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The burden of diseases attributable to air pollution is comparable to those of global health risks such as unhealthy diets and tobacco smoking, with many air pollution sources also emitting climate heating gases. In this UK study we estimated the co-benefits of Net Zero (NZ) climate policy on the health benefits of air pollution reduction, increased active travel, outdoor exposure inequalities and indoor air pollution changes. The study focused on two of the largest UK sources, road transport and building heating, with comparisons made between NZ and UK existing policy, referred to as Business as Usual (BAU). Particulate matter (PM 2.5 ), Nitrogen Dioxide (NO 2 ) and Ozone (O 3 ) projections were made between 2019 and 2050, with emphasis placed upon the NZ co-benefits in 2030 and 2040. We compared the UK BAU scenarios with the Climate Change Committee's (CCC) Balanced Net Zero Pathway (BNZP) and Widespread Innovation (WI) pathway. Compared to BAU predictions, BNZP assumptions lead to more electric vehicles, reduced vehicle km, more low carbon building heating, and reduced emissions of NO 2 and PM 2.5 . By 2040 under BNZP, relative to BAU, the buildings sector was predicted to be three times more effective at reducing PM 2.5 than road transport. To help reduce the inequality gap the NZ building transition was tailored toward those most in need. Outdoor air pollution exposure inequalities prevailed across the socioeconomic spectrum, especially for NO 2 , but were less pronounced due in part to NZ policies. Core air quality health benefits for the BNZP buildings sector were £21.3 billion (16.4 to 26.2) by 2050 and £98.4 billion (75.7 to 121.1) by 2154. For the transport sector the health benefits were £9.1 billion (7.0 to 11.2) by 2050 and £36.5 billion (28.1 to 44.9) by 2154. NZ building sector operating costs did not achieve break-even via efficiency savings, but with Greenhouse Gas (GHG) (lower benefits) break-even was achieved in 2052. With additional air pollution health benefits, building-sector time to break-even improved by between 3.1 (2.5 to 4.7) and 6.3 (4.7 to 7.6) years to between 2046 and 2049. Analysis found that removing gas cooking at home, for NZ, may result in greater concentration reductions than outdoor air pollution for NO 2 . Net Zero health and economic co-benefits are large, as are the changes needed, requiring political leadership and public engagement. Our findings are relevant to other countries facing the NZ transition., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

Background: The UK is committed to achieve net zero greenhouse gas emissions by 2050. The suite of policies needed to reach net zero will lead to improvements in air quality and, consequently, could lessen air pollution inequalities. We assessed air pollution inequalities across different sociodemographic groups in England and Wales and explored how these might be differentially impacted by future air pollution projections in 2030 and 2040 under net zero policies., Methods: We employed a geodemographic classification approach to categorise neighbourhoods into five distinct clusters based on 2021 UK Census sociodemographic variables. We modelled fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) concentrations for the year 2019, and predicted concentrations in 2030 and 2040. We compared a business-as-usual (BAU) scenario and two policy pathways to achieve net zero currently considered by the UK government. We aggregated air pollution concentrations to the neighbourhood level and assessed differential neighbourhood-level concentrations across the geodemographic groups using descriptive statistics and box plots., Results: The Urban Central Professionals group experienced 14 µg/m 3 higher average NO 2 concentrations compared with the Rural Elderly group in 2019. Despite substantial improvements to air quality in 2030 and 2040 of up to 6.3 µg/m 3 for NO 2 based on BAU, and further reductions of up to 2.4 µg/m 3 NO 2 under net zero policies, the overall pattern of inequality persists, but is predicted to be less pronounced., Conclusions: Our findings demonstrate the effectiveness of targeted policies and innovations in reducing both air quality and greenhouse gas emissions and in bridging the environmental inequality gap. Our findings are essential to develop targeted communication campaigns to secure acceptance and willingness across the sociodemographic spectrum to support the significant behavioural changes needed to achieve net zero, by highlighting the wider co-benefits to the environment and health of such policies., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: [Co-authors Heather Walton and Mike Holland declare membership of the Committee on the Medical Effects of Air Pollutants reporting to the UK Department for Health and Social Care. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper]., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

The recent United Kingdom (UK) Environment Act consultation had the intention of setting two targets for PM 2.5 (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 PM 2.5 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 PM 2.5 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 PM 2.5 in London, population weighted concentrations showed full compliance with the WHO interim target of 10 μg m -3 in 2030. However, predicting future PM 2.5 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 PM 2.5 predictions in 2030, current uncertainty was quantified using PM 2.5 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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Crown Copyright © 2023. Published by Elsevier Ltd. All rights reserved.)

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.

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 (NO 2 ) and oxides (NO x ), ozone (O 3 ), particulate matter with an aerodynamic diameter < 10 μm (PM 10 ) and < 2.5 μm (PM 2.5 ) 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 PM 2.5 , NO x and NO 2 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 PM 10 . These longitudinal associations were more pronounced in the subset of non-movers for NO 2 and NO x ., 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., (© 2020. The Author(s).)

Background: 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., Objectives: 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., Methods: 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 (PM 2.5 ) and <10 μm (PM 10 ), ozone (O 3 ), primary traffic air pollutants (nitrogen dioxide, nitrogen oxides, PM 2.5 from traffic exhaust and traffic non-exhaust), and road traffic noise were estimated based on maternal address at birth., Results: An interquartile range increase in O 3 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 PM 2.5 , which was associated with 3% increased odds of preterm birth (Trimester 1) and 7% increased odds stillbirth (Trimester 1 and 2) when adjusted for O 3 . Elevated risk of preterm birth was associated with increasing road traffic noise, but only after adjustment for certain air pollutant exposures., Discussion: Our findings suggest that exposure to higher levels of O 3 and primary traffic non-exhaust related PM 2.5 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., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

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 [NO 2 ]) and particulate matter with a diameter of less than 2·5 μm (PM 2·5 ) and less than 10 μm (PM 10 ) and lung function: postbronchodilator forced expiratory volume in 1 s (FEV 1 , 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 NO 2 (40 μg/m 3 ) fell from 99% (444/450) in 2009 to 34% (150/441) in 2013. Over this period, we identified a reduction in NO 2 at both roadside (median -1·35 μg/m 3 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 PM 10 . The effect on PM 2·5 was equivocal. We found no association between postbronchodilator FEV 1 and annual residential pollutant attributions. By contrast, FVC was inversely correlated with annual NO 2 (-0·0023 L/μg per m 3 ; -0·0044 to -0·0002; p=0·033) and PM 10 (-0·0090 L/μg per m 3 ; -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., (Copyright © 2019 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Objective: To investigate whether the incidence of dementia is related to residential levels of air and noise pollution in London., Design: Retrospective cohort study using primary care data., Setting: 75 Greater London practices., Participants: 130 978 adults aged 50-79 years registered with their general practices on 1 January 2005, with no recorded history of dementia or care home residence., Primary and Secondary Outcome Measures: A first recorded diagnosis of dementia and, where specified, subgroups of Alzheimer's disease and vascular dementia during 2005-2013. The average annual concentrations during 2004 of nitrogen dioxide (NO 2 ), particulate matter with a median aerodynamic diameter ≤2.5 µm (PM 2.5 ) and ozone (O 3 ) were estimated at 20×20 m resolution from dispersion models. Traffic intensity, distance from major road and night-time noise levels (L night ) were estimated at the postcode level. All exposure measures were linked anonymously to clinical data via residential postcode. HRs from Cox models were adjusted for age, sex, ethnicity, smoking and body mass index, with further adjustments explored for area deprivation and comorbidity., Results: 2181 subjects (1.7%) received an incident diagnosis of dementia (39% mentioning Alzheimer's disease, 29% vascular dementia). There was a positive exposure response relationship between dementia and all measures of air pollution except O 3 , which was not readily explained by further adjustment. Adults living in areas with the highest fifth of NO 2 concentration (>41.5 µg/m 3 ) versus the lowest fifth (<31.9 µg/m 3 ) were at a higher risk of dementia (HR=1.40, 95% CI 1.12 to 1.74). Increases in dementia risk were also observed with PM 2.5 , PM 2.5 specifically from primary traffic sources only and L night , but only NO 2 and PM 2.5 remained statistically significant in multipollutant models. Associations were more consistent for Alzheimer's disease than vascular dementia., Conclusions: We have found evidence of a positive association between residential levels of air pollution across London and being diagnosed with dementia, which is unexplained by known confounding factors., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: 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., Methods: 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 (PM 2·5 ), nitrogen dioxide (NO 2 ) 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., Findings: NO 2 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 NO 2 itself. PM 2·5 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 PM 2·5 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 PM 2·5 in the low-greenhouse gas scenario and 1 122 000 more life-years lost in the nuclear power scenario from PM 2·5 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., Interpretation: 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., Funding: National Institute for Health Research., (Copyright © 2018 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Short telomeres are associated with chronic disease and early mortality. Recent studies in adults suggest an association between telomere length and exposure to particulate matter, and that ethnicity may modify the relationship. However associations in children are unknown., Objectives: We examined associations between air pollution and telomere length in an ethnically diverse group of children exposed to high levels of traffic derived pollutants, particularly diesel exhaust, and to environmental tobacco smoke., Methods: Oral DNA from 333 children (8-9years) participating in a study on air quality and respiratory health in 23 inner city London schools was analysed for relative telomere length using monochrome multiplex qPCR. Annual, weekly and daily exposures to nitrogen oxides and particulate matter were obtained from urban dispersion models (2008-10) and tobacco smoke by urinary cotinine. Ethnicity was assessed by self-report and continental ancestry by analysis of 28 random genomic markers. We used linear mixed effects models to examine associations with telomere length., Results: Telomere length increased with increasing annual exposure to NO x (model coefficient 0.003, [0.001, 0.005], p<0.001), NO 2 (0.009 [0.004, 0.015], p<0.001), PM 2.5 (0.041, [0.020, 0.063], p<0.001) and PM 10 (0.096, [0.044, 0.149], p<0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p<0.001) CONCLUSIONS: Pollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms., (Copyright © 2016. Published by Elsevier Ltd.)

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., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: 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., Methods: Patients from the Myocardial Ischaemia National Audit Project database resident in Greater London (n = 1 8,138) 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 20 m × 20 m) 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., Results: 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 (PM(10)) (HR = 1.05 (95% CI 1.00, 1.10), IQR = 1.1 μg/m(3)); oxidant gases (HR = 1.05 (95% CI 1.00, 1.09), IQR = 3.2 μg/m(3)); and the coarse fraction of PM (HR = 1.05 (95% CI 1.00, 1.10), IQR = 0.9 μg/m(3)). Adjustment for traffic noise only slightly attenuated these associations. The association for a 5 dB increase in road-traffic noise with mortality was HR = 1.02 (95% CI 0.99, 1.06) independent of air pollution., Conclusions: 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., (Copyright © 2015 The Authors. Published by Elsevier GmbH.. All rights reserved.)

Long-term exposure to primary traffic pollutants may be harmful for health but few studies have investigated effects on mortality. We examined associations for six primary traffic pollutants with all-cause and cause-specific mortality in 2003-2010 at small-area level using linear and piecewise linear Poisson regression models. In linear models most pollutants showed negative or null association with all-cause, cardiovascular or respiratory mortality. In the piecewise models we observed positive associations in the lowest exposure range (e.g. relative risk (RR) for all-cause mortality 1.07 (95% credible interval (CI) = 1.00-1.15) per 0.15 μg/m(3) increase in exhaust related primary particulate matter ≤2.5 μm (PM2.5)) whereas associations in the highest exposure range were negative (corresponding RR 0.93, 95% CI: 0.91-0.96). Overall, there was only weak evidence of positive associations with mortality. That we found the strongest positive associations in the lowest exposure group may reflect residual confounding by unmeasured confounders that varies by exposure group., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Evidence on the effects of long-term exposure to traffic pollution on health is inconsistent. In Greater London we examined associations between traffic pollution and emergency hospital admissions for cardio-respiratory diseases by applying linear and piecewise linear Poisson regression models in a small-area analysis. For both models the results for children and adults were close to unity. In the elderly, linear models found negative associations whereas piecewise models found non-linear associations characterized by positive risks in the lowest and negative risks in the highest exposure category. An increased risk was observed among those living in areas with the highest socioeconomic deprivation. Estimates were not affected by adjustment for traffic noise. The lack of convincing positive linear associations between primary traffic pollution and hospital admissions agrees with a number of other reports, but may reflect residual confounding. The relatively greater vulnerability of the most deprived populations has important implications for public health., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: 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., Methods and Findings: 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., Conclusions: 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.