed data extraction independently. Random-effects meta-analysis was used to derive the pooled risk estimate per 1 mg/m3 increase in ambient carbon monoxide concentration. Risk of bias in individual studies was assessed using a domain-based assessment tool. The overall certainty of the body of evidence was evaluated using an adapted certainty of evidence assessment framework. Results We evaluated 1,038 articles from the previous review and our updated literature search, of which, 26 satisfied our inclusion criteria. Overall, myocardial infarction was associated with exposure to ambient carbon monoxide concentration (risk ratio of 1.052, 95% confidence interval 1.017–1.089 per 1 mg/m3 increase). A third of studies were assessed to be at high risk of bias (RoB) due to inadequate adjustment for confounding. Using an adaptation of the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework, the overall evidence was assessed to be of moderate certainty. Conclusions This review demonstrated that the pooled risk ratio for myocardial infarction was 1.052 (95% CI 1.017–1.089) per 1 mg/m3 increase in ambient carbon monoxide concentration. However, very few studies originated from low- and middle-income countries.

This study is part of the "Air Polluion Impacts on Cardiopulmonary disease in Beijing: an integrated study of Exposure Science, ToxicologenomicsEnvironmental Epidemiology (APIC-ESTEE)" project under the UK-China joint research programme "Atmospheric Pollution and Human Health in a Chinese Megacity (APHH-China)". The aim is to capture the spatio-temporal variability in people's exposure to fine particles (PM

Air pollution is associated with premature mortality and a wide spectrum of diseases. Traffic-related air pollution (TRAP) is one of the most concerning sources of air pollution for human exposure and health. Until TRAP levels can be significantly reduced on a global scale, there is a need for effective shorter-term strategies to prevent the adverse health effects of TRAP. A growing number of studies suggest that increasing antioxidant intake, through diet or supplementation, may reduce this burden of disease. In this paper, we conducted a non-systematic literature review to assess the available evidence on antioxidant-rich diets and antioxidant supplements as a strategy to mitigate adverse health effects of TRAP in human subjects. We identified 11 studies that fit our inclusion criteria; 3 of which investigated antioxidant-rich diets and 8 of which investigated antioxidant supplements. Overall, we found consistent evidence that dietary intake of antioxidants from adherence to the Mediterranean diet and increased fruit and vegetable consumption is effective in mitigating adverse health effects associated with TRAP. In contrast, antioxidant supplements, including fish oil, olive oil, and vitamin C and E supplements, presented conflicting evidence. Further research is needed to determine why antioxidant supplementation has limited efficacy and whether this relates to effective dose, supplement formulation, timing of administration, or population being studied. There is also a need to better ascertain if susceptible populations, such as children, the elderly, asthmatics and occupational workers consistently exposed to TRAP, should be recommended to increase their antioxidant intake to reduce their burden of disease. Policymakers should consider increasing populations’ antioxidant intake, through antioxidant-rich diets, as a relatively cheap and easy preventive measure to lower the burden of disease associated with TRAP.

Air pollution is associated with staggering levels of morbidity and mortality globally. Emissions from traffic, such as particulate matter and nitrogen dioxide in exhaust, are a prominent source of pollution in urban environments. Specifically, there is a growing body of epidemiological data demonstrating that traffic-related air pollution (TRAP) is linked to widespread effects on health. This chapter provides an overview of mechanistic studies demonstrating the link between TRAP and health effects on the lung, cardiovascular system, and other organs of the body. Special attention is given to the effect of particles in TRAP on the cardiovascular system as an exemplar for the many mechanisms by which these pollutants can exert multiple effects on an organ system through a variety of underlying pathways. These research findings lend biological plausibility to epidemiological observations and emphasize the need to tackle vehicle emissions to reduce the health effects of air pollution.

To assess the cardiovascular benefits of protecting against particulate air pollution and noise, we conducted a randomized crossover study with 40 young healthy college students from March to May 2017 in the underground subway, Beijing. Participants each received 4 treatments (no intervention phase [NIP], respirator intervention phase [RIP], headphone intervention phase [HIP], respirator plus headphone intervention phase [RHIP]) in a randomized order during 4 different study periods with 2-week washout intervals. We measured personal exposure to particulate matter (PM), noise and electrocardiogram (ECG) parameters (heart rate variability (HRV), heart rate (HR) and ST segment changes), ambulatory blood pressure (BP) continuously for 4 hours to investigate the cardiovascular effects. Compared with NIP, most of the HRV parameters increased, especially high frequency (HF) [21.1% (95% CI: 15.7%, 26.9%), 18.2% (95% CI: 12.8%, 23.9%), and 35.5% (95% CI: 29.3%, 42.0%) in RIP, HIP, and RHIP, respectively], whereas ST segment elevation and HR decreased for all 3 modes of interventions. However, no significant differences were observed in BP among the 4 treatments. In summary, short-term wearing of a respirator and/or headphone may be an effective way to minimize cardiovascular risk induced by air pollution in the subway by improving autonomic nervous function.

Background The effect of health status on the relationship between particulate matter (PM) and black carbon (BC) and cardiac autonomic function has not been examined sufficiently directly comparing patients with healthy participants. Objectives To evaluate the association patterns between size-fractioned indoor PM and BC and cardiac autonomic function in chronic obstructive pulmonary disease (COPD) patients and their healthy spouses. Methods Twenty-four-hour heart rate variability (HRV) and heart rate (HR) was measured in eight pairs of stable COPD patients and their healthy spouses. Real-time size-fractioned indoor PM and BC levels were monitored on the same, and preceding, days. Mixed-effects models were used to estimate the changes in health indices and pollutants after controlling for potential confounding variables. Results Increases in size-fractioned PM and BC were associated with alterations in cardiac autonomic function in both COPD patients and their healthy spouses. However, the association patterns differed between the two groups. In COPD group, an IQR (13.65 μg/m3) increase in PM0.5 at 12-h moving average was associated with reductions of 14.62% (95% CI: -21.74%, -6.86%) in total power (TP) and 10.14% (95% CI: -16.11%, -3.76%) in high frequency (HF) power. In healthy volunteers, however, TP and HF declined immediately upon exposure to PM and then returned to normal levels gradually. In this group, an IQR increase in PM0.5 at 5 min moving average was associated a 20.30% (95% CI: -25.49%, -14.73%) reduction in TP and a 31.79% (95% CI: -36.48%, -26.72%) reduction in HF. Conclusions Exposure to indoor PM and BC was associated with cardiac autonomic dysfunction in COPD patients and their healthy spouses. Exposure had a greater lagged effect on HRV in COPD patients than in healthy participants. These findings will aid the formulation of targeted measures to prevent the adverse effects of indoor air pollution for individuals with different health statuses.

Associations between size-fractionated indoor particulate matter (PM) and black carbon (BC) and heart rate variability (HRV) and heart rate (HR) in elderly women remain unclear. Twenty-nine healthy elderly women were measured for 24-hour HRV/HR indices. Real-time size-fractionated indoor PM and BC were monitored on the same day and on the preceding day. Mixed-effects models were applied to investigate the associations between pollutants and HRV/HR indices. Increases in size-fractionated indoor PM were significantly associated with declines in power in the high-frequency band (HF), power in the low-frequency band (LF), and standard deviation of all NN intervals (SDNN). The largest decline in HF was 19% at 5-minute moving average for an interquartile range (IQR) increase (24 μg/m3 ) in PM0.5 . The results showed that smaller particles could lead to greater reductions in HRV indices. The reported associations were modified by body mass index (BMI): Declines in HF at 5-minute average for an IQR increase in PM0.5 were 34.5% and 1.0% for overweight (BMI ≥25 kg/m2 ) and normal-weight (BMI

Titania (TiO2) nanoparticles were surface modified using silica and citrate to implement a ‘safe-by-design' approach for managing potential toxicity of titania nanoparticles by controlling surface redox reactivity. DLS and zeta-potential analyses confirmed the surface modification, and electron microscopy and surface area measurements demonstrated nanoscale dimensions of the particles. Electron paramagnetic resonance (EPR) was used to determine the exogenous generation of reactive oxygen species (ROS). All the produced spray dried nanotitania lowered levels of ROS when compared to the corresponding dispersed nanotitania, suggesting that the spray drying process is an appropriate design strategy for the control of nano TiO2 ROS reactivity. The modification of nanotitania with silica and with citrate resulted in increased levels of ROS generation in exogenous measurements, including photoexcitation for 60 minutes. The dichlorodihydrofluorescein (DCFH) assay of dose-dependent production of oxidative stress, generated by pristine and modified nanotitania in macrophages and alveolar epithelial cells, found no significant change in toxicity originating from the generation of reactive oxygen species. Our findings show that there is no direct correlation between the photocatalytic activity of nanotitania and its oxidative stress-mediated potential toxicity, and it is possible to improve the former, for example adding silica as a modifying agent, without altering the cell redox equilibrium.