Long-term exposure to ambient air pollution and traffic noise and incident hypertension in seven cohorts of the European study of cohorts for air pollution effects (ESCAPE)

We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts. We included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2....

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Vydané v:European heart journal Ročník 38; číslo 13; s. 983
Hlavní autori: Fuks, Kateryna B, Weinmayr, Gudrun, Basagaña, Xavier, Gruzieva, Olena, Hampel, Regina, Oftedal, Bente, Sørensen, Mette, Wolf, Kathrin, Aamodt, Geir, Aasvang, Gunn Marit, Aguilera, Inmaculada, Becker, Thomas, Beelen, Rob, Brunekreef, Bert, Caracciolo, Barbara, Cyrys, Josef, Elosua, Roberto, Eriksen, Kirsten Thorup, Foraster, Maria, Fratiglioni, Laura, Hilding, Agneta, Houthuijs, Danny, Korek, Michal, Künzli, Nino, Marrugat, Jaume, Nieuwenhuijsen, Mark, Östenson, Claes-Göran, Penell, Johanna, Pershagen, Göran, Raaschou-Nielsen, Ole, Swart, Wim J R, Peters, Annette, Hoffmann, Barbara
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England 01.04.2017
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Abstract We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts. We included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), >2.5, and ≤10 µm (PMcoarse), soot (PM2.5 absorbance), and nitrogen oxides at the addresses of participants with land use regression. Residential exposure to traffic noise was modelled at the facade according to the EU Directive 2002/49/EC. We assessed hypertension as (i) self-reported and (ii) measured (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg or intake of BP lowering medication (BPLM). We used Poisson regression with robust variance estimation to analyse associations of traffic-related exposures with incidence of hypertension, controlling for relevant confounders, and combined the results from individual studies with random-effects meta-analysis. Among 41 072 participants free of self-reported hypertension at baseline, 6207 (15.1%) incident cases occurred within 5-9 years of follow-up. Incidence of self-reported hypertension was positively associated with PM2.5 (relative risk (RR) 1.22 [95%-confidence interval (CI):1.08; 1.37] per 5 µg/m³) and PM2.5 absorbance (RR 1.13 [95% CI:1.02; 1.24] per 10 - 5m - 1). These estimates decreased slightly upon adjustment for road traffic noise. Road traffic noise was weakly positively associated with the incidence of self-reported hypertension. Among 10 896 participants at risk, 3549 new cases of measured hypertension occurred. We found no clear associations with measured hypertension. Long-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension.
AbstractList We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts.AimsWe investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts.We included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), >2.5, and ≤10 µm (PMcoarse), soot (PM2.5 absorbance), and nitrogen oxides at the addresses of participants with land use regression. Residential exposure to traffic noise was modelled at the facade according to the EU Directive 2002/49/EC. We assessed hypertension as (i) self-reported and (ii) measured (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg or intake of BP lowering medication (BPLM). We used Poisson regression with robust variance estimation to analyse associations of traffic-related exposures with incidence of hypertension, controlling for relevant confounders, and combined the results from individual studies with random-effects meta-analysis. Among 41 072 participants free of self-reported hypertension at baseline, 6207 (15.1%) incident cases occurred within 5-9 years of follow-up. Incidence of self-reported hypertension was positively associated with PM2.5 (relative risk (RR) 1.22 [95%-confidence interval (CI):1.08; 1.37] per 5 µg/m³) and PM2.5 absorbance (RR 1.13 [95% CI:1.02; 1.24] per 10 - 5m - 1). These estimates decreased slightly upon adjustment for road traffic noise. Road traffic noise was weakly positively associated with the incidence of self-reported hypertension. Among 10 896 participants at risk, 3549 new cases of measured hypertension occurred. We found no clear associations with measured hypertension.Methods and resultsWe included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), >2.5, and ≤10 µm (PMcoarse), soot (PM2.5 absorbance), and nitrogen oxides at the addresses of participants with land use regression. Residential exposure to traffic noise was modelled at the facade according to the EU Directive 2002/49/EC. We assessed hypertension as (i) self-reported and (ii) measured (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg or intake of BP lowering medication (BPLM). We used Poisson regression with robust variance estimation to analyse associations of traffic-related exposures with incidence of hypertension, controlling for relevant confounders, and combined the results from individual studies with random-effects meta-analysis. Among 41 072 participants free of self-reported hypertension at baseline, 6207 (15.1%) incident cases occurred within 5-9 years of follow-up. Incidence of self-reported hypertension was positively associated with PM2.5 (relative risk (RR) 1.22 [95%-confidence interval (CI):1.08; 1.37] per 5 µg/m³) and PM2.5 absorbance (RR 1.13 [95% CI:1.02; 1.24] per 10 - 5m - 1). These estimates decreased slightly upon adjustment for road traffic noise. Road traffic noise was weakly positively associated with the incidence of self-reported hypertension. Among 10 896 participants at risk, 3549 new cases of measured hypertension occurred. We found no clear associations with measured hypertension.Long-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension.ConclusionLong-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension.
We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts. We included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), >2.5, and ≤10 µm (PMcoarse), soot (PM2.5 absorbance), and nitrogen oxides at the addresses of participants with land use regression. Residential exposure to traffic noise was modelled at the facade according to the EU Directive 2002/49/EC. We assessed hypertension as (i) self-reported and (ii) measured (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg or intake of BP lowering medication (BPLM). We used Poisson regression with robust variance estimation to analyse associations of traffic-related exposures with incidence of hypertension, controlling for relevant confounders, and combined the results from individual studies with random-effects meta-analysis. Among 41 072 participants free of self-reported hypertension at baseline, 6207 (15.1%) incident cases occurred within 5-9 years of follow-up. Incidence of self-reported hypertension was positively associated with PM2.5 (relative risk (RR) 1.22 [95%-confidence interval (CI):1.08; 1.37] per 5 µg/m³) and PM2.5 absorbance (RR 1.13 [95% CI:1.02; 1.24] per 10 - 5m - 1). These estimates decreased slightly upon adjustment for road traffic noise. Road traffic noise was weakly positively associated with the incidence of self-reported hypertension. Among 10 896 participants at risk, 3549 new cases of measured hypertension occurred. We found no clear associations with measured hypertension. Long-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension.
Author Fuks, Kateryna B
Wolf, Kathrin
Hilding, Agneta
Fratiglioni, Laura
Swart, Wim J R
Hampel, Regina
Caracciolo, Barbara
Weinmayr, Gudrun
Becker, Thomas
Raaschou-Nielsen, Ole
Foraster, Maria
Östenson, Claes-Göran
Elosua, Roberto
Aasvang, Gunn Marit
Pershagen, Göran
Nieuwenhuijsen, Mark
Basagaña, Xavier
Sørensen, Mette
Oftedal, Bente
Cyrys, Josef
Aguilera, Inmaculada
Houthuijs, Danny
Hoffmann, Barbara
Beelen, Rob
Peters, Annette
Künzli, Nino
Eriksen, Kirsten Thorup
Penell, Johanna
Gruzieva, Olena
Brunekreef, Bert
Marrugat, Jaume
Aamodt, Geir
Korek, Michal
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Issue 13
Keywords Hypertension
Air pollution
Nitrogen oxides
Particulate matter
Road traffic noise
Meta-analysis
Language English
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Snippet We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts. We included seven cohorts of the...
We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts.AimsWe investigated whether...
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pubmed
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Index Database
StartPage 983
SubjectTerms Aged
Air Pollutants - adverse effects
Air Pollutants - analysis
Air Pollution - adverse effects
Air Pollution - analysis
Antihypertensive Agents - therapeutic use
Europe - epidemiology
Female
Humans
Hypertension - drug therapy
Hypertension - epidemiology
Hypertension - etiology
Incidence
Male
Middle Aged
Noise, Transportation - adverse effects
Particulate Matter - adverse effects
Particulate Matter - analysis
Prognosis
Prospective Studies
Self Report
Title Long-term exposure to ambient air pollution and traffic noise and incident hypertension in seven cohorts of the European study of cohorts for air pollution effects (ESCAPE)
URI https://www.ncbi.nlm.nih.gov/pubmed/28417138
https://www.proquest.com/docview/1889381755
Volume 38
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