Imperial College London

ProfessorAnnaHansell

Faculty of MedicineSchool of Public Health

Visiting Professor
 
 
 
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a.hansell

 
 
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UG42Medical SchoolSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
to

194 results found

Douglas P, Freni-Sterrantino A, Leal Sanchez M, Ashworth DC, Ghosh RE, Fecht D, Font A, Blangiardo M, Gulliver J, Toledano MB, Elliott P, De Hoogh K, Fuller GW, Hansell ALet al., 2017, Estimating Particulate Exposure from Modern Municipal Waste Incinerators in Great Britain, Environmental science & technology, Vol: 51, Pages: 7511-7519, ISSN: 0013-936X

Municipal Waste Incineration (MWI) is regulated through the European Union Directive on Industrial Emissions (IED), but there is ongoing public concern regarding potential hazards to health. Using dispersion modeling, we estimated spatial variability in PM10 concentrations arising from MWIs at postcodes (average 12 households) within 10 km of MWIs in Great Britain (GB) in 2003-2010. We also investigated change points in PM10 emissions in relation to introduction of EU Waste Incineration Directive (EU-WID) (subsequently transposed into IED) and correlations of PM10 with SO2, NOx, heavy metals, polychlorinated dibenzo-p-dioxins/furan (PCDD/F), polycyclic aromatic hydrocarbon (PAH) and polychlorinated biphenyl (PCB) emissions. Yearly average modeled PM10 concentrations were 1.00 × 10-5 to 5.53 × 10-2 μg m-3, a small contribution to ambient background levels which were typically 6.59-2.68 × 101 μg m-3, 3-5 orders of magnitude higher. While low, concentration surfaces are likely to represent a spatial proxy of other relevant pollutants. There were statistically significant correlations between PM10 and heavy metal compounds (other heavy metals (r = 0.43, p = <0.001)), PAHs (r = 0.20, p = 0.050), and PCBs (r = 0.19, p = 0.022). No clear change points were detected following EU-WID implementation, possibly as incinerators were operating to EU-WID standards before the implementation date. Results will be used in an epidemiological analysis examining potential associations between MWIs and health outcomes.

Journal article

Cai Y, Hodgson S, Blangiardo M, Gulliver J, Morley D, Vienneau D, de Hoogh K, Key T, Hveem K, Elliott P, Hansell Aet al., 2017, Road traffic noise and incident cardiovascular disease: a joint analysis of HUNT, EPIC-Oxford and UK Biobank, ICBEN 2017 Proceedings

Aims: This study aimed to investigate the effects of long-term exposure to road traffic noise on incident CVD in three large cohorts: HUNT, EPIC-Oxford and UK Biobank. Methods: In a complete-case sample (N=361,699), 4,014 IHD and 2,109 cerebrovascular incident cases were ascertained between baseline (1993-2010) and end of follow-up (2008-2015) through medical record linkage. Annual mean road traffic noise exposure was modelled at baseline address. Individual-level covariate data were harmonised and data were pooled. Analyses used Cox proportional hazards model with adjustments for confounders, including air pollution. Results: For an interquartile range (IQR) (3.9 dBA) higher daytime noise, a non-significant association with incident IHD was seen (Hazard ratio (HR): 1.015, 95% Confidence Interval (CI): 0.989-1.042), fully adjusted. Statistically significant associations and interaction terms were seen in obese individuals (HR: 1.099, 95%CI: 1.029-1.174), and current-smokers (HR: 1.054, 95%CI: 1.007-1.103). No associations were found for ischemic or hemorrhagic stroke. Conclusions: Our study strengthens the evidence base for an effect of road traffic noise on incident IHD, whilst the association with incident stroke remains unclear.

Journal article

Hansell A, Cai Y, Gulliver J, 2017, Cardiovascular Health Effects of Road Traffic Noise, Environmental Impacts of Road Vehicles Past, Present and Future, Publisher: Issues in Environmental Scienc, ISBN: 9781782628927

This book is a comprehensive source of authoritative information for students studying pollution, and for policy-makers concerned with vehicle emissions and road traffic impacts more generally.

Book chapter

Dimakopoulou K, Koutentakis K, Papageorgiou I, Kasdagli M-I, Haralabidis AS, Sourtzi P, Samoli E, Houthuijs D, Swart W, Hansell AL, Katsouyanni Ket al., 2017, Is aircraft noise exposure associated with cardiovascular disease and hypertension? Results from a cohort study in Athens, Greece., Occupational and Environmental Medicine, Vol: 74, Pages: 830-837, ISSN: 1351-0711

BACKGROUND: We followed up, in 2013, the subjects who lived near the Athens International Airport and had participated in the cross-sectional multicountry HYENA study in 2004-2006. OBJECTIVE: To evaluate the association of exposure to aircraft and road traffic noise with the incidence of hypertension and other cardiovascular outcomes. METHODS: From the 780 individuals who participated in the cross-sectional study, 537 were still living in the same area and 420 accepted to participate in the follow-up. Aircraft and road traffic noise exposure was based on the estimations conducted in 2004-2006, linking geocoded residential addresses of the participants to noise levels. We applied multiple logistic regression and Cox proportional hazards models, adjusting for potential confounders. RESULTS: The incidence of hypertension was significantly associated with higher aircraft noise exposure during the night. Specifically, the OR for hypertension per 10 dB increase in Lnight aircraft noise exposure was 2.63 (95% CI 1.21 to 5.71). Doctor-diagnosed cardiac arrhythmia was significantly associated with Lnight aircraft noise exposure, when prevalent and incident cases were considered with an OR of 2.09 (95% CI 1.07 to 4.08). Stroke risk was also increased with increasing noise exposure but the association was not significant. Twenty-four-hour road traffic noise associations with the outcomes considered were weaker and less consistent. CONCLUSIONS: In conclusion, our cohort study suggests that long-term exposure to aircraft noise, particularly during the night, is associated with incident hypertension and possibly, also, cardiovascular effects.

Journal article

Cai Y, Hansell A, Blangiardo M, Burton P, de Hoogh K, Doiron D, Fortier I, Gulliver J, Hveem K, Mbatchou S, Morley D, Stolk R, Zijlema W, Elliott P, Hodgson Set al., 2017, Long-term exposure to road traffic noise, ambient air pollution and cardiovascular risk factors in the HUNT and Lifelines cohorts, European Heart Journal, Vol: 38, Pages: 2290-2296, ISSN: 1522-9645

AimsBlood biochemistry may provide information on associations between road traffic noise, air pollution, and cardiovascular disease risk. We evaluated this in two large European cohorts (HUNT3, Lifelines).Methods and resultsRoad traffic noise exposure was modelled for 2009 using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU). Annual ambient air pollution (PM10, NO2) at residence was estimated for 2007 using a Land Use Regression model. The statistical platform DataSHIELD was used to pool data from 144 082 participants aged ≥20 years to enable individual-level analysis. Generalized linear models were fitted to assess cross-sectional associations between pollutants and high-sensitivity C-reactive protein (hsCRP), blood lipids and for (Lifelines only) fasting blood glucose, for samples taken during recruitment in 2006–2013. Pooling both cohorts, an inter-quartile range (IQR) higher day-time noise (5.1 dB(A)) was associated with 1.1% [95% confidence interval (95% CI: 0.02–2.2%)] higher hsCRP, 0.7% (95% CI: 0.3–1.1%) higher triglycerides, and 0.5% (95% CI: 0.3–0.7%) higher high-density lipoprotein (HDL); only the association with HDL was robust to adjustment for air pollution. An IQR higher PM10 (2.0 µg/m3) or NO2 (7.4 µg/m3) was associated with higher triglycerides (1.9%, 95% CI: 1.5–2.4% and 2.2%, 95% CI: 1.6–2.7%), independent of adjustment for noise. Additionally for NO2, a significant association with hsCRP (1.9%, 95% CI: 0.5–3.3%) was seen. In Lifelines, an IQR higher noise (4.2 dB(A)) and PM10 (2.4 µg/m3) was associated with 0.2% (95% CI: 0.1–0.3%) and 0.6% (95% CI: 0.4–0.7%) higher fasting glucose respectively, with both remaining robust to adjustment for air/noise pollution.ConclusionLong-term exposures to road traffic noise and ambient air pollution were associated with blood biochemistry, providing a possible link b

Journal article

Cai Y, Hodgson S, Blangiardo M, De Hoogh K, Morley D, Gulliver J, Hveem K, Elliott P, Hansell Aet al., 2017, Ambient Air Pollution, Traffic Noise And Adult-Onset Asthma: The Hunt Study, Norway, International Conference of the American-Thoracic-Society (ATS), Publisher: American Thoracic Society, ISSN: 1073-449X

Conference paper

Basner M, Clark C, Hansell A, Hileman JI, Janssen S, Shepherd K, Sparrow Vet al., 2017, Aviation Noise Impacts: State of the Science, Noise and Health, Vol: 19, Pages: 41-50, ISSN: 1463-1741

Noise is defined as “unwanted sound.” Aircraft noise is one, if not the most detrimental environmental effect of aviation. It can cause community annoyance, disrupt sleep, adversely affect academic performance of children, and could increase the risk for cardiovascular disease of people living in the vicinity of airports. In some airports, noise constrains air traffic growth. This consensus paper was prepared by the Impacts of Science Group of the Committee for Aviation Environmental Protection of the International Civil Aviation Organization and summarizes the state of the science of noise effects research in the areas of noise measurement and prediction, community annoyance, children’s learning, sleep disturbance, and health. It also briefly discusses civilian supersonic aircraft as a future source of aviation noise.

Journal article

Wain LV, Shrine N, Artigas MS, Erzurumluoglu AM, Noyvert B, Bossini-Castillo L, Obeidat M, Henrys AP, Portelli MA, Hall RJ, Billington CK, Rimington TL, Fenech AG, John C, Blake T, Jackson VE, Allen RJ, Prins BP, Campbell A, Porteous DJ, Jarvelin M-R, Wielscher M, Jamess AL, Hui J, Wareham NJ, Zhao JH, Wilson JF, Joshi PK, Stubbe B, Rawal R, Schulz H, Imboden M, Probst-Hensch NM, Karrasch S, Gieger C, Deary IJ, Harris SE, Marten J, Rudan I, Enroth S, Gyllensten U, Kerr SM, Polasek O, Kahonen M, Surakka I, Vitart V, Hayward C, Lehtimaki T, Raitakari OT, Evans DM, Henderson AJ, Pennell CE, Wang CA, Sly PD, Wan ES, Busch R, Hobbs BD, Litonjua AA, Sparrow DW, Gulsvik A, Bakke PS, Crapo JD, Beaty TH, Hansel NN, Mathias RA, Ruczinski I, Barnes KC, Bosse Y, Joubert P, van den Berge M, Brandsma C-A, Pare PD, Sin DD, Nickle DC, Hao K, Gottesman O, Dewey FE, Bruse SE, Carey DJ, Kirchner HL, Jonsson S, Thorleifsson G, Jonsdottir I, Gislason T, Stefansson K, Schurmann C, Nadkarni G, Bottinger EP, Loos RJF, Walters RG, Chen Z, Millwood IY, Vaucher J, Kurmi OP, Li L, Hansell AL, Brightling C, Zeggini E, Cho MH, Silverman EK, Sayers I, Trynka G, Morris AP, Strachan DP, Halls IP, Tobin MDet al., 2017, Genome-wide association analyses for lung function and chronic obstructive pulmonary disease identify new loci and potential druggable targets, Nature Genetics, Vol: 49, Pages: 416-425, ISSN: 1061-4036

Chronic obstructive pulmonary disease (COPD) is characterized by reduced lung function and is the third leading cause of death globally. Through genome-wide association discovery in 48,943 individuals, selected from extremes of the lung function distribution in UK Biobank, and follow-up in 95,375 individuals, we increased the yield of independent signals for lung function from 54 to 97. A genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk score (~6 alleles) (95% confidence interval) = 1.24 (1.20–1.27), P = 5.05 × 10−49), and we observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest genetic risk score deciles in UK Biobank. The 97 signals show enrichment in genes for development, elastic fibers and epigenetic regulation pathways. We highlight targets for drugs and compounds in development for COPD and asthma (genes in the inositol phosphate metabolism pathway and CHRM3) and describe targets for potential drug repositioning from other clinical indications.

Journal article

Zijlema W, Cai Y, Doiron D, Mbatchou S, Fortier I, Gulliver J, de Hoogh K, Morley D, Hodgson S, Elliott P, Key T, Kongsgard H, Hveem K, Gaye A, Burton P, Hansell A, Stolk R, Rosmalen Jet al., 2017, Corrigendum to "Road traffic noise, blood pressure and heart rate: Pooled analyses of harmonized data from 88,336 participants" [Envrion. Res. 151 (2016) 804-813], Environmental Research, Vol: 152, Pages: 520-520, ISSN: 0013-9351

Journal article

Dehbi HM, Blangiardo M, Gulliver J, Fecht D, de Hoogh K, Al-Kanaani Z, Tillin T, Hardy R, Chaturvedi N, Hansell ALet al., 2016, Air pollution and cardiovascular mortality with over 25 years follow-up: A combined analysis of two British cohorts, Environment International, Vol: 99, Pages: 275-281, ISSN: 1873-6750

BACKGROUND: Adverse effects of air pollution on cardiovascular disease (CVD) mortality are well established. There are comparatively fewer studies in Europe, and in the UK particularly, than in North America. We examined associations in two British cohorts with >25years of follow-up. METHODS: Annual average NO2, SO2 and black smoke (BS) air pollution exposure estimates for 1991 were obtained from land use regression models using contemporaneous monitoring data. From the European Study of Cohorts and Air Pollution (ESCAPE), air pollution estimates in 2010-11 were obtained for NO2, NOx, PM10, PMcoarse and PM2.5. The exposure estimates were assigned to place of residence 1989 for participants in a national birth cohort born in 1946, the MRC National Study of Health and Development (NSHD), and an adult multi-ethnic London cohort, Southall and Brent Revisited (SABRE) recruited 1988-91. The combined median follow-up was 26years. Single-pollutant competing risk models were employed, adjusting for individual risk factors. RESULTS: Elevated non-significant hazard ratios for CVD mortality were seen with 1991 BS and SO2 and with ESCAPE PM10 and PM2.5 in fully adjusted linear models. Per 10μg/m(3) increase HRs were 1.11 [95% CI: 0.76-1.61] for BS, 1.05 [95% CI: 0.91-1.22] for SO2, 1.16 [95% CI: 0.70-1.92] for PM10 and 1.30 [95% CI: 0.39-4.34] for PM2.5, with largest effects seen in the fourth quartile of BS and PM2.5 compared to the first with HR 1.24 [95% CI: 0.91-1.61] and 1.21 [95% CI: 0.88-1.66] respectively. There were no consistent associations with other ESCAPE pollutants, or with 1991 NO2. Modelling using Cox regression led to similar results. CONCLUSION: Our results support a detrimental long-term effect for air pollutants on cardiovascular mortality.

Journal article

Cai Y, Zijlema WL, Doiron D, Blangiardo M, Burton PR, Fortier I, Gaye A, Gulliver J, de Hoogh K, Hveem K, Mbatchou S, Morley DW, Stolk RP, Elliott P, Hansell AL, Hodgson Set al., 2016, Ambient air pollution, traffic noise and adult asthma prevalence: a BioSHaRE approach, European Respiratory Journal, Vol: 49, ISSN: 0903-1936

We investigated the effects of both ambient air pollution and traffic noise on adult asthma prevalence, using harmonised data from three European cohort studies established in 2006–2013 (HUNT3, Lifelines and UK Biobank).Residential exposures to ambient air pollution (particulate matter with aerodynamic diameter <=10 µm (PM10) and nitrogen dioxide (NO2)) were estimated by a pan-European Land Use Regression model for 2007. Traffic noise for 2009 was modelled at home addresses by adapting a standardised noise assessment framework (CNOSSOS-EU). A cross-sectional analysis of 646 731 participants aged >=20 years was undertaken using DataSHIELD to pool data for individual-level analysis via a “compute to the data” approach. Multivariate logistic regression models were fitted to assess the effects of each exposure on lifetime and current asthma prevalence.PM10 or NO2 higher by 10 µg·m-3 was associated with 12.8% (95% CI 9.5–16.3%) and 1.9% (95% CI 1.1–2.8%) higher lifetime asthma prevalence, respectively, independent of confounders. Effects were larger in those aged >=50 years, ever-smokers and less educated. Noise exposure was not significantly associated with asthma prevalence.This study suggests that long-term ambient PM10 exposure is associated with asthma prevalence in western European adults. Traffic noise is not associated with asthma prevalence, but its potential to impact on asthma exacerbations needs further investigation.Long-term ambient PM10 exposure is associated with asthma prevalence in three European adult cohorts http://ow.ly/En4b3049S7X

Journal article

Bartington SE, Bakolis I, Devakumar D, Kurmi OP, Gulliver J, Chaube G, Manandhar DS, Saville NM, Costello A, Osrin D, Hansell AL, Ayres JGet al., 2016, Patterns of domestic exposure to carbon monoxide and particulate matter in households using biomass fuel in Janakpur, Nepal, Environmental Pollution, Vol: 220, Pages: 38-45, ISSN: 1873-6424

Household Air Pollution (HAP) from biomass cooking fuels is a major cause of morbidity and mortality in low-income settings worldwide. In Nepal the use of open stoves with solid biomass fuels is the primary method of domestic cooking. To assess patterns of domestic air pollution we performed continuous measurement of carbon monoxide (CO) and particulate Matter (PM2.5) in 12 biomass fuel households in Janakpur, Nepal. We measured kitchen PM2.5 and CO concentrations at one-minute intervals for an approximately 48-h period using the TSI DustTrak II 8530/SidePak AM510 (TSI Inc, St. Paul MN, USA) or EL-USB-CO data logger (Lascar Electronics, Erie PA, USA) respectively. We also obtained information regarding fuel, stove and kitchen characteristics and cooking activity patterns. Household cooking was performed in two daily sessions (median total duration 4 h) with diurnal variability in pollutant concentrations reflecting morning and evening cooking sessions and peak concentrations associated with fire-lighting. We observed a strong linear relationship between PM2.5 measurements obtained by co-located photometric and gravimetric monitoring devices, providing local calibration factors of 4.9 (DustTrak) and 2.7 (SidePak). Overall 48-h average CO and PM2.5 concentrations were 5.4 (SD 4.3) ppm (12 households) and 417.6 (SD 686.4) μg/m(3) (8 households), respectively, with higher average concentrations associated with cooking and heating activities. Overall average PM2.5 concentrations and peak 1-h CO concentrations exceeded WHO Indoor Air Quality Guidelines. Average hourly PM2.5 and CO concentrations were moderately correlated (r = 0.52), suggesting that CO has limited utility as a proxy measure for PM2.5 exposure assessment in this setting. Domestic indoor air quality levels associated with biomass fuel combustion in this region exceed WHO Indoor Air Quality standards and are in the hazardous range for human health.

Journal article

Zijlema W, Cai Y, Doiron D, Mbatchou S, Fortier I, Gulliver J, Hoogh KD, Morley D, Hodgson S, Elliott P, Key T, Kongsgard H, Hveem K, Gaye A, Burton P, Hansell A, Stolk R, Rosmalen Jet al., 2016, Road traffic noise, blood pressure and heart rate: Pooled analyses of harmonized data from 88,336 participants, Environmental Research, Vol: 151, Pages: 804-813, ISSN: 0013-9351

Introduction Exposure to road traffic noise may increase blood pressure and heart rate. It is unclear to what extent exposure to air pollution may influence this relationship. We investigated associations between noise, blood pressure and heart rate, with harmonized data from three European cohorts, while taking into account exposure to air pollution. Methods Road traffic noise exposure was assessed using a European noise model based on the Common Noise Assessment Methods in Europe framework (CNOSSOS-EU). Exposure to air pollution was estimated using a European-wide land use regression model. Blood pressure and heart rate were obtained by trained clinical professionals. Pooled cross-sectional analyses of harmonized data were conducted at the individual level and with random-effects meta-analyses. Results We analyzed data from 88,336 participants, across the three participating cohorts (mean age 47.0 (±13.9) years). Each 10 dB(A) increase in noise was associated with a 0.93 (95% CI 0.76;1.11) bpm increase in heart rate, but with a decrease in blood pressure of 0.01 (95% CI −0.24;0.23) mmHg for systolic and 0.38 (95% CI −0.53; −0.24) mmHg for diastolic blood pressure. Adjustments for PM10 or NO2 attenuated the associations, but remained significant for DBP and HR. Results for BP differed by cohort, with negative associations with noise in LifeLines, no significant associations in EPIC-Oxford, and positive associations with noise &gt;60 dB(A) in HUNT3. Conclusions Our study suggests that road traffic noise may be related to increased heart rate. No consistent evidence for a relation between noise and blood pressure was found.

Journal article

Douglas P, Tyrrel SF, Kinnersley RP, Whelan M, Longhurst PJ, Hansell AL, Walsh K, Pollard SJ, Drew GHet al., 2016, Predicting Aspergillus fumigatus exposure from composting facilities using a dispersion model: A conditional calibration and validation., International Journal of Hygiene and Environmental Health, Vol: 220, Pages: 17-28, ISSN: 1618-131X

Bioaerosols are released in elevated quantities from composting facilities and are associated with negative health effects, although dose-response relationships are unclear. Exposure levels are difficult to quantify as established sampling methods are costly, time-consuming and current data provide limited temporal and spatial information. Confidence in dispersion model outputs in this context would be advantageous to provide a more detailed exposure assessment. We present the calibration and validation of a recognised atmospheric dispersion model (ADMS) for bioaerosol exposure assessments. The model was calibrated by a trial and error optimisation of observed Aspergillus fumigatus concentrations at different locations around a composting site. Validation was performed using a second dataset of measured concentrations for a different site. The best fit between modelled and measured data was achieved when emissions were represented as a single area source, with a temperature of 29°C. Predicted bioaerosol concentrations were within an order of magnitude of measured values (1000-10,000CFU/m(3)) at the validation site, once minor adjustments were made to reflect local differences between the sites (r(2)>0.7 at 150, 300, 500 and 600m downwind of source). Results suggest that calibrated dispersion modelling can be applied to make reasonable predictions of bioaerosol exposures at multiple sites and may be used to inform site regulation and operational management.

Journal article

Hansell A, Ghosh R, Bakolis I, Strachan Det al., 2016, Geographical variation in the respiratory health of Great Britain, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Hansell A, Ghosh R, Blangiardo M, Perkins C, Vienneau D, Goffe K, Briggs D, Gulliver Jet al., 2016, Respiratory mortality risks in England and Wales associated with air pollution exposures up to 38 years previously, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Bakolis I, Kelly R, Fecht D, Best N, Millett C, Garwood K, Elliott P, Hansell A, Hodgson Set al., 2016, Protective Effects of Smoke-free Legislation on Birth Outcomes in England: A Regression Discontinuity Design, Epidemiology, Vol: 27, Pages: 810-818, ISSN: 1531-5487

Background: Environmental tobacco smoke has an adverse impact on preterm birth and birthweight. England introduced a new law to make virtually all enclosed public places andworkplaces smoke free on July 1 2007. We investigated the effect of smoke-free legislation onbirth outcomes in England using Hospital Episode Statistics (HES) maternity data.Methods: We used regression discontinuity, a quasi-experimental study design, which canfacilitate valid causal inference, to analyse short-term effects of smoke-free legislation on birthweight, low birth weight, gestational age, preterm birth and small for gestational age.Results: We analysed 1,800,906 pregnancies resulting in singleton live-births in Englandbetween January 1 2005 and December 31 2009. In the one to five months following theintroduction of the smoking-free legislation, for those entering their third trimester, the risk oflow birth weight decreased by between 8% (95% CI: 4%-12%) and 14% (95% CI: 5%-23%),very low birth weight between 28% (95% CI: 19%-36%) and 32% (95% CI: 21%-41%), pretermbirth between 4% (95% CI: 1%-8%) and 9% (95% CI: 2%-16%), and small for gestational agebetween 5% (95% CI: 2%-8%) and 9% (95% CI: 2%-15%). The impact of the smoke-freelegislation varied by maternal age, deprivation, ethnicity and region.Conclusions: The introduction of smoke-free legislation in England had an immediate beneficialimpact on birth outcomes overall, although this benefit was not observed across all age, ethnic, ordeprivation groups.

Journal article

Boulieri A, Blangiardo MB, Hansell AH, 2016, Investigating trends in asthma and COPD through multiple data sources: a small area study, Spatial and Spatio-temporal Epidemiology, Vol: 19, Pages: 28-36, ISSN: 1877-5853

This paper investigates trends in asthma and COPD by using multiple datasources to help understanding the relationships between disease prevalence, morbidityand mortality. GP drug prescriptions, hospital admissions, and deaths are analysedat clinical commissioning group (CCG) level in England from August 2010 to March2011. A Bayesian hierarchical model is used for the analysis, which takes into accountthe complex space and time dependencies of asthma and COPD, while it is alsoable to detect unusual areas. Main findings show important discrepancies across thedifferent data sources, reflecting the different groups of patients that are represented.In addition, the detection mechanism that is provided by the model, together withinference on the spatial, and temporal variation, provide a better picture of therespiratory health problem.

Journal article

Majeed F, Hansell A, Saxena S, Millett C, Ward H, Harris M, Hayhoe B, Car J, Easton G, Donnelly CA, Perneczky R, Jarvelin MR, Ezzati M, Rawaf S, Vineis P, Ferguson N, Riboli Eet al., 2016, How would a decision to leave the European Union affect medical research and health in the United Kingdom?, Journal of the Royal Society of Medicine, Vol: 109, Pages: 216-218, ISSN: 1758-1095

Journal article

Bovenberg JA, de Hoogh K, Knoppers BM, Hveem K, Hansell ALet al., 2016, Don't Take It Personal: European Union Legal Aspects of Procuring and Protecting Environmental Exposure Data in Population Biobanks Through the Use of a Geo-Information-Systems Toolkit, Biopreservation and Biobanking, Vol: 14, Pages: 217-223, ISSN: 1947-5543

Journal article

Gulliver J, de Hoogh K, Hoek G, Vienneau D, Fecht D, Hansell Aet al., 2016, Back-extrapolated and year-specific NO2 land use regression models for Great Britain - Do they yield different exposure assessment?, Environment International, Vol: 92-93, Pages: 202-209, ISSN: 1873-6750

Robust methods to estimate historic population air pollution exposures are important tools for epidemiological studies evaluating long-term health effects. We developed land use regression (LUR) models for NO2 exposure in Great Britain for 1991 and explored whether the choice of year-specific or back-extrapolated LUR yields 1) similar LUR variables and model performance, and 2) similar national and regional address-level and small-area concentrations. We constructed two LUR models for 1991using NO2 concentrations from the diffusion tube monitoring network, one using 75% of all available measurement sites (that over-represent industrial areas), and the other using 75% of a subset of sites proportionate to population by region to study the effects of monitoring site selection bias. We compared, using the remaining (hold-out) 25% of monitoring sites, the performance of the two 1991 models with back-extrapolation of a previously published 2009 model, developed using NO2 concentrations from automatic chemiluminescence monitoring sites and predictor variables from 2006/2007. The 2009 model was back-extrapolated to 1991 using the same predictors (1990 & 1995) used to develop 1991 models. The 1991 models included industrial land use variables, not present for 2009. The hold-out performance of 1991 models (mean-squared-error-based-R2: 0.62–0.64) was up to 8% higher and ~ 1 μg/m3 lower in root mean squared error than the back-extrapolated 2009 model, with best performance from the subset of sites representing population exposures. Year-specific and back-extrapolated exposures for residential addresses (n = 1.338,399) and small areas (n = 10.518) were very highly linearly correlated for Great Britain (r > 0.83). This study suggests that year-specific model for 1991 and back-extrapolation of the 2009 LUR yield similar exposure assessment.

Journal article

Douglas P, Bakolis I, Fecht D, Pearson C, Leal Sanchez M, Kinnersley R, de Hoogh K, Hansell Aet al., 2016, Respiratory hospital admission risk near large composting facilities, International Journal of Hygiene and Environmental Health, Vol: 219, Pages: 372-379, ISSN: 1618-131X

BackgroundLarge-scale composting can release bioaerosols in elevated quantities, but there are few studies of health effects on nearby communitiesMethodsA cross-sectional ecological small area design was used to examine risk of respiratory hospital admissions within 2500 m of all 148 English large-scale composting facilities in 2008–10. Statistical analyses used a random intercept Poisson regression model at Census Output Area (COA) level (mean population 310). Models were adjusted for age, sex, deprivation and tobacco sales.ResultsAnalysing 34,963 respiratory hospital admissions in 4656COAs within 250–2500 m of a site, there were no significant trends using pre-defined distance bands of >250m-750m, >750–1500 m and >1500-2500m. Using a continuous measure of distance, there was a small non-statistically significant (p = 0.054) association with total respiratory admissions corresponding to a 1.5% (95% CI: 0.0–2.9%) decrease in risk if moving from 251 m to 501m. There were no significant associations for subgroups of respiratory infections, asthma or chronic obstructive pulmonary disease.ConclusionThis national study does not provide evidence for increased risks of respiratory hospital admissions in those living beyond 250 m of an outdoor composting area perimeter. Further work using better measures of exposure and exploring associations with symptoms and disease prevalence, especially in vulnerable groups, is recommended to support regulatory approaches.

Journal article

Fecht D, Fortunato L, Morley D, Hansell A, Gulliver Jet al., 2016, Associations between urban metrics and mortality rates in England, Environmental Health, Vol: 15, ISSN: 1832-3367

BackgroundSeventy-five percent of the population in Europe live in urban areas and analysing the effectsof urban form on the health of the urban population is of great public health interest. Notmuch is known, however, on the effects of urban form on the health of city dwellers. Thisstudy uses a novel approach to investigate whether associations exist between differentmeasures of urban form and mortality risks in cities in England.MethodsWe conducted an ecological, cross-sectional study for urban areas in England with more than100,000 residents (n = 50) and included all registered premature deaths (<65 years) between1st January 2002 and 31th December 2009. To describe and categorise urban form wequantified the distribution and density of population, land cover and transport networks andmeasures of geographical characteristics. We used Poisson regression models to examineassociations between the measures of urban form and age-standardised risks of deaths fromall causes, cardiovascular disease, and traffic accidents after adjustment for socioeconomicstatus and smoking. Analysis was stratified by gender to explore differential associationsbetween females and males.ResultsThere were a total of 200,200 premature deaths during the study period (Females: 37%;Males: 63%). Transport network patterns were associated with overall and cardiovascularmortality rates in cities. We saw 12% higher mortality risk after adjustment in cities with highjunction density compared to cities with low density [Females: RR 1.12 (95% CI 1.10 –1.15); Males: RR 1.12 (95% CI 1.10 -1.14)]; the risk was slightly higher for cardiovascularmortality [Females: RR 1.16 (95% CI 1.10 – 1.22); Males: RR 1.12 (95% CI 1.09 – 1.16)].Associations between mortality and population patterns were of similar magnitude [Females: 3RR 1.10 (95% CI 1.09 – 1.13); Males: RR 1.09 (95% CI 1.07 -1.10)]; associations betweenmortality and land cover patterns were inconclusive.ConclusionsWe found an a

Journal article

Fecht D, Hansell A, Morley D, Dajnak D, Vienneau D, Beevers S, Toledano M, Kelly F, Anderson HR, Gulliver Jet al., 2016, Spatial and temporal associations of road traffic noise and air pollution in London: Implications for epidemiological studies, Environment International, Vol: 88, Pages: 235-242, ISSN: 0160-4120

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,24 h, Lden, LAeq,16 h, 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 ≤ 2.5 μm and ≤ 10 μm. 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), 1 km grid squares, air pollution tertiles, 50 m, 100 m and 200 m 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 1 km 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, sugges

Journal article

Hansell A, Ghosh RE, Blangiardo M, Perkins C, Vienneau D, Goffe K, Briggs D, Gulliver Jet al., 2016, Historic air pollution exposure and long-term mortality risks in England and Wales: prospective longitudinal cohort study, Thorax, Vol: 71, Pages: 330-338, ISSN: 1468-3296

Introduction Long-term air pollution exposure contributes to mortality but there are few studies examining effects of very long-term (>25 years) exposures.Methods This study investigated modelled air pollution concentrations at residence for 1971, 1981, 1991 (black smoke (BS) and SO2) and 2001 (PM10) in relation to mortality up to 2009 in 367 658 members of the longitudinal survey, a 1% sample of the English Census. Outcomes were all-cause (excluding accidents), cardiovascular (CV) and respiratory mortality.Results BS and SO2 exposures remained associated with mortality decades after exposure—BS exposure in 1971 was significantly associated with all-cause (OR 1.02 (95% CI 1.01 to 1.04)) and respiratory (OR 1.05 (95% CI 1.01 to 1.09)) mortality in 2002–2009 (ORs expressed per 10 μg/m3). Largest effect sizes were seen for more recent exposures and for respiratory disease. PM10 exposure in 2001 was associated with all outcomes in 2002–2009 with stronger associations for respiratory (OR 1.22 (95% CI 1.04 to 1.44)) than CV mortality (OR 1.12 (95% CI 1.01 to 1.25)). Adjusting PM10 for past BS and SO2 exposures in 1971, 1981 and 1991 reduced the all-cause OR to 1.16 (95% CI 1.07 to 1.26) while CV and respiratory associations lost significance, suggesting confounding by past air pollution exposure, but there was no evidence for effect modification. Limitations include limited information on confounding by smoking and exposure misclassification of historic exposures.Conclusions This large national study suggests that air pollution exposure has long-term effects on mortality that persist decades after exposure, and that historic air pollution exposures influence current estimates of associations between air pollution and mortality.

Journal article

Ghosh RE, Ashworth DC, Hansell AL, Garwood K, Elliott P, Toledano MBet al., 2016, Routinely collected English birth data sets: comparisons and recommendations for reproductive epidemiology., Archives of Disease in Childhood: Fetal and Neonatal edition, Vol: 101, Pages: F451-F457, ISSN: 1359-2998

BACKGROUND: In England there are four national routinely collected data sets on births: Office for National Statistics (ONS) births based on birth registrations; Hospital Episode Statistics (HES) deliveries (mothers' information); HES births (babies' information); and NHS Numbers for Babies (NN4B) based on ONS births plus gestational age and ethnicity information. This study describes and compares these data, with the aim of recommending the most appropriate data set(s) for use in epidemiological research and surveillance. METHODS: We assessed the completeness and quality of the data sets in relation to use in epidemiological research and surveillance and produced detailed descriptive statistics on common reproductive outcomes for each data set including temporal and spatial trends. RESULTS: ONS births is a high quality complete data set but lacks interpretive and clinical information. HES deliveries showed good agreement with ONS births but HES births showed larger amounts of missing or unavailable data. Both HES data sets had improved quality from 2003 onwards, but showed some local spatial variability. NN4B showed excellent agreement with ONS and HES deliveries for the years available (2006-2010). Annual number of births increased by 17.6% comparing 2002 with 2010 (ONS births). Approximately 6% of births were of low birth weight (2.6% term low birth weight) and 0.5% were stillbirths. CONCLUSIONS: Routinely collected data on births provide a valuable resource for researchers. ONS and NN4B offer the most complete and accurate record of births. Where more detailed clinical information is required, HES deliveries offers a high quality data set that captures the majority of English births.

Journal article

Cai TY, Sullivan TR, Ayer JG, Harmer JA, Leeder SR, Toelle BG, Marks GB, Celermajer DS, Skilton MRet al., 2016, Carotid extramedial thickness is associated with local arterial stiffness in children, JOURNAL OF HYPERTENSION, Vol: 34, Pages: 109-115, ISSN: 0263-6352

Journal article

Artigas MS, Wain LV, Miller S, Kheirallah AK, Huffman JE, Ntalla I, Shrine N, Obeidat M, Trochet H, McArdle WL, Alves AC, Hui J, Zhao JH, Joshi PK, Teumer A, Albrecht E, Imboden M, Rawal R, Lopez LM, Marten J, Enroth S, Surakka I, Polasek O, Lyytikainen L-P, Granell R, Hysi PG, Flexeder C, Mahajan A, Beilby J, Bosse Y, Brandsma C-A, Campbell H, Gieger C, Glaeser S, Gonzalez JR, Grallert H, Hammond CJ, Harris SE, Hartikainen A-L, Heliovaara M, Henderson J, Hocking L, Horikoshi M, Hutri-Kahonen N, Ingelsson E, Johansson A, Kemp JP, Kolcic I, Kumar A, Lind L, Melen E, Musk AW, Navarro P, Nickle DC, Padmanabhan S, Raitakari OT, Ried JS, Ripatti S, Schulz H, Scott RA, Sin DD, Starr JM, Vinuela A, Voelzke H, Wild SH, Wright AF, Zemunik T, Jarvis DL, Spector TD, Evans DM, Lehtimaki T, Vitart V, Kahonen M, Gyllensten U, Rudan I, Deary IJ, Karrasch S, Probst-Hensch NM, Heinrich J, Stubbe B, Wilson JF, Wareham NJ, James AL, Morris AP, Jarvelin M-R, Hayward C, Sayers I, Strachan DP, Hall IP, Tobin MD, Deloukas P, Hansell AL, Hubbard R, Jackson VE, Marchini J, Pavord I, Thomson NC, Zeggini Eet al., 2015, Sixteen new lung function signals identified through 1000 Genomes Project reference panel imputation, Nature Communications, Vol: 6, ISSN: 2041-1723

Lung function measures are used in the diagnosis of chronic obstructive pulmonary disease. In 38,199 European ancestry individuals, we studied genome-wide association of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC with 1000 Genomes Project (phase 1)-imputed genotypes and followed up top associations in 54,550 Europeans. We identify 14 novel loci (P<5 × 10−8) in or near ENSA, RNU5F-1, KCNS3, AK097794, ASTN2, LHX3, CCDC91, TBX3, TRIP11, RIN3, TEKT5, LTBP4, MN1 and AP1S2, and two novel signals at known loci NPNT and GPR126, providing a basis for new understanding of the genetic determinants of these traits and pulmonary diseases in which they are altered.

Journal article

Marcon A, de Hoogh K, Gulliver J, Beelen R, Hansell ALet al., 2015, Development and transferability of a nitrogen dioxide land use regression model within the Veneto region of Italy, Atmospheric Environment, Vol: 122, Pages: 696-704, ISSN: 1873-2844

When measurements or other exposure models are unavailable, air pollution concentrations could be estimated by transferring land-use regression (LUR) models from other areas. No studies have looked at transferability of LUR models from regions to cities. We investigated model transferability issues. We developed a LUR model for 2010 using annual average nitrogen dioxide (NO2) concentrations retrieved from 47 regulatory stations of the Veneto region, Northern Italy. We applied this model to 40 independent sites in Verona, a city inside the region, where NO2 had been monitored in the European Study of Cohorts for Air Pollution Effects (ESCAPE) during 2010. We also used this model to estimate average NO2 concentrations at the regulatory network in 2008, 2009 and 2011. Of 33 predictor variables offered, five were retained in the LUR model (R2 = 0.75). The number of buildings in 5000 m buffers, industry surface area in 1000 m buffers and altitude, mainly representing large-scale air pollution dispersion patterns, explained most of the spatial variability in NO2 concentrations (R2 = 0.68), while two local traffic proxy indicators explained little of the variability (R2 = 0.07). The performance of this model transferred to urban sites was poor overall (R2 = 0.18), but it improved when only predicting inner-city background concentrations (R2 = 0.52). Recalibration of LUR coefficients improved model performance when predicting NO2 concentrations at the regulatory sites in 2008, 2009 and 2011 (R2 between 0.67 and 0.80). Models developed for a region using NO2 regulatory data are unable to capture small-scale variability in NO2 concentrations in urban traffic areas. Our study documents limitations in transferring a regional model to a city, even if it is nested within that region.

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