Social connection and mortality in UK Biobank: a prospective cohort analysis.

BACKGROUND: Components of social connection are associated with mortality, but research examining their independent and combined effects in the same dataset is lacking. This study aimed to examine the independent and combined associations between functional and structural components of social connection and mortality. METHODS: Analysis of 458,146 participants with full data from the UK Biobank cohort linked to mortality registers. Social connection was assessed using two functional (frequency of ability to confide in someone close and often feeling lonely) and three structural (frequency of friends/family visits, weekly group activities, and living alone) component measures. Cox proportional hazard models were used to examine the associations with all-cause and cardiovascular disease (CVD) mortality. RESULTS: Over a median of 12.6 years (IQR 11.9-13.3) follow-up, 33,135 (7.2%) participants died, including 5112 (1.1%) CVD deaths. All social connection measures were independently associated with both outcomes. Friends/family visit frequencies < monthly were associated with a higher risk of mortality indicating a threshold effect. There were interactions between living alone and friends/family visits and between living alone and weekly group activity. For example, compared with daily friends/family visits-not living alone, there was higher all-cause mortality for daily visits-living alone (HR 1.19 [95% CI 1.12-1.26]), for never having visits-not living alone (1.33 [1.22-1.46]), and for never having visits-living alone (1.77 [1.61-1.95]). Never having friends/family visits whilst living alone potentially counteracted benefits from other components as mortality risks were highest for those reporting both never having visits and living alone regardless of weekly group activity or functional components. When all measures were combined into overall functional and structural components, there was an interaction between components: compared with participants defined as not isolated by both components, those considered isolated by both components had higher CVD mortality (HR 1.63 [1.51-1.76]) than each component alone (functional isolation 1.17 [1.06-1.29]; structural isolation 1.27 [1.18-1.36]). CONCLUSIONS: This work suggests (1) a potential threshold effect for friends/family visits, (2) that those who live alone with additional concurrent markers of structural isolation may represent a high-risk population, (3) that beneficial associations for some types of social connection might not be felt when other types of social connection are absent, and (4) considering both functional and structural components of social connection may help to identify the most isolated in society.

Delivering spatially comparable inference on the risks of multiple severities of respiratory disease from spatially misaligned disease count data.

Population-level disease risk varies between communities, and public health professionals are interested in mapping this spatial variation to monitor the locations of high-risk areas and the magnitudes of health inequalities. Almost all of these risk maps relate to a single severity of disease outcome, such as hospitalization, which thus ignores any cases of disease of a different severity, such as a mild case treated in a primary care setting. These spatially-varying risk maps are estimated from spatially aggregated disease count data, but the set of areal units to which these disease counts relate often varies by severity. Thus, the statistical challenge is to provide spatially comparable inference from multiple sets of spatially misaligned disease count data, and an additional complexity is that the spatial extents of the areal units for some severities are partially unknown. This paper thus proposes a novel spatial realignment approach for multivariate misaligned count data, and applies it to the first study delivering spatially comparable inference for multiple severities of the same disease. Inference is via a novel spatially smoothed data augmented MCMC algorithm, and the methods are motivated by a new study of respiratory disease risk in Scotland in 2017.

A Bayesian space-time model for clustering areal units based on their disease trends.

Population-level disease risk across a set of non-overlapping areal units varies in space and time, and a large research literature has developed methodology for identifying clusters of areal units exhibiting elevated risks. However, almost no research has extended the clustering paradigm to identify groups of areal units exhibiting similar temporal disease trends. We present a novel Bayesian hierarchical mixture model for achieving this goal, with inference based on a Metropolis-coupled Markov chain Monte Carlo ((MC)$^3$) algorithm. The effectiveness of the (MC)$^3$ algorithm compared to a standard Markov chain Monte Carlo implementation is demonstrated in a simulation study, and the methodology is motivated by two important case studies in the United Kingdom. The first concerns the impact on measles susceptibility of the discredited paper linking the measles, mumps, and rubella vaccination to an increased risk of Autism and investigates whether all areas in the Scotland were equally affected. The second concerns respiratory hospitalizations and investigates over a 10 year period which parts of Glasgow have shown increased, decreased, and no change in risk.

Assessing Risks of Polypharmacy Involving Medications With Anticholinergic Properties.

PURPOSE: Anticholinergic burden (ACB), the cumulative effect of anticholinergic medications, is associated with adverse outcomes in older people but is less studied in middle-aged populations. Numerous scales exist to quantify ACB. The aims of this study were to quantify ACB in a large cohort using the 10 most common anticholinergic scales, to assess the association of each scale with adverse outcomes, and to assess overlap in populations identified by each scale. METHODS: We performed a longitudinal analysis of the UK Biobank community cohort (502,538 participants, baseline age: 37-73 years, median years of follow-up: 6.2). The ACB was calculated at baseline using 10 scales. Baseline data were linked to national mortality register records and hospital episode statistics. The primary outcome was a composite of all-cause mortality and major adverse cardiovascular event (MACE). Secondary outcomes were all-cause mortality, MACE, hospital admission for fall/fracture, and hospital admission with dementia/delirium. Cox proportional hazards models (hazard ratio [HR], 95% CI) quantified associations between ACB scales and outcomes adjusted for age, sex, socioeconomic status, body mass index, smoking status, alcohol use, physical activity, and morbidity count. RESULTS: Anticholinergic medication use varied from 8% to 17.6% depending on the scale used. For the primary outcome, ACB was significantly associated with all-cause mortality/MACE for each scale. The Anticholinergic Drug Scale was most strongly associated with mortality/MACE (HR = 1.12; 95% CI, 1.11-1.14 per 1-point increase in score). The ACB was significantly associated with all secondary outcomes. The Anticholinergic Effect on Cognition scale was most strongly associated with dementia/delirium (HR = 1.45; 95% CI, 1.3-1.61 per 1-point increase). CONCLUSIONS: The ACB was associated with adverse outcomes in a middle- to older-aged population. Populations identified and effect size differed between scales. Scale choice influenced the population identified as potentially requiring reduction in ACB in clinical practice or intervention trials.

Relationship between multimorbidity, demographic factors and mortality: findings from the UK Biobank cohort.

BACKGROUND: Multimorbidity is associated with higher mortality, but the relationship with cancer and cardiovascular mortality is unclear. The influence of demographics and type of condition on the relationship of multimorbidity with mortality remains unknown. We examine the relationship between multimorbidity (number/type) and cause of mortality and the impact of demographic factors on this relationship. METHODS: Data source: the UK Biobank; 500,769 participants; 37-73 years; 53.7% female. Exposure variables: number and type of long-term conditions (LTCs) (N = 43) at baseline, modelled separately. Cox regression models were used to study the impact of LTCs on all-cause/vascular/cancer mortality during median 7-year follow-up. All-cause mortality regression models were stratified by age/sex/socioeconomic status. RESULTS: All-cause mortality is 2.9% (14,348 participants). Of all deaths, 8350 (58.2%) were cancer deaths and 2985 (20.8%) vascular deaths. Dose-response relationship is observed between the increasing number of LTCs and all-cause/cancer/vascular mortality. A strong association is observed between cardiometabolic multimorbidity and all three clinical outcomes; non-cardiometabolic multimorbidity (excluding cancer) is associated with all-cause/vascular mortality. All-cause mortality risk for those with ≥ 4 LTCs was nearly 3 times higher than those with no LTCs (HR 2.79, CI 2.61-2.98); for ≥ 4 cardiometabolic conditions, it was > 3 times higher (HR 3.20, CI 2.56-4.00); and for ≥ 4 non-cardiometabolic conditions (excluding cancer), it was 50% more (HR 1.50, CI 1.36-1.67). For those with ≥ 4 LTCs, morbidity combinations that included cardiometabolic conditions, chronic kidney disease, cancer, epilepsy, chronic obstructive pulmonary disease, depression, osteoporosis and connective tissue disorders had the greatest impact on all-cause mortality. In the stratified model by age/sex, absolute all-cause mortality was higher among the 60-73 age group with an increasing number of LTCs; however, the relative effect size of the increasing number of LTCs on higher mortality risk was larger among those 37-49 years, especially men. While socioeconomic status was a significant predictor of all-cause mortality, mortality risk with increasing number of LTCs remained constant across different socioeconomic gradients. CONCLUSIONS: Multimorbidity is associated with higher all-cause/cancer/vascular mortality. Type, as opposed to number, of LTCs may have an important role in understanding the relationship between multimorbidity and mortality. Multimorbidity had a greater relative impact on all-cause mortality in middle-aged as opposed to older populations, particularly males, which deserves exploration.

A rigorous statistical framework for spatio-temporal pollution prediction and estimation of its long-term impact on health.

In the United Kingdom, air pollution is linked to around 40000 premature deaths each year, but estimating its health effects is challenging in a spatio-temporal study. The challenges include spatial misalignment between the pollution and disease data; uncertainty in the estimated pollution surface; and complex residual spatio-temporal autocorrelation in the disease data. This article develops a two-stage model that addresses these issues. The first stage is a spatio-temporal fusion model linking modeled and measured pollution data, while the second stage links these predictions to the disease data. The methodology is motivated by a new five-year study investigating the effects of multiple pollutants on respiratory hospitalizations in England between 2007 and 2011, using pollution and disease data relating to local and unitary authorities on a monthly time scale.

Multivariate space-time modelling of multiple air pollutants and their health effects accounting for exposure uncertainty.

The long-term health effects of air pollution are often estimated using a spatio-temporal ecological areal unit study, but this design leads to the following statistical challenges: (1) how to estimate spatially representative pollution concentrations for each areal unit; (2) how to allow for the uncertainty in these estimated concentrations when estimating their health effects; and (3) how to simultaneously estimate the joint effects of multiple correlated pollutants. This article proposes a novel 2-stage Bayesian hierarchical model for addressing these 3 challenges, with inference based on Markov chain Monte Carlo simulation. The first stage is a multivariate spatio-temporal fusion model for predicting areal level average concentrations of multiple pollutants from both monitored and modelled pollution data. The second stage is a spatio-temporal model for estimating the health impact of multiple correlated pollutants simultaneously, which accounts for the uncertainty in the estimated pollution concentrations. The novel methodology is motivated by a new study of the impact of both particulate matter and nitrogen dioxide concentrations on respiratory hospital admissions in Scotland between 2007 and 2011, and the results suggest that both pollutants exhibit substantial and independent health effects.

Multimorbidity and co-morbidity in atrial fibrillation and effects on survival: findings from UK Biobank cohort.

Aims: To examine the number and type of co-morbid long-term health conditions (LTCs) and their associations with all-cause mortality in an atrial fibrillation (AF) population. Methods and results: Community cohort participants (UK Biobank n = 502 637) aged 37-73 years were recruited between 2006 and 2010. Self-reported LTCs (n = 42) identified in people with AF at baseline. All-cause mortality was available for a median follow-up of 7 years (interquartile range 76-93 months). Hazard ratios (HRs) examined associations between number and type of co-morbid LTC and all-cause mortality, adjusting for age, sex, socio-economic status, smoking, and anticoagulation status. Three thousand six hundred fifty-one participants (0.7% of the study population) reported AF; mean age was 61.9 years. The all-cause mortality rate was 6.7% (248 participants) at 7 years. Atrial fibrillation participants with ≥4 co-morbidities had a six-fold higher risk of mortality compared to participants without any LTC. Co-morbid heart failure was associated with higher risk of mortality [HR 2.96, 95% confidence interval (CI) 1.83-4.80], whereas the presence of co-morbid stroke did not have a significant association. Among non-cardiometabolic conditions, presence of chronic obstructive pulmonary disease (HR 3.31, 95% CI 2.14-5.11) and osteoporosis (HR 3.13, 95% CI 1.63-6.01) was associated with a higher risk of mortality. Conclusion: Survival in middle-aged to older individuals with self-reported AF is strongly correlated with level of multimorbidity. This group should be targeted for interventions to optimize their management, which in turn may potentially reduce the impact of their co-morbidities on survival. Future AF clinical guidelines need to place greater emphasis on the issue of co-morbidity.

Quantifying the impact of current and future concentrations of air pollutants on respiratory disease risk in England.

BACKGROUND: Estimating the long-term health impact of air pollution in a spatio-temporal ecological study requires representative concentrations of air pollutants to be constructed for each geographical unit and time period. Averaging concentrations in space and time is commonly carried out, but little is known about how robust the estimated health effects are to different aggregation functions. A second under researched question is what impact air pollution is likely to have in the future. METHODS: We conducted a study for England between 2007 and 2011, investigating the relationship between respiratory hospital admissions and different pollutants: nitrogen dioxide (NO2); ozone (O3); particulate matter, the latter including particles with an aerodynamic diameter less than 2.5 micrometers (PM2.5), and less than 10 micrometers (PM10); and sulphur dioxide (SO2). Bayesian Poisson regression models accounting for localised spatio-temporal autocorrelation were used to estimate the relative risks (RRs) of pollution on disease risk, and for each pollutant four representative concentrations were constructed using combinations of spatial and temporal averages and maximums. The estimated RRs were then used to make projections of the numbers of likely respiratory hospital admissions in the 2050s attributable to air pollution, based on emission projections from a number of Representative Concentration Pathways (RCP). RESULTS: NO2 exhibited the largest association with respiratory hospital admissions out of the pollutants considered, with estimated increased risks of between 0.9 and 1.6% for a one standard deviation increase in concentrations. In the future the projected numbers of respiratory hospital admissions attributable to NO2 in the 2050s are lower than present day rates under 3 Representative Concentration Pathways (RCPs): 2.6, 6.0, and 8.5, which is due to projected reductions in future NO2 emissions and concentrations. CONCLUSIONS: NO2 concentrations exhibit consistent substantial present-day health effects regardless of how a representative concentration is constructed in space and time. Thus as concentrations are predicted to remain above limits set by European Union Legislation until the 2030s in parts of urban England, it will remain a substantial health risk for some time.

Spatial clustering of average risks and risk trends in Bayesian disease mapping.

Spatiotemporal disease mapping focuses on estimating the spatial pattern in disease risk across a set of nonoverlapping areal units over a fixed period of time. The key aim of such research is to identify areas that have a high average level of disease risk or where disease risk is increasing over time, thus allowing public health interventions to be focused on these areas. Such aims are well suited to the statistical approach of clustering, and while much research has been done in this area in a purely spatial setting, only a handful of approaches have focused on spatiotemporal clustering of disease risk. Therefore, this paper outlines a new modeling approach for clustering spatiotemporal disease risk data, by clustering areas based on both their mean risk levels and the behavior of their temporal trends. The efficacy of the methodology is established by a simulation study, and is illustrated by a study of respiratory disease risk in Glasgow, Scotland.

Identifying clusters in Bayesian disease mapping.

Disease mapping is the field of spatial epidemiology interested in estimating the spatial pattern in disease risk across [Formula: see text] areal units. One aim is to identify units exhibiting elevated disease risks, so that public health interventions can be made. Bayesian hierarchical models with a spatially smooth conditional autoregressive prior are used for this purpose, but they cannot identify the spatial extent of high-risk clusters. Therefore, we propose a two-stage solution to this problem, with the first stage being a spatially adjusted hierarchical agglomerative clustering algorithm. This algorithm is applied to data prior to the study period, and produces [Formula: see text] potential cluster structures for the disease data. The second stage fits a separate Poisson log-linear model to the study data for each cluster structure, which allows for step-changes in risk where two clusters meet. The most appropriate cluster structure is chosen by model comparison techniques, specifically by minimizing the Deviance Information Criterion. The efficacy of the methodology is established by a simulation study, and is illustrated by a study of respiratory disease risk in Glasgow, Scotland.

Improving spatial nitrogen dioxide prediction using diffusion tubes: A case study in West Central Scotland.

It has been well documented that air pollution adversely affects health, and epidemiological pollution-health studies utilise pollution data from automatic monitors. However, these automatic monitors are small in number and hence spatially sparse, which does not allow an accurate representation of the spatial variation in pollution concentrations required for these epidemiological health studies. Nitrogen dioxide (NO2) diffusion tubes are also used to measure concentrations, and due to their lower cost compared to automatic monitors are much more prevalent. However, even combining both data sets still does not provide sufficient spatial coverage of NO2 for epidemiological studies, and modelled concentrations on a regular grid from atmospheric dispersion models are also available. This paper proposes the first modelling approach to using all three sources of NO2 data to make fine scale spatial predictions for use in epidemiological health studies. We propose a geostatistical fusion model that regresses combined NO2 concentrations from both automatic monitors and diffusion tubes against modelled NO2 concentrations from an atmospheric dispersion model in order to predict fine scale NO2 concentrations across our West Central Scotland study region. Our model exhibits a 47% improvement in fine scale spatial prediction of NO2 compared to using the automatic monitors alone, and we use it to predict NO2 concentrations across West Central Scotland in 2006.

Controlling for unmeasured confounding and spatial misalignment in long-term air pollution and health studies.

The health impact of long-term exposure to air pollution is now routinely estimated using spatial ecological studies, owing to the recent widespread availability of spatial referenced pollution and disease data. However, this areal unit study design presents a number of statistical challenges, which if ignored have the potential to bias the estimated pollution-health relationship. One such challenge is how to control for the spatial autocorrelation present in the data after accounting for the known covariates, which is caused by unmeasured confounding. A second challenge is how to adjust the functional form of the model to account for the spatial misalignment between the pollution and disease data, which causes within-area variation in the pollution data. These challenges have largely been ignored in existing long-term spatial air pollution and health studies, so here we propose a novel Bayesian hierarchical model that addresses both challenges and provide software to allow others to apply our model to their own data. The effectiveness of the proposed model is compared by simulation against a number of state-of-the-art alternatives proposed in the literature and is then used to estimate the impact of nitrogen dioxide and particulate matter concentrations on respiratory hospital admissions in a new epidemiological study in England in 2010 at the local authority level. © 2015 The Authors. Environmetrics published by John Wiley & Sons Ltd.

A Bayesian localized conditional autoregressive model for estimating the health effects of air pollution.

Estimation of the long-term health effects of air pollution is a challenging task, especially when modeling spatial small-area disease incidence data in an ecological study design. The challenge comes from the unobserved underlying spatial autocorrelation structure in these data, which is accounted for using random effects modeled by a globally smooth conditional autoregressive model. These smooth random effects confound the effects of air pollution, which are also globally smooth. To avoid this collinearity a Bayesian localized conditional autoregressive model is developed for the random effects. This localized model is flexible spatially, in the sense that it is not only able to model areas of spatial smoothness, but also it is able to capture step changes in the random effects surface. This methodological development allows us to improve the estimation performance of the covariate effects, compared to using traditional conditional auto-regressive models. These results are established using a simulation study, and are then illustrated with our motivating study on air pollution and respiratory ill health in Greater Glasgow, Scotland in 2011. The model shows substantial health effects of particulate matter air pollution and nitrogen dioxide, whose effects have been consistently attenuated by the currently available globally smooth models.

Variable-stiffness prosthesis improves biomechanics of walking across speeds compared to a passive device.

Ankle push-off power plays an important role in healthy walking, contributing to center-of-mass acceleration, swing leg dynamics, and accounting for 45% of total leg power. The majority of existing passive energy storage and return prostheses for people with below-knee (transtibial) amputation are stiffer than the biological ankle, particularly at slower walking speeds. Additionally, passive devices provide insufficient levels of energy return and push-off power, negatively impacting biomechanics of gait. Here, we present a clinical study evaluating the kinematics and kinetics of walking with a microprocessor-controlled, variable-stiffness ankle-foot prosthesis (945 g) compared to a standard low-mass passive prosthesis (Ottobock Taleo, 463 g) with 7 study participants having unilateral transtibial amputation. By modulating prosthesis stiffness under computer control across walking speeds, we demonstrate that there exists a stiffness that increases prosthetic-side energy return, peak power, and center-of-mass push-off work, and decreases contralateral limb peak ground reaction force compared to the standard passive prosthesis across all evaluated walking speeds. We demonstrate a significant increase in center-of-mass push-off work of 26.1%, 26.2%, 29.6% and 29.9% at 0.75 m/s, 1.0 m/s, 1.25 m/s, and 1.5 m/s, respectively, and a significant decrease in contralateral limb ground reaction force of 3.1%, 3.9%, and 3.2% at 1.0 m/s, 1.25 m/s, and 1.5 m/s, respectively. This study demonstrates the potential for a quasi-passive microprocessor-controlled variable-stiffness prosthesis to increase push-off power and energy return during gait at a range of walking speeds compared to a passive device of a fixed stiffness.

Mental Health Admissions to Paediatric Wards Study (MAPS): protocol of a prospective study of mental health admissions to paediatric wards in England using surveillance and qualitative methods.

INTRODUCTION: Children and young people (CYP) presenting with a mental health (MH) crisis are frequently admitted to general acute paediatric wards as a place of safety. Prior to the pandemic, a survey in England showed that CYP occupied 6% of general paediatric inpatient beds due to an MH crisis, and there have been longstanding concerns about the quality of care to support these patients in this setting. MAPS aims to generate a Theory of Change (ToC) model to improve the quality of care for CYP admitted to acute paediatric services after presenting with an MH crisis. Here, we describe work packages (WPs) 2 and 3 of the study, which have been granted ethics approval. METHODS AND ANALYSIS: We will undertake a national (England), sequential, mixed-methods study to inform a ToC framework alongside a stakeholder group consisting of patients, families/carers and healthcare professionals (HCPs). Our study consists of four WPs undertaken over 30 months. WP2 is limited to working with stakeholders to develop a data collection instrument and then use this in a prospective study of MH admissions over 6 months in 15 purposively recruited acute paediatric wards across England. WP3 consists of gathering the views of CYP, their families/carers and HCPs during admissions using semistructured interviews. ETHICS AND DISSEMINATION: WP2 and WP3 received ethical approval (ref: 23/LO/0349). We will publish the overall synthesis of data and the final ToC to improve care of CYP with MH crisis admitted to general acute paediatric settings. As co-producers of the ToC, we will work with our stakeholder group to ensure wide dissemination of findings. Potential impacts will be upon service development, new models of care, training and workforce planning. PROSPERO REGISTRATION NUMBER: CRD42022350655.

Mental Health Admissions to Paediatric Wards Study (MAPS): a protocol for the analysis of Hospital Episode Statistics (HES) data.

INTRODUCTION: Children and young people (CYP) presenting with a mental health (MH) crisis are frequently admitted to general acute paediatric wards as a place of safety. Prior to the pandemic, a survey in England showed that CYP occupied 6% of general paediatric inpatient beds due to an MH crisis, and there have been longstanding concerns about the quality of care to support these patients in this setting. Mental Health Admissions to Paediatric Wards Study aims to generate a theory of change (ToC) model to improve the quality of care for CYP admitted to acute paediatric services after presenting in a MH crisis. METHODS AND ANALYSIS: We will undertake a national (England), sequential, mixed methods study to inform a ToC framework alongside a stakeholder group consisting of patients, families/carers and healthcare professionals (HCPs). Our study consists of four work packages (WP) undertaken over 30 months. WP1 is limited to using national routine administrative data to identify and characterise trends in MH admissions in acute paediatric wards in England between 2015- 2022. ETHICS AND DISSEMINATION: WP1 received ethical approval (Ref 23/NW/0192). We will publish the overall synthesis of data and the final ToC to improve care of CYP with MH crisis admitted to general acute paediatric settings. As coproducers of the ToC, we will work with our stakeholder group to ensure wide dissemination of findings. Potential impacts will be on service development, new models of care, training and workforce planning.

Boundary detection in disease mapping studies.

In disease mapping, the aim is to estimate the spatial pattern in disease risk over an extended geographical region, so that areas with elevated risks can be identified. A Bayesian hierarchical approach is typically used to produce such maps, which represents the risk surface with a set of random effects that exhibit a single global level of spatial smoothness. However, in complex urban settings, the risk surface is likely to exhibit localized rather than global spatial structure, including areas where the risk varies smoothly over space, as well as boundaries separating populations that are geographically adjacent but have very different risk profiles. Therefore, this paper proposes an approach for capturing localized spatial structure, including the identification of such risk boundaries. The effectiveness of the approach is tested by simulation, before being applied to lung cancer incidence data in Greater Glasgow, UK, between 2001 and 2005.

Incorporating spatial variability within epidemiological studies of environmental exposures.

Recently there has been great interest in modelling the association between aggregate disease counts and environmental exposures measured at point locations, for example via air pollution monitors. In such cases, the standard approach is to average the observed measurements from the individual monitors and use this in a log-linear health model. Hence such studies are ecological in nature being based on spatially aggregated health and exposure data. Here we investigate the potential for biases in the estimates of the effects on health in such settings. Such ecological bias may occur if a simple summary measure, such as a daily mean, is not a suitable summary of a spatially variable pollution surface. We assess the performance of commonly used models when confronted with such issues using simulation studies and compare their performance with a model specifically designed to acknowledge the effects of exposure aggregation. In addition to simulation studies, we apply the models to a case study of the short-term effects of particulate matter on respiratory mortality using data from Greater London for the period 2002-2005.

National lockdowns in England: The same restrictions for all, but do the impacts on COVID-19 mortality risks vary geographically?

Quantifying the impact of lockdowns on COVID-19 mortality risks is an important priority in the public health fight against the virus, but almost all of the existing research has only conducted macro country-wide assessments or limited multi-country comparisons. In contrast, the extent of within-country variation in the impacts of a nation-wide lockdown is yet to be thoroughly investigated, which is the gap in the knowledge base that this paper fills. Our study focuses on England, which was subject to 3 national lockdowns between March 2020 and March 2021. We model weekly COVID-19 mortality counts for the 312 Local Authority Districts in mainland England, and our aim is to understand the impact that lockdowns had at both a national and a regional level. Specifically, we aim to quantify how long after the implementation of a lockdown do mortality risks reduce at a national level, the extent to which these impacts vary regionally within a country, and which parts of England exhibit similar impacts. As the spatially aggregated weekly COVID-19 mortality counts are small in size we estimate the spatio-temporal trends in mortality risks with a Poisson log-linear smoothing model that borrows strength in the estimation between neighbouring data points. Inference is based in a Bayesian paradigm, using Markov chain Monte Carlo simulation. Our main findings are that mortality risks typically begin to reduce between 3 and 4 weeks after lockdown, and that there appears to be an urban-rural divide in lockdown impacts.