Mortality In London Research Articles

Modeled temperature, mortality impact and external benefits of cool roofs and rooftop photovoltaics in London

Population exposure to high temperatures poses health risks and increases mortality. ‘Cool roofs’ (high-albedo roofs) and rooftop photovoltaics (RPV) may reduce temperatures in urban areas. Here, using advanced urban climate modeling, we model impacts of these measures on air temperature and heat-related mortality in London during the record-breaking hot summer of 2018. We estimate changes in mean near-surface air temperature of −0.3 °C in the RPV scenario and −0.8 °C in the cool roof scenario. We find that the heat-related mortality in this period (estimated 655–920) could have been reduced by 96 (12%) by RPV, or 249 (32%) by cool roofs, in scenarios where all roofs have these measures. Monetized using value of statistical life, we estimate benefits for RPV and cool roofs of £237 M and £615 M, respectively. We estimate that up to 20 TWh of electrical energy would be generated in the full RPV scenario. We show that, for conditions such as in London June–August 2018, RPV or cool roofs may reduce near-surface air temperatures and associated heat-related mortality, with cool roofs having a larger effect.

Associations between short-term exposure to airborne carbonaceous particles and mortality: A time-series study in London during 2010–2019

Exposure to ambient particulate matter (PM) has been identified as a major global health concern; however, the importance of specific chemical PM components remains uncertain. Recent studies have suggested that carbonaceous aerosols are important detrimental components of the particle mixture. Using time-series methods, we investigated associations between short-term exposure to carbonaceous particles and mortality in London, UK. Daily counts of non-accidental, respiratory, and cardiovascular deaths were obtained between 2010 and 2019. For the same period, daily concentrations of carbonaceous particles: organic (OC), elemental (EC), wood-burning (WC), total carbon (TC) and equivalent black carbon (eBC) were sourced from two centrally located monitoring sites (one urban-traffic and one urban-background). Generalized additive models were used to estimate the percentage change in mortality risk associated with interquartile range increases in particulate concentrations. Lagged effects up to 3 days were examined. Stratified analyses were conducted by age, sex, and season, separate analyses were also performed by site-type. For non-accidental mortality, positive associations were observed for all particle species at lag1, including statistically significant percentage risk changes in WC (0.51% (95%CI: 0.19%, 0.82%) per IQR (0.68 μg/m3)) and OC (0.45% (95%CI: 0.04%, 0.87% per IQR (2.36 μg/m3)). For respiratory deaths, associations were greatest for particulate concentrations averaged over the current and previous 3 days, with increases in risk of 1.70% (95%CI: 0.64%, 2.77%) for WC and 1.31% (95%CI: −0.08%, 2.71%) for OC. No associations were found with cardiovascular mortality. Results were robust to adjustment for particle mass concentrations. Stratified analyses suggested particulate effects were greatest in the summer and respiratory associations more pronounced in females. Our findings are supportive of an association between carbonaceous particles and non-accidental and respiratory mortality. The strongest evidence of an effect was for WC; this is of significance given the rising popularity of wood-burning for residential space heating and energy production across Europe.

London Fog: A Century of Pollution and Mortality, 1866–1965

Abstract This study draws on London’s long experience with air pollution in order to improve our understanding of the overall effects of pollution exposure and how and why these effects evolve as locations develop. I compare uniquely detailed new mortality data covering 1866 to 1965 to the timing of London’s famous fog events, which trapped emissions in the city. I show that air pollution was a major contributor to mortality in London over this period and that it interacted strongly with specific infectious diseases. As a consequence of this interaction, reductions in the infectious disease burden substantially altered the health costs of pollution.

The potential of urban trees to reduce heat-related mortality in London

Increasing temperatures and more frequent heatwave events pose threats to population health, particularly in urban environments due to the urban heat island (UHI) effect. Greening, in particular planting trees, is widely discussed as a means of reducing heat exposure and associated mortality in cities. This study aims to use data from personal weather stations (PWS) across the Greater London Authority to understand how urban temperatures vary according to tree canopy coverage and estimate the heat-health impacts of London’s urban trees. Data from Netatmo PWS from 2015–2022 were cleaned, combined with official Met Office temperatures, and spatially linked to tree canopy coverage and built environment data. A generalized additive model was used to predict daily average urban temperatures under different tree canopy coverage scenarios for historical and projected future summers, and subsequent health impacts estimated. Results show areas of London with higher canopy coverage have lower urban temperatures, with average maximum daytime temperatures 0.8 °C and minimum temperatures 2.0 °C lower in the top decile versus bottom decile canopy coverage during the 2022 heatwaves. We estimate that London’s urban forest helped avoid 153 heat attributable deaths from 2015–2022 (including 16 excess deaths during the 2022 heatwaves), representing around 16% of UHI-related mortality. Increasing tree coverage 10% in-line with the London strategy would have reduced UHI-related mortality by a further 10%, while a maximal tree coverage would have reduced it 55%. By 2061–2080, under RCP8.5, we estimate that London’s current tree planting strategy can help avoid an additional 23 heat-attributable deaths a year, with maximal coverage increasing this to 131. Substantial benefits would also be seen for carbon storage and sequestration. Results of this study support increasing urban tree coverage as part of a wider public health effort to mitigate high urban temperatures.

Contribution of Cold Versus Climate Change to Mortality in London, UK, 1976-2019.

Objectives. To quantify past reductions in cold-related mortality attributable to anthropogenic climate change. Methods. We performed a daily time-series regression analysis employing distributed lag nonlinear models of 1 203 981 deaths in Greater London, United Kingdom, in winter months (November-March) during 1976 to 2019. We made attribution assessment by comparing differential cold-related mortality impacts associated with observed temperatures to those using counterfactual temperatures representing no climate change. Results. Over the past decade, the average number of cold days (below 8 °C) per year was 120 in the observed series and 158 in the counterfactual series. Since 1976, we estimate 447 (95% confidence interval = 330, 559) annual cold-related all-cause deaths have been avoided because of milder temperatures associated with climate change. Annually, 241 cardiovascular and 73 respiratory disease deaths have been avoided. Conclusions. Anthropogenic climate change made some contribution to reducing previous cold-related deaths in London; however, cold remains an important public health risk factor. Public Health Implications. Better adaptation to both heat and cold should be promoted in public health measures to protect against climate change. In England, this has been addressed by the development of a new year-round Adverse Weather and Health Plan. (Am J Public Health. 2024;114(4):398-402. https://doi.org/10.2105/AJPH.2023.307552).

The Potential of Urban Trees to Reduce Heat-related Mortality in London

The Potential of Urban Trees to Reduce Heat-related Mortality in London

Associations between residential greenspace exposure and premature mortality in London, UK: a data-linkage study

BackgroundUrban greenspaces might reduce non-communicable disease risk. The links between greenspaces and mortality related to non-communicable disease remain unclear. We estimated the associations between residential greenspace quantity and access with all-cause, cardiovascular disease, cancer, respiratory, and type 2 diabetes mortality. MethodsWe linked 2011 UK Census data of London-dwelling adults (aged ≥18 years) to data from the UK death registry and the Greenspace Information for Greater London resource (N=4 645 581). We calculated percent greenspace area, access point density (access points per km2), and distance (metres) to the nearest access point for each respondent's residential neighbourhood (defined as 1000-m street network buffers) for greenspaces overall and by park type using a geographic information system. We estimated associations using Cox proportional hazards models, adjusted for a range of confounders. Ethics approval was granted by the London School of Hygiene and Tropical Medicine's Observational/Interventions Research Ethics Committee. FindingsRespondents were followed for 8·4 years (SD 1·4). A one percentage point increase in pocket park area was associated with a 6% decrease in all-cause mortality risk (hazard ratio [HR] 0·94 [95% CI 0·92–0·97]) and an increase of ten pocket park access points per km2 was associated with an 8% decreased respiratory mortality risk (0·92 [0·85–0·99]). Other associations were observed but the estimated effects were 3% or less. For example, all-cause mortality risk for increases of one percentage point in regional park area (0·99 [0·99–1·00]) and increases of ten small open space access points per km2 (1·03 [1·02–1·03]). InterpretationIncreasing pocket park quantity and access might mitigate premature mortality risk. More research is needed to elucidate the mechanisms that could explain these associations. FundingHealth Data Research UK.

Socioeconomic disparities in cancer incidence and mortality in England and the impact of age-at-diagnosis on cancer mortality.

BackgroundWe identify socioeconomic disparities by region in cancer morbidity and mortality in England for all-cancer and type-specific cancers, and use incidence data to quantify the impact of cancer diagnosis delays on cancer deaths between 2001–2016.Methods and findingsWe obtain population cancer morbidity and mortality rates at various age, year, gender, deprivation, and region levels based on a Bayesian approach. A significant increase in type-specific cancer deaths, which can also vary among regions, is shown as a result of delay in cancer diagnoses. Our analysis suggests increase of 7.75% (7.42% to 8.25%) in female lung cancer mortality in London, as an impact of 12-month delay in cancer diagnosis, and a 3.39% (3.29% to 3.48%) increase in male lung cancer mortality across all regions. The same delay can cause a 23.56% (23.09% to 24.30%) increase in male bowel cancer mortality. Furthermore, for all-cancer mortality, the highest increase in deprivation gap happened in the East Midlands, from 199 (186 to 212) in 2001, to 239 (224 to 252) in 2016 for males, and from 114 (107 to 121) to 163 (155 to 171) for females. Also, for female lung cancer, the deprivation gap has widened with the highest change in the North West, e.g. for incidence from 180 (172 to 188) to 272 (261 to 282), whereas it has narrowed for prostate cancer incidence with the biggest reduction in the South West from 165 (139 to 190) in 2001 to 95 (72 to 117) in 2016.ConclusionsThe analysis reveals considerable disparities in all-cancer and some type-specific cancers with respect to socioeconomic status. Furthermore, a significant increase in cancer deaths is shown as a result of delays in cancer diagnoses which can be linked to concerns about the effect of delay in cancer screening and diagnosis during the COVID-19 pandemic. Public health interventions at regional and deprivation level can contribute to prevention of cancer deaths.

Projecting the impacts of housing on temperature-related mortality in London during typical future years

Climate change means the UK will experience warmer winters and hotter summers in the future. Concurrent energy efficiency improvements to housing may modify indoor exposures to heat or cold, while population aging may increase susceptibility to temperature-related mortality. We estimate heat and cold mortality and energy consumption in London for typical (non-extreme) future climates, given projected changes in population and housing. Building physics models are used to simulate summertime and wintertime indoor temperatures and space heating energy consumption of London dwellings for ‘baseline’ (2005–2014) and future (2030s, 2050s) periods using data from the English Housing Survey, historical weather data, and projected future weather data with temperatures representative of ‘typical’ years. Linking to population projections, we calculate future heat and cold attributable mortality and energy consumption with demolition, construction, and alternative scenarios of energy efficiency retrofit. At current retrofit rates, around 168–174 annual cold-related deaths per million population would typically be avoided by the 2050s, or 261–269 deaths per million under ambitious retrofit rates. Annual heat deaths would typically increase by 1 per million per year under the current retrofit rate, and 12–13 per million under ambitious rates without population adaptation to heat. During typical future summers, an estimated 38–73% of heat-related deaths can be avoided using external shutters on windows, with their effectiveness lower during hotter weather. Despite warmer winters, ambitious retrofit rates are necessary to reduce typical annual energy consumption for heating below baseline levels, assuming no improvement in heating system efficiencies. Concerns over future overheating in energy efficient housing are valid but increases in heat attributable mortality during typical and hot (but not extreme) summers are more than offset by significant reductions in cold mortality and easily mitigated using passive measures. More ambitious retrofit rates are critical to reduce energy consumption and offer co-benefits for reducing cold-related mortality.

Associations between sources of particle number and mortality in four European cities

BackgroundThe evidence on the association between ultrafine (UFP) particles and mortality is still inconsistent. Moreover, health effects of specific UFP sources have not been explored. We assessed the impact of UFP sources on daily mortality in Barcelona, Helsinki, London, and Zurich. MethodsUFP sources were previously identified and quantified for the four cities: daily contributions of photonucleation, two traffic sources (fresh traffic and urban, with size mode around 30 nm and 70 nm, respectively), and secondary aerosols were obtained from data from an urban background station. Different periods were investigated in each city: Barcelona 2013–2016, Helsinki 2009–2016, London 2010–2016, and Zurich 2011–2014. The associations between total particle number concentrations (PNC) and UFP sources and daily (natural, cardiovascular [CVD], and respiratory) mortality were investigated using city-specific generalized linear models (GLM) with quasi-Poisson regression. ResultsWe found inconsistent results across cities, sources, and lags for associations with natural, CVD, and respiratory mortality. Increased risk was observed for total PNC and natural mortality in Helsinki (lag 2; 1.3% [0.07%, 2.5%]), CVD mortality in Barcelona (lag 1; 3.7% [0.17%, 7.4%]) and Zurich (lag 0; 3.8% [0.31%, 7.4%]), and respiratory mortality in London (lag 3; 2.6% [0.84%, 4.45%]) and Zurich (lag 1; 9.4% [1.0%, 17.9%]). A similar pattern of associations between health outcomes and total PNC was followed by the fresh traffic source, for which we also found the same associations and lags as for total PNC. The urban source (mostly aged traffic) was associated with respiratory mortality in Zurich (lag 1; 12.5% [1.7%, 24.2%]) and London (lag 3; 2.4% [0.90%, 4.0%]) while the secondary source was associated with respiratory mortality in Zurich (lag 1: 12.0% [0.63%, 24.5%]) and Helsinki (4.7% [0.11%, 9.5%]). Reduced risk for the photonucleation source was observed for respiratory mortality in Barcelona (lag 2, −8.6% [−14.5%, −2.4%]) and for CVD mortality in Helsinki, as this source is present only in clean atmospheres (lag 1, −1.48 [−2.75, −0.21]). ConclusionsWe found inconsistent results across cities, sources and lags for associations with natural, CVD, and respiratory mortality.

Patterns of smallpox mortality in London, England, over three centuries.

Smallpox is unique among infectious diseases in the degree to which it devastated human populations, its long history of control interventions, and the fact that it has been successfully eradicated. Mortality from smallpox in London, England was carefully documented, weekly, for nearly 300 years, providing a rare and valuable source for the study of ecology and evolution of infectious disease. We describe and analyze smallpox mortality in London from 1664 to 1930. We digitized the weekly records published in the London Bills of Mortality (LBoM) and the Registrar General's Weekly Returns (RGWRs). We annotated the resulting time series with a sequence of historical events that might have influenced smallpox dynamics in London. We present a spectral analysis that reveals how periodicities in reported smallpox mortality changed over decades and centuries; many of these changes in epidemic patterns are correlated with changes in control interventions and public health policies. We also examine how the seasonality of reported smallpox mortality changed from the 17th to 20th centuries in London.

Difference-in-Difference in the Time of Cholera: a Gentle Introduction for Epidemiologists.

The goal of this article is to provide an introduction to the intuition behind the difference-in-difference method for epidemiologists. We focus on the theoretical aspects of this tool, including the types of questions for which difference-in-difference is appropriate, and what assumptions must hold for the results to be causally interpretable. While currently under-utilized in epidemiologic research, the difference-in-difference method is a useful tool to examine effects of population-level exposures, but relies on strong assumptions. We use the famous example of John Snow's investigation of the cause of cholera mortality in London to illustrate the difference-in-difference approach and corresponding assumptions. We conclude by arguing that this method deserves a second-look from epidemiologists interested in asking causal questions about the impact of a population-level exposure change on a population-level outcome for the group that experienced the change.

Variation in quality of acute stroke care by day and time of admission: prospective cohort study of weekday and weekend centralised hyperacute stroke unit care and non-centralised services

ObjectiveTo investigate variations in quality of acute stroke care and outcomes by day and time of admission in London hyperacute stroke units compared with the rest of England.DesignProspective cohort study...

Traffic-Related Air Pollution, Noise and Infant Mortality in London

BackgroundThere is evidence that ambient air pollution is associated with increased risk of infant mortality. Road traffic is a major contributor to ambient air pollution, but it also generates noise. This study investigates long-term exposure to both traffic-related air and noise pollution and risk of infant mortality. MethodsWe conducted a matched case-control study of infant deaths (deaths occurring in 1st year of life) from singleton births across Greater London from 2003-2010. Controls were singleton births in the study area between 2003-2010 surviving to age 1. Cases were matched to controls (n=29) on birthdate and sex. Monthly concentrations of NO2, NOX, source-specific traffic-related PM2.5, PM2.5, PM10 and ozone were estimated at 20x20m resolution using a dispersion model, and time-weighted averages calculated for pregnancy/trimesters and birth to case death at address-level. Road traffic noise was modelled at address-level. We analysed the relationship between air pollutants/noise and infant mortality using conditional logistic regression, with adjustment for confounding. ResultsThe study population comprises 3390 infant deaths (69% neonatal, 31% postneonatal). Average air pollutant exposures for cases from birth to death were 42μg/m3 NO2, 77μg/m3 NOx, 15μg/m3 PM2.5, 24μg/m3 PM10 and 31μg/m3 O3. Average day- and night-time noise levels were 58 and 53 dB respectively. Higher road traffic air pollution and noise exposures were particularly associated with non-White ethnicity and lower socio-economic status. Preliminary results from adjusted single-pollutant models suggest increased risk of infant mortality associated with higher ozone exposure, but not with other air pollutants or noise. Analyses of joint air pollution–noise exposures are currently underway. ConclusionsTo our knowledge, this is the first epidemiological study to investigate risk of infant mortality in relation to both road traffic air pollution and noise co-exposures.

Effect of night-time temperatures on cause and age-specific mortality in London.

High ambient temperatures are associated with an acute increase in mortality risk. Although heat exposure during the night is anecdotally cited as being important, this has not been rigorously demonstrated in the epidemiological literature. We quantified the contribution of nighttime temperatures using time-series quasi-Poisson regression on cause and age-specific daily mortality in London between 1993 and 2015. Daytime and nighttime exposures were characterized by average temperatures between 9 am and 9 pm and between 4 am and 8 am, respectively, lagged by 7 days. We also examined the differential impacts of hot and cool nights preceded by very hot days. All models were adjusted for air quality, season, and day of the week. Nighttime models were additionally adjusted for daytime exposure. Effects from nighttime exposure persisted after adjusting for daytime exposure. This was highest for stroke, RR (relative risk) = 1.65 (95% confidence interval (CI) = 1.27 to 2.14) estimated by comparing mortality risk at the 80th and 99th temperature percentiles. Compared to daytime exposure, nighttime exposure had a higher mortality risk on chronic ischemic and stroke and in the younger age groups. Respiratory mortality was most sensitive to daytime temperatures. Hot days followed by hot nights had a greater mortality risk than hot days followed by cool nights. Nighttime exposures make an additional important contribution to heat-related mortality. This impact was highest on warm nights that were preceded by a hot day, which justifies the alert criteria in heat-health warning system that is based on hot days followed by hot nights. The highest mortality risk was from stroke; targeted interventions would benefit patients most susceptible to stroke.

Examining the Long-Term Association of Personality With Cause-Specific Mortality in London: Four Decades of Mortality Surveillance in the Original Whitehall Smoking Cessation Trial.

The personality domains of extraversion and neuroticism are regarded as being stable individual psychological characteristics, yet it remains unclear whether they are associated with chronic disease over an extended period of time. In a randomized controlled trial of smoking cessation nested within the original prospective Whitehall Study (1967-2012), the Eysenck Personality Questionnaire was administered to 832 male self-declared smokers who had undergone a medical examination during which their levels of extraversion and neuroticism were quantified. In the 42-year follow-up period, there were 781 deaths. In analyses in which participants from both trial arms were pooled, there was little evidence of a robust relation of either personality domain with death from all causes, coronary heart disease, stroke, respiratory disease, or cancer in any of our analyses. We therefore found no support for a role of either extraversion or neuroticism as determinants of long-term mortality risk.

Traffic-related Air and Noise Pollution, Birth Outcomes and Infant Mortality in London

Introduction Traffic pollution comprises toxic air pollutants and noise. Air pollution has been associated with infant mortality, and there is also evidence for small effects on birth weight. Research on noise and birth outcomes is limited, but an association with low birthweight is suggested. This study investigates traffic-related air and noise pollution exposures in relation to birth outcomes and infant mortality. Methods The study population comprises 882713 live births and 5452 stillbirths in the Greater London area from 2003-2010. Monthly concentrations of primary traffic air pollutants (NO2, NOx, exhaust and non-exhaust PM2.5 and PM10) and regional/urban background air pollutants (Ozone, and total PM2.5 and PM10) have been estimated using a dispersion model at 20m x 20m resolution. Time-weighted average air pollution estimates at address-level have been calculated for pregnancy and post-natal time windows. Annual road traffic noise levels have been modeled at address-level using the TRAffic Noise EXposure (TRANEX) model. We are analysing the relationship between air pollutant/noise exposures and birth weight, small-for-gestational-age (SGA), stillbirth and infant mortality, adjusting for potential confounders (e.g. maternal age, smoking and deprivation). Results Mean time-weighted average pregnancy exposures were 75μg/m3 for NOx, 15μg/m3 for PM2.5 and 24μg/m3 for PM10, and mean noise exposures were 58dB (day-time) and 53dB (night-time). Preliminary results suggest that traffic-related air pollution and noise exposures during pregnancy are independently associated with reduced mean birth weight and elevated risk of SGA. Conclusions The study is in progress and will be the largest to date examining environmental noise exposures and birth outcomes. This study combines highly spatially refined address-level exposure assessment for both noise and air pollutants, and will improve understanding of the relative influences of these co-exposures upon fetal/infant health.

Assessing the health burden of long-term exposure to nitrogen dioxide and mortality in London

Introduction The health impact of air pollution in London was previously based on fine particulate matter (PM2.5) alone. In this work, the mortality burden for PM2.5 has been updated and, for the first time, a scoping exercise performed for the potential mortality burden of long-term exposure to nitrogen dioxide (NO2) in London. Methods The methods for PM2.5 followed Committee on the Medical Effects of Air Pollutants recommendations. Methods for NO2 followed the same principles but used the coefficient recommended by the World Health Organisation. We assumed up to a 30% overlap with PM2.5, quantifying down to zero as the upper limit for the size of the effect (down to 20 μg m-3 in sensitivity analysis). Concentrations were modelled using the London Air Quality Modelling toolkit based on the London Atmospheric Emissions Inventory at a 20mx20m grid and then population-weighted at output area level. Estimates for individual London boroughs were summed to give the London figure. Results The total mortality burden of anthropogenic PM2.5 in London for the year 2010 was estimated to be 52,500 life-years lost, equivalent to 3,500 deaths at typical ages. Whilst much less certain than for PM2.5., the total mortality burden of NO2 was estimated to be up to 88,000 life-years lost, equivalent to 5,900 deaths at typical ages (assuming a 30% overlap between the effects of PM2.5 and NO2 and a counterfactual of 0 μg m-3. Some of this effect may be due to other traffic pollutants. The total mortality burden in 2010 from PM2.5 and NO2 if added, with caveats, gives a range from the 52,500 life-years lost, equivalent to 3,500 deaths at typical ages from PM2.5 alone up to as much as 141,000 life-years lost, equivalent to 9,500 deaths at typical ages. Conclusions Inclusion of estimates for NO2 potentially increases the estimated total mortality burden substantially, highlighting the importance of further research on the overlap in effects between NO2, PM2.5 and other traffic pollutants.

An evaluation of multi pollutant profiles and cardiovascular mortality in London and Oxford.

An evaluation of multi pollutant profiles and cardiovascular mortality in London and Oxford.

Short-term exposure to traffic-related air pollution and daily mortality in London, UK.

Epidemiological studies have linked daily concentrations of urban air pollution to mortality, but few have investigated specific traffic sources that can inform abatement policies. We assembled a database of >100 daily, measured and modelled pollutant concentrations characterizing air pollution in London between 2011 and 2012. Based on the analyses of temporal patterns and correlations between the metrics, knowledge of local emission sources and reference to the existing literature, we selected, a priori, markers of traffic pollution: oxides of nitrogen (general traffic); elemental and black carbon (EC/BC) (diesel exhaust); carbon monoxide (petrol exhaust); copper (tyre), zinc (brake) and aluminium (mineral dust). Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death associated with an interquartile increment of each pollutant. Associations were generally small with confidence intervals that spanned 0% and tended to be negative for cardiovascular mortality and positive for respiratory mortality. The strongest positive associations were for EC and BC adjusted for particle mass and respiratory mortality, 2.66% (95% confidence interval: 0.11, 5.28) and 2.72% (0.09, 5.42) per 0.8 and 1.0 μg/m3, respectively. These associations were robust to adjustment for other traffic metrics and regional pollutants, suggesting a degree of specificity with respiratory mortality and diesel exhaust containing EC/BC.