Traffic pollution and the incidence of cardiorespiratory outcomes in an adult cohort in London.

OBJECTIVES: The epidemiological evidence for adverse health effects of long-term exposure to air and noise pollution from traffic is not coherent. Further, the relative roles of background versus near traffic pollution concentrations in this process are unclear. We investigated relationships between modelled concentrations of air and noise pollution from traffic and incident cardiorespiratory disease in London. METHODS: Among 211 016 adults aged 40-79 years registered in 75 Greater London practices between 2005 and 2011, the first diagnosis for a range of cardiovascular and respiratory outcomes were identified from primary care and hospital records. Annual baseline concentrations for nitrogen oxide (NOx), particulate matter with a median aerodynamic diameter <2.5 μm (PM2.5) attributable to exhaust and non-exhaust sources, traffic intensity and noise were estimated at 20 m(2) resolution from dispersion models, linked to clinical data via residential postcode. HRs were adjusted for confounders including smoking and area deprivation. RESULTS: The largest observed associations were between traffic-related air pollution and heart failure (HR=1.10 for 20 μg/m(3) change in NOx, 95% CI 1.01 to 1.21). However, no other outcomes were consistently associated with any of the pollution indicators, including noise. The greater variations in modelled air pollution from traffic between practices, versus within, hampered meaningful fine spatial scale analyses. CONCLUSIONS: The associations observed with heart failure may suggest exacerbatory effects rather than underlying chronic disease. However, the overall failure to observe wider associations with traffic pollution may reflect that exposure estimates based on residence inadequately represent the relevant pattern of personal exposure, and future studies must address this issue

Impacts of air pollution and noise on risk of preterm birth and stillbirth in London

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 (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. Results 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. Discussion 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

Long-term traffic air and noise pollution in relation to mortality and hospital readmission among myocardial infarction survivors.

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

Long-term exposure to traffic pollution and hospital admissions in London.

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

Air pollution, ethnicity and telomere length in east London schoolchildren: An observational study

This study was funded/supported by the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London, Dr. and Mrs. Lee Iu Cheung Fund, and Hackney Primary Care Trust (PCT)

Air pollution and trajectories of adolescent conduct problems: the roles of ethnicity and racism; evidence from the DASH longitudinal study.

PURPOSE: No known UK empirical research has investigated prospective associations between ambient air pollutants and conduct problems in adolescence. Ethnic minority children are disproportionately exposed to structural factors that could moderate any observed relationships. This prospective study examined whether exposure to PM2.5 and NO2 concentrations is associated with conduct problems in adolescence, and whether racism or ethnicity moderate such associations. METHODS: Longitudinal associations between annual mean estimated PM2.5 and NO2 concentrations at the residential address and trajectories of conduct problems, and the potential influence of racism and ethnicity were examined school-based sample of 4775 participants (2002-2003 to 2005-2006) in London, using growth curve models. RESULTS: Overall, in the fully adjusted model, exposure to lower concentrations of PM2.5 and NO2 was associated with a decrease in conduct problems during adolescence, while exposure to higher concentrations was associated with a flattened trajectory of conduct symptoms. Racism amplified the effect of PM2.5 (β = 0.05 (95% CI 0.01 to 0.10, p < 0.01)) on adolescent trajectories of conduct problems over time. At higher concentrations of PM2.5, there was a divergence of trajectories of adolescent conduct problems between ethnic minority groups, with White British and Black Caribbean adolescents experiencing an increase in conduct problems over time. CONCLUSION: These findings suggest that the intersections between air pollution, ethnicity, and racism are important influences on the development of conduct problems in adolescence

Associations between air pollutants and blood pressure in an ethnically diverse cohort of adolescents in London, England

Longitudinal evidence on the association between air pollution and blood pressure (BP) in adolescence is scarce. We explored this association in an ethnically diverse cohort of schoolchildren. Sex-stratified, linear random-effects modelling was used to examine how modelled residential exposure to annual average nitrogen dioxide (NO2), particulate matter (PM2.5, PM10) and ozone (O3), measures in μg/m3, associated with blood pressure. Estimates were based on 3,284 adolescents; 80% from ethnic minority groups, recruited from 51 schools, and followed up from 11–13 to 14–16 years old. Ethnic minorities were exposed to higher modelled annual average concentrations of pollution at residential postcode level than their White UK peers. A two-pollutant model (NO2 &amp; PM2.5), adjusted for ethnicity, age, anthropometry, and pubertal status, highlighted associations with systolic, but not diastolic BP. A μg/m3 increase in NO2 was associated with a 0.30 mmHg (95% CI 0.18 to 0.40) decrease in systolic BP for girls and 0.19 mmHg (95% CI 0.07 to 0.31) decrease in systolic BP for boys. In contrast, a 1 μg/m3 increase in PM2.5 was associated with 1.34 mmHg (95% CI 0.85 to 1.82) increase in systolic BP for girls and 0.57 mmHg (95% CI 0.04 to 1.03) increase in systolic BP for boys. Associations did not vary by ethnicity, body size or socio-economic advantage. Associations were robust to adjustments for noise levels and lung function at 11–13 years. In summary, higher ambient levels of NO2 were associated with lower and PM2.5 with higher systolic BP across adolescence, with stronger associations for girls

Eddy covariance measurements highlight sources of nitrogen oxide emissions missing from inventories for central London

During March–June 2017 emissions of nitrogen oxides were measured via eddy covariance at the British Telecom Tower in central London, UK. Through the use of a footprint model the expected emissions were simulated from the spatially resolved National Atmospheric Emissions Inventory for 2017 and compared with the measured emissions. These simulated emissions were shown to underestimate measured emissions during the daytime by a factor of 1.48, but they agreed well overnight. Furthermore, underestimations were spatially mapped, and the areas around the measurement site responsible for differences in measured and simulated emissions were inferred. It was observed that areas of higher traffic, such as major roads near national rail stations, showed the greatest underestimation by the simulated emissions. These discrepancies are partially attributed to a combination of the inventory not fully capturing traffic conditions in central London and both the spatial and temporal resolution of the inventory not fully describing the high heterogeneity of the urban centre. Understanding of this underestimation may be further improved with longer measurement time series to better understand temporal variation and improved temporal scaling factors to better simulate sub-annual emissions