This paper develops the idea of bivariate polar plots as a method for source detection and characterisation. Bivariate polar plots provide a graphical method for showing the joint wind speed, wind ...direction dependence of air pollutant concentrations. Bivariate polar plots provide an effective graphical means of discriminating different source types and characteristics. In the current work we apply k-means clustering techniques directly to bivariate polar plots to identify and group similar features. The technique is analogous to clustering applied to back trajectories at the regional scale. When applied to data from a monitoring site with high source complexity it is shown that the technique is able to identify important clusters in ambient monitoring data that additional analysis shows to exhibit different source characteristics. Importantly, this paper links identified clusters to known emission characteristics to confirm the inferences made in the analysis. The approaches developed should have wide application to the analysis of air pollution monitoring data and have been made freely available as part of the openair R package.
•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.
Evidence linking ozone to depression and anxiety disorders remains sparse and results are heterogeneous. It remains unknown whether omega-3 fatty acid, or genetic susceptibility of mental disorders ...modify the impacts of ozone. The aim is to assess the associations of ambient ozone with depression and anxiety, and further explore the potential modification effects of omega-3 fatty acid and genetic susceptibility.
In total of 257,534 participants were enrolled from 2006 to 2010 and followed up to 2016. Depression and anxiety were assessed using mental health questionnaires, primary care records and hospital admission records. The annual average concentrations of ozone were calculated and linked to individuals by home address. Dietary intake and plasma concentration were selected to reflect levels of omega-3 fatty acid. Polygenetic risk scores were selected to reflect genetic susceptibility. We examined the associations of ozone and incident mental disorders, and potential modification of omega-3 fatty acid and genetic susceptibility.
Incidences of depression (N = 6957) and anxiety (N = 6944) was associated with increase of ozone. Higher levels of omega-3 fatty acid might attenuate the ozone related depression risk. However, the modification effects of genetic susceptibility were not found.
Long-term exposure to ambient ozone increase the risk of mental disorders among the middle aged and older adults, and omega-3 fatty acid could reduce the adverse effects of ozone on mental health. Higher intake of omega-3 fatty acid is a potential strategy to prevent the risks caused by ozone on public mental health.
•Long-term exposure to ozone was associated with increased incidence of depression and anxiety.•Habitual intake of omega-3 fatty acid was observed reducing the association between long-term ozone and depression.•Genetic susceptibility has not been observed to modify the risk of ozone related mental disorders.
Summary We used Comparative Risk Assessment methods to estimate the health effects of alternative urban land transport scenarios for two settings—London, UK, and Delhi, India. For each setting, we ...compared a business-as-usual 2030 projection (without policies for reduction of greenhouse gases) with alternative scenarios—lower-carbon-emission motor vehicles, increased active travel, and a combination of the two. We developed separate models that linked transport scenarios with physical activity, air pollution, and risk of road traffic injury. In both cities, we noted that reduction in carbon dioxide emissions through an increase in active travel and less use of motor vehicles had larger health benefits per million population (7332 disability-adjusted life-years DALYs in London, and 12 516 in Delhi in 1 year) than from the increased use of lower-emission motor vehicles (160 DALYs in London, and 1696 in Delhi). However, combination of active travel and lower-emission motor vehicles would give the largest benefits (7439 DALYs in London, 12 995 in Delhi), notably from a reduction in the number of years of life lost from ischaemic heart disease (10–19% in London, 11–25% in Delhi). Although uncertainties remain, climate change mitigation in transport should benefit public health substantially. Policies to increase the acceptability, appeal, and safety of active urban travel, and discourage travel in private motor vehicles would provide larger health benefits than would policies that focus solely on lower-emission motor vehicles.
Road traffic noise has been associated with hypertension but evidence for the long-term effects on hospital admissions and mortality is limited. We examined the effects of long-term exposure to road ...traffic noise on hospital admissions and mortality in the general population.
The study population consisted of 8.6 million inhabitants of London, one of Europe's largest cities. We assessed small-area-level associations of day- (7:00-22:59) and nighttime (23:00-06:59) road traffic noise with cardiovascular hospital admissions and all-cause and cardiovascular mortality in all adults (≥25 years) and elderly (≥75 years) through Poisson regression models. We adjusted models for age, sex, area-level socioeconomic deprivation, ethnicity, smoking, air pollution, and neighbourhood spatial structure. Median daytime exposure to road traffic noise was 55.6 dB. Daytime road traffic noise increased the risk of hospital admission for stroke with relative risk (RR) 1.05 95% confidence interval (CI): 1.02-1.09 in adults, and 1.09 (95% CI: 1.04-1.14) in the elderly in areas >60 vs. <55 dB. Nighttime noise was associated with stroke admissions only among the elderly. Daytime noise was significantly associated with all-cause mortality in adults RR 1.04 (95% CI: 1.00-1.07) in areas >60 vs. <55 dB. Positive but non-significant associations were seen with mortality for cardiovascular and ischaemic heart disease, and stroke. Results were similar for the elderly.
Long-term exposure to road traffic noise was associated with small increased risks of all-cause mortality and cardiovascular mortality and morbidity in the general population, particularly for stroke in the elderly.
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•Exposure to air pollution, greenspace, food environment, road safety around schools.•Used Bayesian nonparametrics to find clusters with similar exposure profiles.•Identified ...predominant exposure to urban feature for each cluster.•Investigated associations with deprivation and ethnicity.•Useful to compare schools’ exposure and prioritize interventions based on needs.
Creating healthy environments around schools is important to promote healthy childhood development and is a critical component of public health. In this paper we present a tool to characterize exposure to multiple urban environment features within 400 m (5–10 min walking distance) of schools in Greater London. We modelled joint exposure to air pollution (NO2 and PM2.5), access to public greenspace, food environment, and road safety for 2,929 schools, employing a Bayesian non-parametric approach based on the Dirichlet Process Mixture modelling. We identified 12 latent clusters of schools with similar exposure profiles and observed some spatial clustering patterns. Socioeconomic and ethnicity disparities were manifested with respect to exposure profiles. Specifically, three clusters (containing 645 schools) showed the highest joint exposure to air pollution, poor food environment, and unsafe roads and were characterized with high deprivation. The neighbourhood of the most deprived cluster of schools had a median of 2.5 ha greenspace, 29.0 µg/m3 of NO2, 19.3 µg/m3 of PM2.5, 20 fast food retailers, and five child pedestrian crashes over a three-year period. The neighbourhood of the least deprived cluster of schools had a median of 21.8 ha greenspace, 15.6 µg/m3 of NO2, 15.1 µg/m3 of PM2.5, 2 fast food retailers, and one child pedestrian crash over a three-year period. To have a school-level understanding of exposure levels, we then benchmarked schools based on the probability of exceeding the median exposure to various features of interest. Our study accounts for multiple exposures, enabling us to highlight spatial distribution of exposure profile clusters, and to identify predominant exposure to urban environment features for each cluster of schools. Our findings can help relevant stakeholders, such as schools and public health authorities, to compare schools based on their exposure levels, prioritize interventions, and design local policies that target the schools most in need.
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.
Few studies have examined the association between air pollutants and ischemic stroke subtypes. We examined acute effects of outdoor air pollutants (PM10, NO2, O3, CO, SO2) on subtypes and severity of ...incident ischemic stroke and investigated if pre-existing risk factors increased susceptibility.
We used a time stratified case-crossover study and stroke cases from the South London Stroke Register set up to capture all incident cases of first ever stroke occurring amongst residents in a geographically defined area. The Oxford clinical and TOAST etiological classifications were used to classify subtypes. A pragmatic clinical classification system was used to assess severity. Air pollution concentrations from the nearest background air pollution monitoring stations to patients' residential postcode centroids were used. Lags from 0 to 6 days were investigated.
There were 2590 incident cases of ischemic stroke (1995-2006). While there were associations at various lag times with several pollutants, overall, there was no consistent pattern between exposure and risk of ischemic stroke subtypes or severity. The possible exception was the association between NO2 exposure and small vessel disease stroke-adjusted odds ratio of 1.51 (1.12-2.02) associated with an inter-quartile range increase in the lag 0-6 day average for NO2. There were no clear associations in relation to pre-existing risk factors.
Overall, we found little consistent evidence of association between air pollutants and ischemic stroke subtypes and severity. There was however a suggestion that increasing NO2 exposure might be associated with higher risk of stroke caused by cerebrovascular small vessel disease.
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Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
ObjectiveTo investigate whether the incidence of dementia is related to residential levels of air and noise pollution in London.DesignRetrospective cohort study using primary care data.Setting75 ...Greater London practices.Participants130 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 measuresA 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 (NO2), particulate matter with a median aerodynamic diameter ≤2.5 µm (PM2.5) and ozone (O3) were estimated at 20×20 m resolution from dispersion models. Traffic intensity, distance from major road and night-time noise levels (Lnight) 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.Results2181 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 O3, which was not readily explained by further adjustment. Adults living in areas with the highest fifth of NO2 concentration (>41.5 µg/m3) versus the lowest fifth (<31.9 µg/m3) 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 PM2.5, PM2.5 specifically from primary traffic sources only and Lnight, but only NO2 and PM2.5 remained statistically significant in multipollutant models. Associations were more consistent for Alzheimer’s disease than vascular dementia.ConclusionsWe 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.
Here we describe the development of the London Hybrid Exposure Model (LHEM), which calculates exposure of the Greater London population to outdoor air pollution sources, in-buildings, in-vehicles, ...and outdoors, using survey data of when and where people spend their time. For comparison and to estimate exposure misclassification we compared Londoners LHEM exposure with exposure at the residential address, a commonly used exposure metric in epidemiological research. In 2011, the mean annual LHEM exposure to outdoor sources was estimated to be 37% lower for PM2.5 and 63% lower for NO2 than at the residential address. These decreased estimates reflect the effects of reduced exposure indoors, the amount of time spent indoors (∼95%), and the mode and duration of travel in London. We find that an individual’s exposure to PM2.5 and NO2 outside their residential address is highly correlated (Pearson’s R of 0.9). In contrast, LHEM exposure estimates for PM2.5 and NO2 suggest that the degree of correlation is influenced by their exposure in different transport modes. Further development of the LHEM has the potential to increase the understanding of exposure error and bias in time-series and cohort studies and thus better distinguish the independent effects of NO2 and PM2.5.
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