•The first study of long-term road traffic noise in relation to stillbirth.•Largest study to date of air and noise pollution in relation to birth outcomes.•Ambient ozone linked to increased risk of ...preterm birth and stillbirth.•Traffic non-exhaust PM2.5 linked to increased risk of preterm birth and stillbirth.•Traffic noise linked to risk of preterm birth, after accounting for air pollution.
Evidence for associations between ambient air pollution and preterm birth and stillbirth is inconsistent. Road traffic produces both air pollutants and noise, but few studies have examined these co-exposures together and none to date with all-cause or cause-specific stillbirths.
To analyse the relationship between long-term exposure to air pollution and noise at address level during pregnancy and risk of preterm birth and stillbirth.
The study population comprised 581,774 live and still births in the Greater London area, 2006–2010. Outcomes were preterm birth (<37 completed weeks gestation), all-cause stillbirth and cause-specific stillbirth. Exposures during pregnancy to particulate matter with diameter <2.5 μm (PM2.5) and <10 μm (PM10), ozone (O3), primary traffic air pollutants (nitrogen dioxide, nitrogen oxides, PM2.5 from traffic exhaust and traffic non-exhaust), and road traffic noise were estimated based on maternal address at birth.
An interquartile range increase in O3 exposure was associated with elevated risk of preterm birth (OR 1.15 95% CI: 1.11, 1.18, for both Trimester 1 and 2), all-cause stillbirth (Trimester 1 OR 1.17 95% CI: 1.07, 1.27; Trimester 2 OR 1.20 95% CI: 1.09, 1.32) and asphyxia-related stillbirth (Trimester 1 OR 1.22 95% CI: 1.01, 1.49). Odds ratios with the other air pollutant exposures examined were null or <1, except for primary traffic non-exhaust related PM2.5, which was associated with 3% increased odds of preterm birth (Trimester 1) and 7% increased odds stillbirth (Trimester 1 and 2) when adjusted for O3. Elevated risk of preterm birth was associated with increasing road traffic noise, but only after adjustment for certain air pollutant exposures.
Our findings suggest that exposure to higher levels of O3 and primary traffic non-exhaust related PM2.5 during pregnancy may increase risk of preterm birth and stillbirth; and a possible relationship between long-term traffic-related noise and risk of preterm birth. These findings extend and strengthen the evidence base for important public health impacts of ambient ozone, particulate matter and noise in early life.
Road traffic gives rise to noise and air pollution exposures, both of which are associated with adverse health effects especially for cardiovascular disease, but mechanisms may differ. Understanding ...the variability in correlations between these pollutants is essential to understand better their separate and joint effects on human health.
We explored associations between modelled noise and air pollutants using different spatial units and area characteristics in London in 2003–2010.
We modelled annual average exposures to road traffic noise (LAeq,24h, Lden, LAeq,16h, Lnight) for ~190,000 postcode centroids in London using the UK Calculation of Road Traffic Noise (CRTN) method. We used a dispersion model (KCLurban) to model nitrogen dioxide, nitrogen oxide, ozone, total and the traffic-only component of particulate matter ≤2.5μm and ≤10μm. We analysed noise and air pollution correlations at the postcode level (~50 people), postcodes stratified by London Boroughs (~240,000 people), neighbourhoods (Lower layer Super Output Areas) (~1600 people), 1km grid squares, air pollution tertiles, 50m, 100m and 200m in distance from major roads and by deprivation tertiles.
Across all London postcodes, we observed overall moderate correlations between modelled noise and air pollution that were stable over time (Spearman's rho range: |0.34–0.55|). Correlations, however, varied considerably depending on the spatial unit: largest ranges were seen in neighbourhoods and 1km grid squares (both Spearman's rho range: |0.01–0.87|) and was less for Boroughs (Spearman's rho range: |0.21–0.78|). There was little difference in correlations between exposure tertiles, distance from road or deprivation tertiles.
Associations between noise and air pollution at the relevant geographical unit of analysis need to be carefully considered in any epidemiological analysis, in particular in complex urban areas. Low correlations near roads, however, suggest that independent effects of road noise and traffic-related air pollution can be reliably determined within London.
•Largest study of the relationship of noise and air pollution in space and time.•Correlations of noise and air pollution metrics across different spatial units.•Overall moderate correlations between levels of noise and air pollution in London.•Correlations vary greatly in magnitude by size of spatial unit.•Studies should consider the variability in co-linearity of noise and air pollution.
The recent United Kingdom (UK) Environment Act consultation had the intention of setting two targets for PM2.5 (particles with an aerodynamic diameter less than 2.5 μm), one related to meeting an ...annual average concentration and the second to reducing population exposure. As part of the consultation, predictions of PM2.5 concentrations in 2030 were made by combining European Union (EU) and UK government's emissions forecasts, with the Climate Change Committee's (CCC) Net Zero vehicle forecasts, and in London with the addition of local policies based on the London Environment Strategy (LES). Predictions in 2018 showed 6.4% of the UK's area and 82.6% of London's area had PM2.5 concentrations above the World Health Organization (WHO) interim target of 10 μg m-3, but by 2030, over 99% of the UK's area was predicted to be below it. However, kerbside concentrations in London and other major cities were still at risk of exceeding 10 μg m-3. With local action on PM2.5 in London, population weighted concentrations showed full compliance with the WHO interim target of 10 μg m-3 in 2030. However, predicting future PM2.5 concentrations and interpreting the results will always be difficult and uncertain for many reasons, such as imperfect models and the difficulty in estimating future emissions. To help understand the sensitivity of the model's PM2.5 predictions in 2030, current uncertainty was quantified using PM2.5 measurements and showed large areas in the UK that were still at risk of exceeding the WHO interim target despite the model predictions being below 10 μg m-3. Our results do however point to the benefits that policy at EU, UK and city level can have on achieving the WHO interim target of 10 μg m-3. These results were submitted to the UK Environment Act consultation. Nevertheless, the issues addressed here could be applicable to other European cities.
•Adds high spatially-resolved exposure data compared to previous studies.•Mutually adjusted estimates for air and noise pollution in susceptible population.•Primary traffic pollutants were not more ...strongly associated with prognosis.•Traffic noise only moderately correlated with air pollution.•Modest association between traffic noise and mortality independent of air pollution.
There is relatively little evidence of health effects of long-term exposure to traffic-related pollution in susceptible populations. We investigated whether long-term exposure to traffic air and noise pollution was associated with all-cause mortality or hospital readmission for myocardial infarction (MI) among survivors of hospital admission for MI.
Patients from the Myocardial Ischaemia National Audit Project database resident in Greater London (n=18,138) were followed for death or readmission for MI. High spatially-resolved annual average air pollution (11 metrics of primary traffic, regional or urban background) derived from a dispersion model (resolution 20m×20m) and road traffic noise for the years 2003–2010 were used to assign exposure at residence. Hazard ratios (HR, 95% confidence interval (CI)) were estimated using Cox proportional hazards models.
Most air pollutants were positively associated with all-cause mortality alone and in combination with hospital readmission. The largest associations with mortality per interquartile range (IQR) increase of pollutant were observed for non-exhaust particulate matter (PM10) (HR=1.05 (95% CI 1.00, 1.10), IQR=1.1μg/m3); oxidant gases (HR=1.05 (95% CI 1.00, 1.09), IQR=3.2μg/m3); and the coarse fraction of PM (HR=1.05 (95% CI 1.00, 1.10), IQR=0.9μg/m3). Adjustment for traffic noise only slightly attenuated these associations. The association for a 5dB increase in road-traffic noise with mortality was HR=1.02 (95% CI 0.99, 1.06) independent of air pollution.
These data support a relationship of primary traffic and regional/urban background air pollution with poor prognosis among MI survivors. Although imprecise, traffic noise appeared to have a modest association with prognosis independent of air pollution.
There is widespread concern about the possible health effects of traffic-related air pollution. Nitrogen dioxide (NO2) is a convenient marker of primary pollution. We investigated the associations ...between lung function and current residential exposure to a range of air pollutants (particularly NO2, NO, NOx and particulate matter) in London children. Moreover, we placed the results for NO2 in context with a meta-analysis of published estimates of the association.
Associations between primary traffic pollutants and lung function were investigated in 4884 children aged 9-10 years who participated in the Child Heart and Health Study in England (CHASE). A systematic literature search identified 13 studies eligible for inclusion in a meta-analysis. We combined results from the meta-analysis with the distribution of the values of FEV1 in CHASE to estimate the prevalence of children with abnormal lung function (FEV1<80% of predicted value) expected under different scenarios of NO2 exposure. In CHASE, there were non-significant inverse associations between all pollutants except ozone and both FEV1 and FVC. In the meta-analysis, a 10 μg/m3 increase in NO2 was associated with an 8 ml lower FEV1 (95% CI: -14 to -1 ml; p: 0.016). The observed effect was not modified by a reported asthma diagnosis. On the basis of these results, a 10 μg/m3 increase in NO2 level would translate into a 7% (95% CI: 4% to 12%) increase of the prevalence of children with abnormal lung function.
Exposure to traffic pollution may cause a small overall reduction in lung function and increase the prevalence of children with clinically relevant declines in lung function.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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.
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.
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).
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.
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.
Climate change poses a dangerous and immediate threat to the health of populations in the UK and worldwide. We aimed to model different scenarios to assess the health co-benefits that result from ...mitigation actions.
In this modelling study, we combined a detailed techno-economic energy systems model (UK TIMES), air pollutant emission inventories, a sophisticated air pollution model (Community Multi-scale Air Quality), and previously published associations between concentrations and health outcomes. We used four scenarios and focused on the air pollution implications from fine particulate matter (PM2·5), nitrogen dioxide (NO2) and ozone. The four scenarios were baseline, which assumed no further climate actions beyond those already achieved and did not meet the UK's Climate Change Act (at least an 80% reduction in carbon dioxide equivalent emissions by 2050 compared with 1990) target; nuclear power, which met the Climate Change Act target with a limited increase in nuclear power; low-greenhouse gas, which met the Climate Change Act target without any policy constraint on nuclear build; and a constant scenario that held 2011 air pollutant concentrations constant until 2050. We predicted the health and economic impacts from air pollution for the scenarios until 2050, and the inequalities in exposure across different socioeconomic groups.
NO2 concentrations declined leading to 4 892 000 life-years saved for the nuclear power scenario and 7 178 000 life-years saved for the low-greenhouse gas scenario from 2011 to 2154. However, the associations that we used might overestimate the effects of NO2 itself. PM2·5 concentrations in Great Britain are predicted to decrease between 42% and 44% by 2050 compared with 2011 in the scenarios that met the Climate Change Act targets, especially those from road traffic and off-road machinery. These reductions in PM2·5 are tempered by a 2035 peak (and subsequent decline) in biomass (wood burning), and by a large, projected increase in future demand for transport leading to potential increases in non-exhaust particulate matter emissions. The potential use of biomass in poorly controlled technologies to meet the Climate Change Act commitments would represent an important missed opportunity (resulting in 472 000 more life-years lost from PM2·5 in the low-greenhouse gas scenario and 1 122 000 more life-years lost in the nuclear power scenario from PM2·5 than the baseline scenario). Although substantial overall improvements in absolute amounts of exposure are seen compared with 2011, these outcomes mask the fact that health inequalities seen (in which socioeconomically disadvantaged populations are among the most exposed) are projected to be maintained up to 2050.
The modelling infrastructure created will help future researchers explore a wider range of climate policy scenarios, including local, European, and global scenarios. The need to strengthen the links between climate change policy objectives and public health imperatives, and the benefits to societal wellbeing that might result is urgent.
National Institute for Health Research.
BackgroundLittle is known about the role of air pollution in how people with dementia use mental health services.ObjectiveWe examined longitudinal associations between air pollution exposure and ...mental health service use in people with dementia.MethodsIn 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.FindingsIn 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.ConclusionsResidential air pollution exposure is associated with increased CMHT usage among people with dementia.Clinical implicationsEfforts 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.
This paper describes the development of a model for assessing TRAffic Noise EXposure (TRANEX) in an open-source geographic information system. Instead of using proprietary software we developed our ...own model for two main reasons: 1) so that the treatment of source geometry, traffic information (flows/speeds/spatially varying diurnal traffic profiles) and receptors matched as closely as possible to that of the air pollution modelling being undertaken in the TRAFFIC project, and 2) to optimize model performance for practical reasons of needing to implement a noise model with detailed source geometry, over a large geographical area, to produce noise estimates at up to several million address locations, with limited computing resources. To evaluate TRANEX, noise estimates were compared with noise measurements made in the British cities of Leicester and Norwich. High correlation was seen between modelled and measured LAeq,1hr (Norwich: r = 0.85, p = .000; Leicester: r = 0.95, p = .000) with average model errors of 3.1 dB. TRANEX was used to estimate noise exposures (LAeq,1hr, LAeq,16hr, Lnight) for the resident population of London (2003–2010). Results suggest that 1.03 million (12%) people are exposed to daytime road traffic noise levels ≥ 65 dB(A) and 1.63 million (19%) people are exposed to night-time road traffic noise levels ≥ 55 dB(A). Differences in noise levels between 2010 and 2003 were on average relatively small: 0.25 dB (standard deviation: 0.89) and 0.26 dB (standard deviation: 0.87) for LAeq,16hr and Lnight.
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•Adaptation of the Calculation of Road Traffic Noise method for exposure assessment.•Freely available open-source software (R with PostgreSQL and GRASS GIS).•Model estimates compared well to noise measurements (r: ∼0.85–0.95).•Noise level exposures modelled for 8.61 million London residents (2003–2010).•Over 1 million residents exposed to high daytime and night-time noise levels.
Objective To investigate the relation between exposure to both air and noise pollution from road traffic and birth weight outcomes.Design Retrospective population based cohort study.Setting Greater ...London and surrounding counties up to the M25 motorway (2317 km2), UK, from 2006 to 2010.Participants 540 365 singleton term live births.Main outcome measures Term low birth weight (LBW), small for gestational age (SGA) at term, and term birth weight.Results Average air pollutant exposures across pregnancy were 41 μg/m3 nitrogen dioxide (NO2), 73 μg/m3 nitrogen oxides (NOx), 14 μg/m3 particulate matter with aerodynamic diameter <2.5 μm (PM2.5), 23 μg/m3 particulate matter with aerodynamic diameter <10 μm (PM10), and 32 μg/m3 ozone (O3). Average daytime (LAeq,16hr) and night-time (Lnight) road traffic A-weighted noise levels were 58 dB and 53 dB respectively. Interquartile range increases in NO2, NOx, PM2.5, PM10, and source specific PM2.5 from traffic exhaust (PM2.5 traffic exhaust) and traffic non-exhaust (brake or tyre wear and resuspension) (PM2.5 traffic non-exhaust) were associated with 2% to 6% increased odds of term LBW, and 1% to 3% increased odds of term SGA. Air pollutant associations were robust to adjustment for road traffic noise. Trends of decreasing birth weight across increasing road traffic noise categories were observed, but were strongly attenuated when adjusted for primary traffic related air pollutants. Only PM2.5 traffic exhaust and PM2.5 were consistently associated with increased risk of term LBW after adjustment for each of the other air pollutants. It was estimated that 3% of term LBW cases in London are directly attributable to residential exposure to PM2.5>13.8 μg/m3during pregnancy.Conclusions The findings suggest that air pollution from road traffic in London is adversely affecting fetal growth. The results suggest little evidence for an independent exposure-response effect of traffic related noise on birth weight outcomes.
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