Benjamin Barratt

Ozone, heat and mortality: acute effects in 15 British conurbations

Background Acute associations between mortality and ozone are largely accepted, though recent evidence is less conclusive. Evidence on ozone–heat interaction is sparse. We assess effects of ozone, heat, and their interaction, on mortality in Britain. Methods Acute effects of summer ozone on mortality were estimated using data from 15 conurbations in England and Wales (May–September, 1993–2003). 2-day means of daily maximum 8-h ozone were entered into case series analyses, controlling for particulate matter with aerodynamic diameter of <10 μm, natural cubic splines of temperature, and other factors. Heat effects were estimated, comparing adjusted mortality rates at 97.5th and 75th percentiles of 2-day mean temperature. A separate model employed interaction terms to assess whether ozone effects increased on ‘hot days’ (where 2-day mean temperature exceeded the whole-year 95th percentile). Other heat metrics, and non-linear ozone effects, were also examined. Results Adverse ozone and heat effects occurred in nearly all conurbations. The mean mortality rate ratio for heat effect across conurbations was 1.071 (1.050–1.093). The mean ozone rate ratio was 1.003 per 10 μg/m3 ozone increase (95% CI 1.001 to 1.005). On ‘hot days’ the mean ozone effect reached 1.006 (1.002–1.009) per 10 μg/m3, though ozone–heat interaction was significant in London only. On substituting maximum for mean temperature, the overall ozone effect reduced to null, though evidence remained of effects on hot days, particularly in London. An estimated ozone effect threshold was below current guidelines in ‘mean temperature’ models. Conclusion While heat showed robust effects on summer mortality, estimates for ozone depended upon the modelling of temperature. However, there was some evidence that ozone effects were worse on hot days, whichever temperature measure was used.

Carbon in airway macrophages from children with asthma

Background Airway macrophage (AM) phagocytosis is impaired in severe asthma. Prostaglandin (PG) E2 and D2 are increased in severe asthma and suppress AM phagocytic function in vitro. In this study, we sought evidence for PG-mediated impairment of phagocytosis of inhalable carbonaceous particulate matter (PM) by AM in children with severe asthma compared with mild asthmatics and healthy controls. Methods AM were obtained from children with asthma and healthy controls using induced sputum. AM carbon area (μm2) was assessed by image analysis. In a subgroup of asthmatics, urinary PGE2 and PGD2 metabolites were measured by high-performance liquid chromatography, and PM exposure at the home address was modelled. Phagocytosis of PM by human monocyte-derived macrophages and rat AM was assessed in vitro by image analysis. Results AM carbon was 51% lower in children with moderate-to-severe asthma (n=36) compared with mild asthmatics (n=12, p<0.01) and healthy controls (n=47, p<0.01). There was no association between modelled PM exposure and AM carbon in 33 asthmatics who had a urine sample, but there was an inverse association between AM carbon and urinary metabolites of PGE2 and D2 (n=33, rs=−0.40, p<0.05, and rs=−0.44, p<0.01). PGE2 10−6 M, but not PGD2 10−6 M, suppressed phagocytosis of PM10 by human macrophages in vitro (p<0.05 vs control). PGE2 10−6 M also suppressed phagocytosis of PM10 by rat AM in vitro (p<0.01 vs control). Conclusions Phagocytosis of inhaled carbonaceous PM by AMs is impaired in severe asthma. PGE2 may contribute to impaired AM phagocytic function in severe asthma.

Land use regression modelling of air pollution in high density high rise cities: A case study in Hong Kong

Land use regression (LUR) is a common method of predicting spatial variability of air pollution to estimate exposure. Nitrogen dioxide (NO2), nitric oxide (NO), fine particulate matter (PM2.5), and black carbon (BC) concentrations were measured during two sampling campaigns (April-May and November-January) in Hong Kong (a prototypical high-density high-rise city). Along with 365 potential geospatial predictor variables, these concentrations were used to build two-dimensional land use regression (LUR) models for the territory. Summary statistics for combined measurements over both campaigns were: a) NO2 (Mean=106μg/m3, SD=38.5, N=95), b) NO (M=147μg/m3, SD=88.9, N=40), c) PM2.5 (M=35μg/m3, SD=6.3, N=64), and BC (M=10.6μg/m3, SD=5.3, N=76). Final LUR models had the following statistics: a) NO2 (R2=0.46, RMSE=28μg/m3) b) NO (R2=0.50, RMSE=62μg/m3), c) PM2.5 (R2=0.59; RMSE=4μg/m3), and d) BC (R2=0.50, RMSE=4μg/m3). Traditional LUR predictors such as road length, car park density, and land use types were included in most models. The NO2 prediction surface values were highest in Kowloon and the northern region of Hong Kong Island (downtown Hong Kong). NO showed a similar pattern in the built-up region. Both PM2.5 and BC predictions exhibited a northwest-southeast gradient, with higher concentrations in the north (close to mainland China). For BC, the port was also an area of elevated predicted concentrations. The results matched with existing literature on spatial variation in concentrations of air pollutants and in relation to important emission sources in Hong Kong. The success of these models suggests LUR is appropriate in high-density, high-rise cities.

Just good enough data: Figuring data citizenships through air pollution sensing and data stories

Citizen sensing, or the use of low-cost and accessible digital technologies to monitor environments, has contributed to new types of environmental data and data practices. Through a discussion of participatory research into air pollution sensing with residents of northeastern Pennsylvania concerned about the effects of hydraulic fracturing, we examine how new technologies for generating environmental data also give rise to new problems for analysing and making sense of citizen-gathered data. After first outlining the citizen data practices we collaboratively developed with residents for monitoring air quality, we then describe the data stories that we created along with citizens as a method and technique for composing data. We further mobilise the concept of ‘just good enough data’ to discuss the ways in which citizen data gives rise to alternative ways of creating, valuing and interpreting datasets. We specifically consider how environmental data raises different concerns and possibilities in relation to Big Data, which can be distinct from security or social media studies. We then suggest ways in which citizen datasets could generate different practices and interpretive insights that go beyond the usual uses of environmental data for regulation, compliance and modelling to generate expanded data citizenships.

Methods to Estimate Acclimatization to the Urban Heat Island Effects on Heat- and Cold-Related Mortality.

Background: Investigators have examined whether heat mortality risk is increased in neighborhoods subject to the urban heat island (UHI) effect but have not identified degrees of difference in susceptibility to heat and cold between cool and hot areas, which we call acclimatization to the UHI. Objectives: We developed methods to examine and quantify the degree of acclimatization to heat- and cold-related mortality in relation to UHI anomalies and applied these methods to London, UK. Methods: Case–crossover analyses were undertaken on 1993–2006 mortality data from London UHI decile groups defined by anomalies from the London average of modeled air temperature at a 1-km grid resolution. We estimated how UHI anomalies modified excess mortality on cold and hot days for London overall and displaced a fixed-shape temperature-mortality function (“shifted spline” model). We also compared the observed associations with those expected under no or full acclimatization to the UHI. Results: The relative risk of death on hot versus normal days differed very little across UHI decile groups. A 1°C UHI anomaly multiplied the risk of heat death by 1.004 (95% CI: 0.950, 1.061) (interaction rate ratio) compared with the expected value of 1.070 (1.057, 1.082) if there were no acclimatization. The corresponding UHI interaction for cold was 1.020 (0.979, 1.063) versus 1.030 (1.026, 1.034) (actual versus expected under no acclimatization, respectively). Fitted splines for heat shifted little across UHI decile groups, again suggesting acclimatization. For cold, the splines shifted somewhat in the direction of no acclimatization, but did not exclude acclimatization. Conclusions: We have proposed two analytical methods for estimating the degree of acclimatization to the heat- and cold-related mortality burdens associated with UHIs. The results for London suggest relatively complete acclimatization to the UHI effect on summer heat–related mortality, but less clear evidence for cold–related mortality. Citation: Milojevic A, Armstrong BG, Gasparrini A, Bohnenstengel SI, Barratt B, Wilkinson P. 2016. Methods to estimate acclimatization to urban heat island effects on heat- and cold-related mortality. Environ Health Perspect 124:1016–1022; http://dx.doi.org/10.1289/ehp.1510109

Associations between exhaust and non-exhaust particulate matter and stroke incidence by stroke subtype in South London

BACKGROUND Airborne particulate matter (PM) consists of particles from diverse sources, including vehicle exhausts. Associations between short-term PM changes and stroke incidence have been shown. Cumulative exposures over several months, or years, are less well studied; few studies examined ischaemic subtypes or PM source. AIMS This study combines a high resolution urban air quality model with a population-based stroke register to explore associations between long-term exposure to PM and stroke incidence. METHOD Data from the South London Stroke Register from 2005-2012 were included. Poisson regression explored association between stroke incidence and long-term (averaged across the study period) exposure to PM2.5(PM<2.5μm diameter) and PM10(PM<10μm), nitric oxide, nitrogen dioxide, nitrogen oxides and ozone, at the output area level (average population=309). Estimates were standardised for age and sex and adjusted for socio-economic deprivation. Models were stratified for ischaemic and haemorrhagic strokes and further broken down by Oxford Community Stroke Project classification and Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification. RESULTS 1800 strokes were recorded (incidence=42.6/100,000 person-years). No associations were observed between PM and overall ischaemic or haemorrhagic incidence. For an interquartile range increase in PM2.5, there was a 23% increase in incidence (Incidence rate ratio=1.23 (95%CI: 1.03-1.44)) of total anterior circulation infarcts (TACI) and 20% increase for PM2.5 from exhausts (1.20(1.01-1.41)). There were similar associations with PM10, overall (1.21(1.01-1.44)) and from exhausts (1.20(1.01-1.41)). TACI incidence was not associated with non-exhaust sources. There were no associations with other stroke subtypes or pollutants. CONCLUSION Outdoor air pollution, particularly that arising from vehicle exhausts, may increase risk of TACI but not other stroke subtypes.

The human circulating miRNome reflects multiple organ disease risks in association with short-term exposure to traffic-related air pollution

Traffic-related air pollution is a complex mixture of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide (NO2). PM exposure contributes to the pathogenesis of many diseases including several types of cancer, as well as pulmonary, cardiovascular and neurodegenerative diseases. Also exposure to NO2 has been related to increased cardiovascular mortality. In search of an early diagnostic biomarker for improved air pollution-associated health risk assessment, recent human studies have shown that certain circulating miRNAs are altered upon exposure to traffic-related air pollutants. Here, we present for the first time a global analysis of the circulating miRNA genome in an experimental cross-over study of a human population exposed to traffic-related air pollution. By utilizing next-generation sequencing technology and detailed real-time exposure measurements we identified 54 circulating miRNAs to be dose- and pollutant species-dependently associated with PM10, PM2.5, black carbon, ultrafine particles and NO2 already after 2 h of exposure. Bioinformatics analysis suggests that these circulating miRNAs actually reflect the adverse consequences of traffic pollution-induced toxicity in target tissues including the lung, heart, kidney and brain. This study shows the strong potential of circulating miRNAs as novel biomarkers for environmental health risk assessment.

Effect of Exhaust- and Nonexhaust-Related Components of Particulate Matter on Long-Term Survival After Stroke

Background and Purpose— Outdoor air pollution represents a potentially modifiable risk factor for stroke. We examined the link between ambient pollution and mortality up to 5 years poststroke, especially for pollutants associated with vehicle exhaust. Methods— Data from the South London Stroke Register, a population-based register covering an urban, multiethnic population, were used. Hazard ratios (HR) for a 1 interquartile range increase in particulate matter <2.5 µm diameter (PM2.5) and PM <10 µm (PM10) were estimated poststroke using Cox regression, overall and broken down into exhaust and nonexhaust components. Analysis was stratified for ischemic and hemorrhagic strokes and was further broken down by Oxford Community Stroke Project classification. Results— The hazard of death associated with PM2.5 up to 5 years after stroke was significantly elevated (P=0.006) for all strokes (HR=1.28; 95% confidence interval [CI], 1.08–1.53) and ischemic strokes (HR, 1.32; 95% CI, 1.08–1.62). Within ischemic subtypes, PM2.5 pollution increased mortality risk for total anterior circulation infarcts by 2-fold (HR, 2.01; 95% CI, 1.17–3.48; P=0.012) and by 78% for lacunar infarcts (HR, 1.78; 95% CI, 1.18–2.66; P=0.006). PM10 pollution was associated with 45% increased mortality risk for lacunar infarct strokes (HR, 1.45; 95% CI, 1.06–2.00; P=0.022). Separating PM2.5 and PM10 into exhaust and nonexhaust components did not show increased mortality. Conclusions— Exposure to certain outdoor PM pollution, particularly PM2.5, increased mortality risk poststroke up to 5 years after the initial stroke.

Air pollution and the incidence of ischaemic and haemorrhagic stroke in the South London Stroke Register: a case–cross-over analysis

Background Few European studies investigating associations between short-term exposure to air pollution and incident stroke have considered stroke subtypes. Using information from the South London Stroke Register for 2005–2012, we investigated associations between daily concentrations of gaseous and particulate air pollutants and incident stroke subtypes in an ethnically diverse area of London, UK. Methods Modelled daily pollutant concentrations based on a combination of measurements and dispersion modelling were linked at postcode level to incident stroke events stratified by haemorrhagic and ischaemic subtypes. The data were analysed using a time-stratified case–cross-over approach. Conditional logistic regression models included natural cubic splines for daily mean temperature and daily mean relative humidity, a binary term for public holidays and a sine–cosine annual cycle. Of primary interest were same day mean concentrations of particulate matter <2.5 and <10 µm in diameter (PM2.5, PM10), ozone (O3), nitrogen dioxide (NO2) and NO2+nitrogen oxide (NOX). Results Our analysis was based on 1758 incident strokes (1311 were ischaemic and 256 were haemorrhagic). We found no evidence of an association between all stroke or ischaemic stroke and same day exposure to PM2.5, PM10, O3, NO2 or NOX. For haemorrhagic stroke, we found a negative association with PM10 suggestive of a 14.6% (95% CI 0.7% to 26.5%) fall in risk per 10 µg/m3 increase in pollutant. Conclusions Using data from the South London Stroke Register, we found no evidence of a positive association between outdoor air pollution and incident stroke or its subtypes. These results, though in contrast to recent meta-analyses, are not inconsistent with the mixed findings of other UK studies.

Linking e-health records, patient-reported symptoms and environmental exposure data to characterise and model COPD exacerbations: protocol for the COPE study

Introduction Relationships between exacerbations of chronic obstructive pulmonary disease (COPD) and environmental factors such as temperature, humidity and air pollution are not well characterised, due in part to oversimplification in the assignment of exposure estimates to individuals and populations. New developments in miniature environmental sensors mean that patients can now carry a personal air quality monitor for long periods of time as they go about their daily lives. This creates the potential for capturing a direct link between individual activities, environmental exposures and the health of patients with COPD. Direct associations then have the potential to be scaled up to population levels and tested using advanced human exposure models linked to electronic health records. Methods and analysis This study has 5 stages: (1) development and deployment of personal air monitors; (2) recruitment and monitoring of a cohort of 160 patients with COPD for up to 6 months with recruitment of participants through the Clinical Practice Research Datalink (CPRD); (3) statistical associations between personal exposure with COPD-related health outcomes; (4) validation of a time-activity exposure model and (5) development of a COPD prediction model for London. Ethics and dissemination The Research Ethics Committee for Camden and Islington has provided ethical approval for the conduct of the study. Approval has also been granted by National Health Service (NHS) Research and Development and the Independent Scientific Advisory Committee. The results of the study will be disseminated through appropriate conference presentations and peer-reviewed journals.