Imperial College London

DR YUTONG SAMUEL CAI

Faculty of MedicineSchool of Public Health

Honorary Research Fellow
 
 
 
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yutong.cai

 
 
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155Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

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22 results found

Doiron D, de Hoogh K, Probst-Hensch N, Fortier I, Cai Y, De Matteis S, Hansell Aet al., Air pollution, lung function and COPD: results from the population-based UK Biobank study, European Respiratory Journal, ISSN: 0903-1936

Ambient air pollution increases the risk of respiratory mortality but evidence for impacts on lung function and chronic obstructive pulmonary disease (COPD)is less well established. The aim was toevaluatewhether ambient air pollution isassociated with lung function andCOPD, and explore potential vulnerability factors. We used UK Biobank data on 303,887 individuals aged 40-69 years, with complete covariate data and valid lung function measures. Cross-sectional analysesexamined associations ofLand Use Regression-based estimates ofparticulate matter (PM2.5, PM1035and PMcoarse) and nitrogen dioxide (NO2) concentrations withforced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), the FEV1/FVC ratio, and COPD (FEV1/FVC 37< lower limit of normal). Effect modificationwas investigated for sex, age, obesity, smoking status, household income, asthma status, and occupations previously linked to COPD.40Higher exposures to each pollutant weresignificantly associated with lower lung function. A 5 μg/m3increase in PM2.5concentrationwas associated with lower FEV1(-83.13 mL [95%CI: -92.50, -73.75]) and FVC (-62.62 mL [95%CI:-73.91, -51.32]). COPD prevalence was associated with higher concentrations of PM2.5 (OR 1.52 [95%CI: 1.,1.62], per 5 μg/m3),PM10 (OR 1.08 [95%CI: 1.00,1.16], per 5 μg/m3), andNO2(OR 1.12 [95%CI: 1.10, 1.14], per 10 μg/m3), but not with PMcoarse.Stronger lung functionassociations were 46seenfor males, individuals from lower income households,and ‘at-risk’ occupations, and higher COPD associations for obese, lower income,and non-asthmatic participants. Ambient air pollution wasassociated with lowerlung function and increased COPD prevalencein this large study.

Journal article

Cai Y, Liang L, Barratt B, Kelly F, Hansell A, Tong Z, Lyu B, Chan Q, Xie W, Zhang Det al., Associations between daily air quality and hospitalisations for acute exacerbation of chronic obstructive pulmonary disease in Beijing, 2013-2017, Lancet Planetary Health, ISSN: 2542-5196

Background: Air pollution in Beijing hasbeen improving throughimplementation of the Air Pollution Prevention and Control Action Plan(2013-2017)but the implication for respiratory morbidity hasnot been directly investigated.Methods: Daily city-wide average concentrations of PM10, PM2·5, PMcoarse, NO2, SO2, CO and O3 in 2013-17 were averaged from 35 monitoring stationsacross the city.A generalized additive Poisson time-series model was applied to estimate the relative riskwith 95% confidence interval (CI) on hospitalisationsratesfor acute exacerbation of chronic obstructive pulmonary disease (AECOPD) in Beijing.Findings: During 18/January/2013-31/December/2017, 161,613 AECOPD hospitalisationswere recorded.Ambient concentrations of SO2and PM2·5 decreased by 68% and 33% over this five-year period.Relative risk for AECOPD hospitalisation was1·029 (95%CI: 1·023-1·035), 1·028(95%CI:1·021-1·034), 1·018(95%CI:1·013-1·022), 1·036(95%CI:1·028-1·044), 1·019(95%CI:1·013-1·024), 1·024(95%CI:1·018-1·029) and 1·027(95%CI:1·010-1·044) forsame day PM10,PM2·5, PMcoarse, NO2, SO2,COand O3 (warm season) respectivelyper interquartile rangeincrement.Femalesor patients aged ≥65 years were more susceptible.In 2013, there were 12,679 AECOPD casesadvanced by PM2·5pollution over expected rates if daily levels had not exceeded the World Health Organisationtarget, whereas in 2017 the respective figure was 7,377 cases.Interpretation: Increased acuteair pollution episodesweresignificantly associated with increasedhospitalisations for AECOPDin Beijingdespite improvement in overall air quality.Our findings however highlight the importance and effectiveness of stringent air pollution control policieson reducing COPD morbidity and provide rationale

Journal article

Cai Y, Hansell A, Hodgson S, Elliott P, Fecht D, Gulliver J, Key T, de Hoogh K, Hveem K, Morley D, Vienneau D, Blangiardo Met al., Road traffic noise, air pollution and incident cardiovascular disease: a joint analysis of the HUNT, EPIC-Oxford and UK Biobank cohorts, Environment International, ISSN: 0160-4120

Background: This study aimed to investigate the effects of long-term exposure to road traffic noiseand air pollutionon incident cardiovascular disease (CVD)in three large cohorts: HUNT, EPIC-Oxford and UK Biobank. Methods: In pooled complete-casesample of the three cohorts from Norway and the United Kingdom(N=355,732), 21,081 incident all CVD cases including 5,259ischemic heart disease (IHD)and 2,871cerebrovascular cases were ascertained between baseline (1993-2010)and end of follow-up (2008-2013)through medical recordlinkage. Annual mean 24-hour weighted road traffic noise(Lden) and air pollution (particulate matter with aerodynamic diameter ≤10 μm [PM10],≤2.5 μm [PM2.5]andnitrogen 39dioxide[NO2])exposure at baseline address was modelled using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU)and European-wide Land Use Regression models.Individual-level covariate data were harmonised and physically pooled across the three cohorts. Analysis was via Cox proportional hazard model with mutual adjustmentsforboth noise and air pollution andpotential confounders. Results: No significant associations were found between annual mean Ldenand incidentCVD,IHD or cerebrovascular disease in the overall populationexcept that the association withincident IHD was significantamong current-smokers.In the fully adjusted models including adjustmentfor Lden, an interquartile range (IQR) higher PM10(4.1μg/m3) or PM2.5(1.4μg/m3) was associated witha5.8% (95%CI: 2.5%-9.3%) and 3.7% (95%CI: 0.2%-7.4%) higherrisk for all incident CVD respectively. No significant associations were found between NO2and any of the CVD outcomes. Conclusions: We found suggestive evidence of a possible association between road traffic noise and incident IHD, consistent with current literature. Long-term particulate air pollution exposure, even at concentrations below current European air quality standards, w

Journal article

Gulliver J, Elliott P, Hansell A, Cai Y, McCrea A, Garwood K, Fecht D, Briggs Det al., 2018, Local- and regional-scale air pollution modelling (PM10) and exposure assessment for pregnancy trimesters, infancy, and childhood to age 15 years: Avon Longitudinal Study of Parents And Children (ALSPAC)., Environment International, Vol: 113, Pages: 10-19, ISSN: 0160-4120

We established air pollution modelling to study particle (PM10) exposures during pregnancy and infancy (1990–1993) through childhood and adolescence up to age ~15 years (1991–2008) for the Avon Longitudinal Study of Parents And Children (ALSPAC) birth cohort. For pregnancy trimesters and infancy (birth to 6 months; 7 to 12 months) we used local (ADMS-Urban) and regional/long-range (NAME-III) air pollution models, with a model constant for local, non-anthropogenic sources. For longer exposure periods (annually and the average of birth to age ~8 and to age ~15 years to coincide with relevant follow-up clinics) we assessed spatial contrasts in local sources of PM10 with a yearly-varying concentration for all background sources. We modelled PM10 (μg/m3) for 36,986 address locations over 19 years and then accounted for changes in address in calculating exposures for different periods: trimesters/infancy (n = 11,929); each year of life to age ~15 (n = 10,383). Intra-subject exposure contrasts were largest between pregnancy trimesters (5th to 95th centile: 24.4–37.3 μg/m3) and mostly related to temporal variability in regional/long-range PM10. PM10 exposures fell on average by 11.6 μg/m3 from first year of life (mean concentration = 31.2 μg/m3) to age ~15 (mean = 19.6 μg/m3), and 5.4 μg/m3 between follow-up clinics (age ~8 to age ~15). Spatial contrasts in 8-year average PM10 exposures (5th to 95th centile) were relatively low: 25.4–30.0 μg/m3 to age ~8 years and 20.7–23.9 μg/m3 from age ~8 to age ~15 years. The contribution of local sources to total PM10 was 18.5%–19.5% during pregnancy and infancy, and 14.4%–17.0% for periods leading up to follow-up clinics. Main roads within the study area contributed on average ~3.0% to total PM10 exposures in all periods; 9.5% of address locations were within 50 m of a main road. Exposure estimates will be used in a number of planned epidemiological studies.

Journal article

Doiron D, de Hoogh K, Probst-Hensch N, Mbatchou S, Eeftens M, Cai Y, Schindler C, Fortier I, Hodgson S, Gaye A, Stolk R, Hansell Aet al., 2017, Residential Air Pollution and Associations with Wheeze and Shortness of Breath in Adults: A Combined Analysis of Cross-Sectional Data from Two Large European Cohorts., Environmental Health Perspectives, Vol: 125, ISSN: 0091-6765

BACKGROUND: Research examining associations between air pollution exposure and respiratory symptoms in adults has generally been inconclusive. This may be related in part to sample size issues, which also preclude analysis in potentially vulnerable subgroups. OBJECTIVES: We estimated associations between air pollution exposures and the prevalence of wheeze and shortness of breath using harmonized baseline data from two very large European cohorts, Lifelines (2006-2013) and UK Biobank (2006-2010). Our aim was also to determine whether the relationship between air pollution and respiratory symptom prevalence differed between individuals with different characteristics. METHODS: Cross-sectional analyses explored associations between prevalence of self-reported wheeze and shortness of breath and annual mean particulate matter with aerodynamic diameter <2.5μm, 2.5-10μm, and <10μm (PM2.5, PMcoarse, and PM10, respectively) and nitrogen dioxide (NO2) concentrations at place of residence using logistic regression. Subgroup analyses and tests for interaction were performed for age, sex, smoking status, household income, obesity status, and asthma status. RESULTS: All PM exposures were associated with respiratory symptoms based on single-pollutant models, with the largest associations seen for PM2.5 with prevalence of wheezing {odds ratio (OR)=1.16 per 5μg/m³ [95% confidence interval (CI): 1.11, 1.21]} and shortness of breath [OR=1.61 per 5μg/m³ (95% CI: 1.45, 1.78)]. The association between shortness of breath and a 5-μg/m³ increment in PM2.5 was significantly higher for individuals from lower-[OR=1.73 (95% CI: 1.52, 1.97)] versus higher-income households [OR=1.31 (95% CI: 1.11, 1.55); p-interaction=0.005), whereas the association between PM2.5 and wheeze was limited to lower-income participants [OR=1.30 (95% CI: 1.22, 1.38) vs. OR=1.02; (95% CI: 0.96, 1.08); p-interaction<0.001]. Exposure to NO2 also showed positive associations with

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

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

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

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

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

Cai Y, Shaheen SO, Hardy R, Kuh D, Hansell ALet al., 2015, Birth weight, early childhood growth and lung function in middle to early old age: 1946 British birth cohort, Thorax, Vol: 71, Pages: 916-922, ISSN: 1468-3296

Background Findings from previous studies investigating the relationship between birth weight and adult lung function have been inconsistent, and data on birth weight and adult lung function decline are lacking. Few studies have investigated the relation between early childhood growth and adult lung function.Methods FEV1 and FVC were measured at ages 43 years, 53 years and 60–64 years in the 1946 British birth cohort study. Multiple linear regression models were fitted to study associations with birth weight and weight gain at age 0–2 years. Multilevel models assessed how associations changed with age, with FEV1 and FVC as repeated outcomes.Results 3276 and 3249 participants were included in FEV1 and FVC analyses, respectively. In women, there was a decreasing association between birth weight and FVC with age. From the multilevel model, for every 1 kg higher birth weight, FVC was higher on average by 66.3 mL (95% CI 0.5 to 132) at 43 years, but significance was lost at 53 years and 60–64 years. Similar associations were seen with FEV1, but linear change (decline) from age 43 years lost statistical significance after full adjustment. In men, associations with birth weight were null in multilevel models. Higher early life weight gain was associated with higher FEV1 at age 43 years in men and women combined but not in each sex.Conclusions Birth weight is positively associated with adult lung function in middle age, particularly in women, but the association diminishes with age, potentially due to accumulating environmental influences over the life course.

Journal article

Jacquemin B, Siroux V, Sanchez M, Carsin AE, Schikowski T, Adam M, Bellisario V, Buschka A, Bono R, Brunekreef B, Cai Y, Cirach M, Clavel-Chapelon F, Declercq C, Marco RD, Nazelle AD, Ducret-Stich RE, Ferretti VV, Gerbase MW, Hardy R, Heinrich J, Janson C, Jarvis D, Kanaani ZA, Keidel D, Kuh D, Moual NL, Nieuwenhuijsen MJ, Marcon A, Modig L, Pin I, Rochat T, Schindler C, Sugiri D, Stempfelet M, Temam S, Tsai MY, Varraso R, Vienneau D, Vierkotter A, Hansell AL, Kramer U, Probst-Hensch NM, Sunyer J, Kunzli N, Kauffmann Fet al., 2015, Ambient Air Pollution and Adult Asthma Incidence in Six European Cohorts (ESCAPE), Environmental Health Perspectives, Vol: 123, Pages: 613-621, ISSN: 1552-9924

BACKGROUND: Short-term exposure to air pollution has adverse effects among patients with asthma, whether long-term exposure to air pollution is a cause of adult-onset asthma is unclear. OBJECTIVE: To investigate the association between air pollution and adult onset asthma. METHODS: Asthma incidence was prospectively assessed in six European cohorts. Exposures studied were annual average concentrations at home addresses for nitrogen oxides assessed for 23,704 participants (including 1,257 incident cases) and particulate matter assessed for 17,909 participants through ESCAPE land-use regression models, and traffic exposure indicators. Meta-analyses of cohort-specific logistic regression on asthma incidence were performed. Models were adjusted on age, sex, overweight, education and smoking and included city/area within each cohort as a random effect. RESULTS: In this longitudinal analysis, asthma incidence was positively, but not significantly, associated with all exposure metrics, except for PMcoarse. Positive associations of borderline significance were observed for NO2, (adjusted OR = 1.10; 95% CI: 0.99, 1.21 per 10 mug/m3; p=0.10) and NOx (1.04; 95% CI: 0.99, 1.08 per 20 mug/m3; p=0.08). Non-significant positive associations were estimated for PM10 (1.04; 95% CI: 0.88, 1.23 per 10 mug/m3), PM2.5 (1.04; 95% CI: 0.88, 1.23 per 5 mug/m3), PM2.5absorbance (1.06; 95% CI: 0.95, 1.19 per 10-5/m), traffic load (1.10; 95% CI: 0.93, 1.30 per four million vehicles x m/day on major roads in a 100m buffer) and traffic intensity (1.10; 95% CI: 0.93, 1.30 per 5,000 vehicles/day on the nearest road). A non-significant negative association was estimated for PMcoarse (0.98; 95% CI: 0.87, 1.14 per 5 mug/m3). CONCLUSIONS: Results are suggestive of a deleterious effect of ambient air pollution on asthma incidence in adults. Further research with improved personal-level exposure assessment (versus residential exposure assessment only) and phenotypic characterization is needed.

Journal article

Adam M, Schikowski T, Carsin AE, Cai Y, Jacquemin B, Sanchez M, Vierkötter A, Marcon A, Keidel D, Sugiri D, Al Kanani Z, Nadif R, Siroux V, Hardy R, Kuh D, Rochat T, Bridevaux P-O, Eeftens M, Tsai M-Y, Villani S, Phuleria HC, Birk M, Cyrys J, Cirach M, de Nazelle A, Nieuwenhuijsen MJ, Forsberg B, de Hoogh K, Declerq C, Bono R, Piccioni P, Quass U, Heinrich J, Jarvis D, Pin I, Beelen R, Hoek G, Brunekreef B, Schindler C, Sunyer J, Krämer U, Kauffmann F, Hansell AL, Künzli N, Probst-Hensch Net al., 2014, Adult lung function and long-term air pollution exposure. ESCAPE: a multicentre cohort study and meta-analysis, European Respiratory Journal, Vol: 45, Pages: 38-50, ISSN: 1399-3003

The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE).Residential exposure to nitrogen oxides (NO2, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis.We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 μg·m−3 increase in NO2 exposure was associated with lower levels of FEV1 (−14.0 mL, 95%CI −25.8– −2.1) and FVC (−14.9 mL, 95% CI −28.7– −1.1). An increase of 10 μg·m−3 in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV1 (−44.6 mL, 95% CI −85.4– −3.8) and FVC (−59.0 mL, 95% CI −112.3– −5.6). The associations were particularly strong in obese persons.This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe.

Journal article

Cai Y, Schikowski T, Adam M, Buschka A, Carsin A, Jacquemin B, Marcon A, Sanchez M, Vierkötter A, Al-Kanaani Z, Beelen R, Birk M, Brunekreef B, Cirach M, Clavel-Chapelon F, Declercq C, de Hoogh K, de Nazelle A, Ducret-Stich RE, Valeria Ferretti V, Forsberg B, Gerbase MW, Hardy R, Heinrich J, Hoek G, Jarvis D, Keidel D, Kuh D, Nieuwenhuijsen MJ, Ragettli MS, Ranzi A, Rochat T, Schindler C, Sugiri D, Temam S, Tsai M, Varraso R, Kauffmann F, Krämer U, Sunyer J, Künzli N, Probst-Hensch N, Hansell ALet al., 2014, Cross-sectional associations between air pollution and chronic bronchitis: an ESCAPE meta-analysis across five cohorts, Thorax, Vol: 69, Pages: 1005-1014, ISSN: 0040-6376

Background This study aimed to assess associations of outdoor air pollution on prevalence of chronic bronchitis symptoms in adults in five cohort studies (Asthma-E3N, ECRHS, NSHD, SALIA, SAPALDIA) participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE) project.Methods Annual average particulate matter (PM10, PM2.5, PMabsorbance, PMcoarse), NO2, nitrogen oxides (NOx) and road traffic measures modelled from ESCAPE measurement campaigns 2008–2011 were assigned to home address at most recent assessments (1998–2011). Symptoms examined were chronic bronchitis (cough and phlegm for ≥3 months of the year for ≥2 years), chronic cough (with/without phlegm) and chronic phlegm (with/without cough). Cohort-specific cross-sectional multivariable logistic regression analyses were conducted using common confounder sets (age, sex, smoking, interview season, education), followed by meta-analysis.Results 15 279 and 10 537 participants respectively were included in the main NO2 and PM analyses at assessments in 1998–2011. Overall, there were no statistically significant associations with any air pollutant or traffic exposure. Sensitivity analyses including in asthmatics only, females only or using back-extrapolated NO2 and PM10 for assessments in 1985–2002 (ECRHS, NSHD, SALIA, SAPALDIA) did not alter conclusions. In never-smokers, all associations were positive, but reached statistical significance only for chronic phlegm with PMcoarse OR 1.31 (1.05 to 1.64) per 5 µg/m3 increase and PM10 with similar effect size. Sensitivity analyses of older cohorts showed increased risk of chronic cough with PM2.5abs (black carbon) exposures.Conclusions Results do not show consistent associations between chronic bronchitis symptoms and current traffic-related air pollution in adult European populations.

Journal article

Schikowski T, Adam M, Marcon A, Cai Y, Vierkotter A, Carsin AE, Jacquemin B, Al KZ, Beelen R, Birk M, Bridevaux PO, Brunekeef B, Burney P, Cirach M, Cyrys J, de HK, de MR, de NA, Declercq C, Forsberg B, Hardy R, Heinrich J, Hoek G, Jarvis D, Keidel D, Kuh D, Kuhlbusch T, Migliore E, Mosler G, Nieuwenhuijsen MJ, Phuleria H, Rochat T, Schindler C, Villani S, Tsai MY, Zemp E, Hansell A, Kauffmann F, Sunyer J, Probst-Hensch N, Kramer U, Kunzli Net al., 2014, Association of ambient air pollution with the prevalence and incidence of COPD, Eur.Respir.J.

The role of air pollution in chronic obstructive pulmonary disease (COPD) remains uncertain.The aim was to assess the impact of chronic exposure to air pollution on COPD in four cohorts using the standardised ESCAPE exposure estimates. Annual average particulate matter (PM), nitrogen oxides (NOx) and road traffic exposure were assigned to home addresses using land-use regression models. COPD was defined by NHANES reference equation (forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) less than the lower limit of normal) and the Global Initiative for Chronic Obstructive Lung Disease criterion (FEV1/FVC <0.70) and categorised by severity in non-asthmatics.We included 6550 subjects with assigned NOx and 3692 with PM measures. COPD was not associated with NO2 or PM10 in any individual cohort. In meta-analyses only NO2, NOx, PM10 and the traffic indicators were positively, although not significantly, associated with COPD. The only statistically significant associations were seen in females (COPD prevalence using GOLD: OR 1.57, 95% CI 1.11-2.23; and incidence: OR 1.79, 95% CI 1.21-2.68).None of the principal results were statistically significant, the weak positive associations of exposure with COPD and the significant subgroup findings need to be evaluated in further well standardised cohorts followed up for longer time, and with time-matched exposure assignments

Journal article

Cai Y, Blangiardo M, De Hoogh K, Gulliver J, Morley D, Doiron D, Elliott P, Hansell A, Hodgson Set al., 2014, Road traffic noise, air pollution and cardio-respiratory health in European cohorts: A harmonised approach in the BioSHaRE project

Background and aims: Few studies have investigated joint effects of road traffic noise and air pollution on cardiovascular outcomes. This project aims to quantify the joint and separate effects of both exposures on prevalent and incident cardiovascular disease and asthma as part of the EU-funded BioSHaRE project involving five European cohorts (EPIC-Oxford, EPIC-Turin, HUNT, Lifelines, UK Biobank). Methods: Health outcomes have been ascertained by self-report (prevalence) and medical record (incidence) and retrospectively harmonised across the five cohorts. Residential road traffic noise exposures for each participant are being estimated using a European noise model based on Common Noise Assessment Methods in Europe (CNOSSOS-EU). Cross-sectional epidemiological analyses are in progress, virtually pooled using DataSHIELD methods. Results: In total, 716,945 men and women are included, mostly >40 years. Initial analysis of EPIC-Oxford and Lifelines showed prevalence of self-reported hypertension to be 26%, high blood lipids 15% and asthma 11% and mean annual 24-hour noise estimates of 56.4 dB(A) (EPIC-Oxford) and 65.8 dB(A) (Lifelines). Correlations between noise estimates and NO2 are generally low (r~0.1 to 0.4). Conclusions: Pooling of individual level harmonised data from established cohorts offers the large sample sizes needed to investigate effects of road traffic noise and ambient air pollution on cardio-respiratory diseases.

Conference paper

Cai Y, Schikowski T, Carsin A-E, et alet al., 2013, Effect of air pollution on prevalence of chronic bronchitis symptoms-a cross-sectional analysis of 5 cohort studies, International Society for Environmental Epidemiology (ISEE) Annual Conference 2013, Publisher: Environ Health Perspect

Conference paper

Cai Y, de Hoogh K, Hodgson S, et alet al., 2013, Methods to harmonise air pollution and noise assessment in EU Biobanks, International Society for Environmental Epidemiology (ISEE) Annual Conference 2013, Publisher: Environ Health Perspect

Conference paper

Schikowski T, Adam M, Cai Y, et alet al., 2013, Association between long-term exposure to traffic-related air pollution and COPD, International Society for Environmental Epidemiology (ISEE) Annual Conference 2013, Publisher: Environ Health Perspect

Conference paper

Alhyas L, Cai Y, Majeed A, 2012, Type 2 diabetes care for patients in a tertiary care setting in UAE: a retrospective cohort study., JRSM Short Rep, Vol: 3

OBJECTIVE: We aimed to examine the quality of type 2 diabetes mellitus (T2DM) care in Al-Ain, in the United Arab Emirates (UAE). DESIGN: A retrospective cohort study from 2008 to 2010. SETTING: A diabetes centre located in a tertiary care hospital in Al-Ain, UAE. PARTICIPANTS: People with T2DM receiving care from the diabetes centre. RESULTS: 382 Emirates patients with T2DM were included in the analysis. Overall in 2010, proportions of people with T2DM reaching the following targets were: glycated haemoglobin (HbA1c) 41%, low-density lipoprotein (LDL) 72%, systolic and diastolic blood pressure (SBP/DBP) 47% and 73%, respectively. There was a significant improvement from 2008 to 2010, respectively, in the mean for the following: (1) HbA1c (8.5% [95% confidence interval, CI: 8.33-8.67] versus 7.5% [95% CI: 7.36-7.63]); (2) LDL (2.60 mmol/L [95% CI: 2.51-2.70] versus 2.27 mmol/L [95% CI: 2.21-2.33]); and (3) SBP (133.1 mmHg [95% CI: 131.7-134.4] versus 131.0 [95% CI: 130.1-131.9]). Glycaemic and lipid control were similar in men and women; however, HbA1c levels in men and women aged 60+ years were significantly lower by (0.7% [P = 0.01] versus 0.8% [P < 0.001], respectively) than for those aged between 18 and 39 years. CONCLUSION: This study demonstrates that there is encouraging progress in diabetes care in Al-Ain, UAE as reflected by the overall improvement in the mean of HbA1c, LDL and SBP, and the increase in the number of people reaching the target for the same indicators from 2008 to 2010. The results however show that there is scope for additional enhancement of care, especially for better glycaemic control among young patients and better SBP control among men.

Journal article

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