Long-term air pollution exposure and risk of SARS-CoV-2 infection: A UK-wide cohort study.

BACKGROUND: The association between air quality and risk of SARS-CoV-2 infection is poorly understood. We investigated this association using serological individual-level data adjusting for a wide range of confounders, in a large population-based cohort (COVIDENCE UK). METHODS: We assessed the associations between long-term (2015-19) nitrogen dioxide (NO2) and fine particulate matter with an aerodynamic diameter of ≤2.5 µm (PM2.5), exposures with SARS-CoV-2 infection, level of antibody response among those infected, and COVID-19 disease severity. We used serological data from 10,489 participants in the COVIDENCE UK cohort, and estimated annual average air pollution exposure at each participant's home postcode. RESULTS: After controlling for potential confounders, we found a positive association between 5-year NO2 and PM2.5 exposures and the risk of seropositivity: 10 unit increase in NO2 (µg/m3) was associated with an increasing risk of seropositivity by 1.092 (95% CI 1.02 to 1.17; p-for-trend 0.012). For PM2.5, 10 unit increase (µg/m3) was associated with an increasing risk of seropositivity by 1.65 (95% CI 1.015-2.68; p-for-trend 0·049). In addition, we found that NO2 was positively associated with higher antibody titres (p-for-trend 0·013) among seropositive participants, with no evidence of an association for PM2.5. CONCLUSION: Our findings suggest that the long-term burden of air pollution increased the risks of SARS-CoV-2 infection and has important implications for future pandemic preparedness. This evidence strengthens the case for reducing long-term air pollution exposures to reduce the vulnerability of individuals to respiratory viruses.

Investigating the impact of London's ultra low emission zone on children's health: children's health in London and Luton (CHILL) protocol for a prospective parallel cohort study.

BACKGROUND: Air pollution harms health across the life course. Children are at particular risk of adverse effects during development, which may impact on health in later life. Interventions that improve air quality are urgently needed both to improve public health now, and prevent longer-term increased vulnerability to chronic disease. Low Emission Zones are a public health policy intervention aimed at reducing traffic-derived contributions to urban air pollution, but evidence that they deliver health benefits is lacking. We describe a natural experiment study (CHILL: Children's Health in London and Luton) to evaluate the impacts of the introduction of London's Ultra Low Emission Zone (ULEZ) on children's health. METHODS: CHILL is a prospective two-arm parallel longitudinal cohort study recruiting children at age 6-9 years from primary schools in Central London (the focus of the first phase of the ULEZ) and Luton (a comparator site), with the primary outcome being the impact of changes in annual air pollutant exposures (nitrogen oxides [NOx], nitrogen dioxide [NO2], particulate matter with a diameter of less than 2.5micrograms [PM2.5], and less than 10 micrograms [PM10]) across the two sites on lung function growth, measured as post-bronchodilator forced expiratory volume in one second (FEV1) over five years. Secondary outcomes include physical activity, cognitive development, mental health, quality of life, health inequalities, and a range of respiratory and health economic data. DISCUSSION: CHILL's prospective parallel cohort design will enable robust conclusions to be drawn on the effectiveness of the ULEZ at improving air quality and delivering improvements in children's respiratory health. With increasing proportions of the world's population now living in large urban areas exceeding World Health Organisation air pollution limit guidelines, our study findings will have important implications for the design and implementation of Low Emission and Clean Air Zones in the UK, and worldwide. CLINICALTRIALS: GOV: NCT04695093 (05/01/2021).

Vitamin D3 regulates PM-driven primary human neutrophil inflammatory responses.

Recent evidence has demonstrated that both acute and chronic exposure to particulate air pollution are risk factors for respiratory tract infections and increased mortality from sepsis. There is therefore an urgent need to establish the impact of ambient particulate matter (PM) on innate immune cells and to establish potential strategies to mitigate against adverse effects. PM has previously been reported to have potential adverse effects on neutrophil function. In the present study, we investigated the impact of standard urban PM (SRM1648a, NIST) and PM2.5 collected from Chiang Mai, Thailand, on human peripheral blood neutrophil functions, including LPS-induced migration, IL-8 production, and bacterial killing. Both NIST and the PM2.5, being collected in Chiang Mai, Thailand, increased IL-8 production, but reduced CXCR2 expression and migration of human primary neutrophils stimulated with Escherichia coli LPS. Moreover, PM-pretreated neutrophils from vitamin D-insufficient participants showed reduced E. coli-killing activity. Furthermore, in vitro vitamin D3 supplementation attenuated IL-8 production and improved bacterial killing by cells from vitamin D-insufficient participants. Our findings suggest that provision of vitamin D to individuals with insufficiency may attenuate adverse acute neutrophilic responses to ambient PM.

Associations between air pollution and mental health service use in dementia: a retrospective cohort study.

BACKGROUND: Little is known about the role of air pollution in how people with dementia use mental health services. OBJECTIVE: We examined longitudinal associations between air pollution exposure and mental health service use in people with dementia. METHODS: In 5024 people aged 65 years or older with dementia in South London, high resolution estimates of nitrogen dioxide (NO2) and particulate matter (PM2.5 and PM10) levels in ambient air were linked to residential addresses. Associations between air pollution and Community Mental Health Team (CMHT) events (recorded over 9 years) were examined using negative binomial regression models. Cognitive function was measured using the Mini Mental State Examination (MMSE) and health and social functioning was measured using the Health of the Nation Outcomes Scale (HoNOS65+). Associations between air pollution and both MMSE and HoNOS65+ scores were assessed using linear regression models. FINDINGS: In the first year of follow-up, increased exposure to all air pollutants was associated with an increase in the use of CMHTs in a dose-response manner. These associations were strongest when we compared the highest air pollution quartile (quartile 4: Q4) with the lowest quartile (Q1) (eg, NO2: adjusted incidence rate ratio (aIRR) 1.27, 95% CI 1.11 to 1.45, p<0.001). Dose-response patterns between PM2.5 and CMHT events remained at 5 and 9 years. Associations were strongest for patients with vascular dementia. NO2 levels were linked with poor functional status, but not cognitive function. CONCLUSIONS: Residential air pollution exposure is associated with increased CMHT usage among people with dementia. CLINICAL IMPLICATIONS: Efforts to reduce pollutant exposures in urban settings might reduce the use of mental health services in people with dementia, freeing up resources in already considerably stretched psychiatric services.

Device-Measured Change in Physical Activity in Primary School Children During the UK COVID-19 Pandemic Lockdown: A Longitudinal Study.

BACKGROUND: Lockdown measures, including school closures, due to the COVID-19 pandemic have caused widespread disruption to children's lives. The aim of this study was to explore the impact of a national lockdown on children's physical activity using seasonally matched accelerometry data. METHODS: Using a pre/post observational design, 179 children aged 8 to 11 years provided physical activity data measured using hip-worn triaxial accelerometers worn for 5 consecutive days prepandemic and during the January to March 2021 lockdown. Multilevel regression analyses adjusted for covariates were used to assess the impact of lockdown on time spent in sedentary and moderate to vigorous physical activity. RESULTS: A 10.8-minute reduction in daily time spent in moderate to vigorous physical activity (standard error: 2.3 min/d, P < .001) and a 33.2-minute increase in daily sedentary activity (standard error: 5.5 min/d, P < .001) were observed during lockdown. This reflected a reduction in daily moderate to vigorous physical activity for those unable to attend school (-13.1 [2.3] min/d, P < .001) during lockdown, with no significant change for those who continued to attend school (0.4 [4.0] min/d, P < .925). CONCLUSION: These findings suggest that the loss of in-person schooling was the single largest impact on physical activity in this cohort of primary school children in London, Luton, and Dunstable, United Kingdom.

The Contribution of Environmental Science to Mental Health Research: A Scoping Review.

Mental health is influenced by multiple complex and interacting genetic, psychological, social, and environmental factors. As such, developing state-of-the-art mental health knowledge requires collaboration across academic disciplines, including environmental science. To assess the current contribution of environmental science to this field, a scoping review of the literature on environmental influences on mental health (including conditions of cognitive development and decline) was conducted. The review protocol was developed in consultation with experts working across mental health and environmental science. The scoping review included 202 English-language papers, published between 2010 and 2020 (prior to the COVID-19 pandemic), on environmental themes that had not already been the subject of recent systematic reviews; 26 reviews on climate change, flooding, air pollution, and urban green space were additionally considered. Studies largely focused on populations in the USA, China, or Europe and involved limited environmental science input. Environmental science research methods are primarily focused on quantitative approaches utilising secondary datasets or field data. Mental health measurement was dominated by the use of self-report psychometric scales. Measures of environmental states or exposures were often lacking in specificity (e.g., limited to the presence or absence of an environmental state). Based on the scoping review findings and our synthesis of the recent reviews, a research agenda for environmental science's future contribution to mental health scholarship is set out. This includes recommendations to expand the geographical scope and broaden the representation of different environmental science areas, improve measurement of environmental exposure, prioritise experimental and longitudinal research designs, and giving greater consideration to variation between and within communities and the mediating pathways by which environment influences mental health. There is also considerable opportunity to increase interdisciplinarity within the field via the integration of conceptual models, the inclusion of mixed methods and qualitative approaches, as well as further consideration of the socio-political context and the environmental states that can help support good mental health. The findings were used to propose a conceptual model to parse contributions and connections between environmental science and mental health to inform future studies.

A Review of Road Traffic-Derived Non-Exhaust Particles: Emissions, Physicochemical Characteristics, Health Risks, and Mitigation Measures.

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.

Acute cardiovascular effects of controlled exposure to dilute Petrodiesel and biodiesel exhaust in healthy volunteers: a crossover study.

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.

Characterising professional drivers' exposure to traffic-related air pollution: Evidence for reduction strategies from in-vehicle personal exposure monitoring.

Professional drivers working in congested urban areas are required to work near harmful traffic related pollutants for extended periods, representing a significant, but understudied occupational risk. This study collected personal black carbon (BC) exposures for 141 drivers across seven sectors in London. The aim of the study was to assess the magnitude and the primary determinants of their exposure, leading to the formulation of targeted exposure reduction strategies for the occupation. Each participant's personal BC exposures were continuously measured using real-time monitors for 96 h, incorporating four shifts per participant. 'At work' BC exposures (3.1 ± 3.5 µg/m3) were 2.6 times higher compared to when 'not at work' (1.2 ± 0.7 µg/m3). Workers spent 19% of their time 'at work driving', however this activity contributed 36% of total BC exposure, highlighting the disproportionate effect driving had on their daily exposure. Taxi drivers experienced the highest BC exposures due to the time they spent working in congested central London, while emergency services had the lowest. Spikes in exposure were observed while driving and were at times greater than 100 µg/m3. The most significant determinants of drivers' exposures were driving in tunnels, congestion, location, day of week and time of shift. Driving with closed windows significantly reduced exposures and is a simple behaviour change drivers could implement. Our results highlight strategies by which employers and local policy makers can reduce professional drivers' exposure to traffic-related air pollution.

Air Pollution and Asthma: Mechanisms of Harm and Considerations for Clinical Interventions.

There is global concern regarding the harmful impact of polluted air on the respiratory health of patients with asthma. Multiple epidemiologic studies have shown ongoing associations between high levels of air pollution and poor early life lung growth, development of allergic sensitization, development of asthma, airway inflammation, acutely impaired lung function, respiratory tract infections, and asthma exacerbations. However, studies have often yielded inconsistent findings, and not all studies have found significant associations; this may be related to both variations in statistical, measurement, and modeling methodologies between studies as well as differences in the concentrations and composition of air pollution globally. Overall, this variation in findings suggests we still do not fully understand the effects of ambient pollution on the lungs and on the evolution and exacerbation of airway diseases. There is clearly a need to augment epidemiologic studies with experimental studies to clarify the underlying mechanistic basis for the adverse responses reported and to identify the key gaseous and particle-related components within the complex air pollution mixture driving these outcomes. Some progress toward these aims has been made. This article reviews studies providing an improved understanding of causal pathways linking air pollution to asthma development and exacerbation. The article also considers potential strategies to reduce asthma morbidity and mortality through regulation and behavioral/pharmacologic interventions, including a consideration of pollutant avoidance strategies and antioxidant and/or vitamin D supplementation.

Air Pollution and Asthma: Critical Targets for Effective Action.

Evidence to advocate for cleaner air for people with asthma is not in short supply. We know that air pollution is associated with the development and worsening of the condition and that mitigating interventions can improve respiratory outcomes. We have clear targets, particularly traffic emissions, especially in urban areas, and plenty of potentially effective actions. Road traffic must be reduced, and what remains should be cleaner and greener. Urban green spaces, safe cycle networks and wider pavements will promote active travel and leisure time exercise. Healthcare professionals must ensure people are aware of their air quality, its impact on asthma and the appropriate behaviour to safeguard health. What remains are realistic policies and effective measures, based on the correct scientific evidence, to be taken forth with political courage and investment so that air pollution no longer contributes to the development or worsening of respiratory ill health.

Association between air pollution exposure and mental health service use among individuals with first presentations of psychotic and mood disorders: retrospective cohort study.

BACKGROUND: Growing evidence suggests that air pollution exposure may adversely affect the brain and increase risk for psychiatric disorders such as schizophrenia and depression. However, little is known about the potential role of air pollution in severity and relapse following illness onset. AIMS: To examine the longitudinal association between residential air pollution exposure and mental health service use (an indicator of illness severity and relapse) among individuals with first presentations of psychotic and mood disorders. METHOD: We identified individuals aged ≥15 years who had first contact with the South London and Maudsley NHS Foundation Trust for psychotic and mood disorders in 2008-2012 (n = 13 887). High-resolution (20 × 20 m) estimates of nitrogen dioxide (NO2), nitrogen oxides (NOx) and particulate matter (PM2.5 and PM10) levels in ambient air were linked to residential addresses. In-patient days and community mental health service (CMHS) events were recorded over 1-year and 7-year follow-up periods. RESULTS: Following covariate adjustment, interquartile range increases in NO2, NOx and PM2.5 were associated with 18% (95% CI 5-34%), 18% (95% CI 5-34%) and 11% (95% CI 3-19%) increased risk for in-patient days after 1 year. Similarly, interquartile range increases in NO2, NOx, PM2.5 and PM10 were associated with 32% (95% CI 25-38%), 31% (95% CI 24-37%), 7% (95% CI 4-11%) and 9% (95% CI 5-14%) increased risk for CMHS events after 1 year. Associations persisted after 7 years. CONCLUSIONS: Residential air pollution exposure is associated with increased mental health service use among people recently diagnosed with psychotic and mood disorders. Assuming causality, interventions to reduce air pollution exposure could improve mental health prognoses and reduce healthcare costs.

Mental health consequences of urban air pollution: prospective population-based longitudinal survey.

PURPOSE: The World Health Organisation (WHO) recently ranked air pollution as the major environmental cause of premature death. However, the significant potential health and societal costs of poor mental health in relation to air quality are not represented in the WHO report due to limited evidence. We aimed to test the hypothesis that long-term exposure to air pollution is associated with poor mental health. METHODS: A prospective longitudinal population-based mental health survey was conducted of 1698 adults living in 1075 households in South East London, from 2008 to 2013. High-resolution quarterly average air pollution concentrations of nitrogen dioxide (NO2) and oxides (NOx), ozone (O3), particulate matter with an aerodynamic diameter < 10 µm (PM10) and < 2.5 µm (PM2.5) were linked to the home addresses of the study participants. Associations with mental health were analysed with the use of multilevel generalised linear models, after adjusting for large number of confounders, including the individuals' socioeconomic position and exposure to road-traffic noise. RESULTS: We found robust evidence for interquartile range increases in PM2.5, NOx and NO2 to be associated with 18-39% increased odds of common mental disorders, 19-30% increased odds of poor physical symptoms and 33% of psychotic experiences only for PM10. These longitudinal associations were more pronounced in the subset of non-movers for NO2 and NOx. CONCLUSIONS: The findings suggest that traffic-related air pollution is adversely affecting mental health. Whilst causation cannot be proved, this work suggests substantial morbidity from mental disorders could be avoided with improved air quality.

WITHDRAWN: Allergic mechanisms of asthma are enhanced during the summer with oxidant PM10 components.

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.

Impact of London's low emission zone on air quality and children's respiratory health: a sequential annual cross-sectional study.

BACKGROUND: Low emission zones (LEZ) are an increasingly common, but unevaluated, intervention aimed at improving urban air quality and public health. We investigated the impact of London's LEZ on air quality and children's respiratory health. METHODS: We did a sequential annual cross-sectional study of 2164 children aged 8-9 years attending primary schools between 2009-10 and 2013-14 in central London, UK, following the introduction of London's LEZ in February, 2008. We examined the association between modelled pollutant exposures of nitrogen oxides (including nitrogen dioxide [NO2]) and particulate matter with a diameter of less than 2·5 µm (PM2·5) and less than 10 µm (PM10) and lung function: postbronchodilator forced expiratory volume in 1 s (FEV1, primary outcome), forced vital capacity (FVC), and respiratory or allergic symptoms. We assigned annual exposures by each child's home and school address, as well as spatially resolved estimates for the 3 h (0600-0900 h), 24 h, and 7 days before each child's assessment, to isolate long-term from short-term effects. FINDINGS: The percentage of children living at addresses exceeding the EU limit value for annual NO2 (40 µg/m3) fell from 99% (444/450) in 2009 to 34% (150/441) in 2013. Over this period, we identified a reduction in NO2 at both roadside (median -1·35 µg/m3 per year; 95% CI -2·09 to -0·61; p=0·0004) and background locations (-0·97; -1·56 to -0·38; p=0·0013), but not for PM10. The effect on PM2·5 was equivocal. We found no association between postbronchodilator FEV1 and annual residential pollutant attributions. By contrast, FVC was inversely correlated with annual NO2 (-0·0023 L/µg per m3; -0·0044 to -0·0002; p=0·033) and PM10 (-0·0090 L/µg per m3; -0·0175 to -0·0005; p=0·038). INTERPRETATION: Within London's LEZ, a smaller lung volume in children was associated with higher annual air pollutant exposures. We found no evidence of a reduction in the proportion of children with small lungs over this period, despite small improvements in air quality in highly polluted urban areas during the implementation of London's LEZ. Interventions that deliver larger reductions in emissions might yield improvements in children's health. FUNDING: National Institute for Health Research Biomedical Research Centre at Guy's and St Thomas' National Health Service (NHS) Foundation Trust and King's College London, NHS Hackney, Lee Him donation, and Felicity Wilde Charitable Trust.

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter.

BACKGROUND: Particulate matter (PM) pollutant exposure, which induces oxidative stress and inflammation, and vitamin D insufficiency, which compromises immune regulation, are detrimental in asthma. OBJECTIVES: Mechanistic cell culture experiments were undertaken to ascertain whether vitamin D abrogates PM-induced inflammatory responses of human bronchial epithelial cells (HBECs) through enhancement of antioxidant pathways. METHODS: Transcriptome analysis, PCR and ELISA were undertaken to delineate markers of inflammation and oxidative stress; with comparison of expression in primary HBECs from healthy and asthmatic donors cultured with reference urban PM in the presence/absence of vitamin D. RESULTS: Transcriptome analysis identified over 500 genes significantly perturbed by PM-stimulation, including multiple pro-inflammatory cytokines. Vitamin D altered expression of a subset of these PM-induced genes, including suppressing IL6. Addition of vitamin D suppressed PM-stimulated IL-6 production, although to significantly greater extent in healthy versus asthmatic donor cultures. Vitamin D also differentially affected PM-stimulated GM-CSF, with suppression in healthy HBECs and enhancement in asthmatic cultures. Vitamin D increased HBEC expression of the antioxidant pathway gene G6PD, increased the ratio of reduced to oxidised glutathione, and in PM-stimulated cultures decreased the formation of 8-isoprostane. Pre-treatment with vitamin D decreased CXCL8 and further decreased IL-6 production in PM-stimulated cultures, an effect abrogated by inhibition of G6PD with DHEA, supporting a role for this pathway in the anti-inflammatory actions of vitamin D. CONCLUSIONS: In a study using HBECs from 18 donors, vitamin D enhanced HBEC antioxidant responses and modulated the immune response to PM, suggesting that vitamin D may protect the airways from pathological pollution-induced inflammation.