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The mediating role of lung function on air pollution-induced cardiopulmonary mortality in elderly women: The SALIA cohort study with 22-year mortality follow-up

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61988987%3A17110%2F21%3AA2202BQO" target="_blank" >RIV/61988987:17110/21:A2202BQO - isvavai.cz</a>

  • Výsledek na webu

    <a href="https://www.sciencedirect.com/science/article/pii/S1438463921000183?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S1438463921000183?via%3Dihub</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.ijheh.2021.113705" target="_blank" >10.1016/j.ijheh.2021.113705</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    The mediating role of lung function on air pollution-induced cardiopulmonary mortality in elderly women: The SALIA cohort study with 22-year mortality follow-up

  • Popis výsledku v původním jazyce

    Air pollution exposure is associated with reduced lung function and increased cardio-pulmonary mortality (CPM). Objectives: We analyzed the potential mediating effect of reduced lung function on the association between air pollution exposure and CPM. Methods: We used data from the German SALIA cohort including 2527 elderly women (aged 51–56 years at baseline 1985–1994) with 22-year follow-up to CPM. Exposures to PM10, PM2.5, PM2.5 absorbance, NO2 and NOx were assessed by land-use regression modelling and back-extrapolated to estimate exposures at baseline. Lung function (FVC, FEV1) was measured by spirometry and transformed to GLI z-scores. Adjusted Cox proportional hazards and causal proportional hazards mediation analysis models were fitted. Results: The survival analysis showed that reduced lung function (z-scores of FVC or FEV1 below 5% predicted) reflected significantly lower survival probability from CPM (p <0.0001). Longterm exposures to NOx and NO2 were associated with increased risks of CPM (eg. HR =1.215; 95%CI: 1.017–1.452 for IQR increase in NOx and HR =1.209; 95%CI: 1.011–1.445 for IQR increase in NO2) after adjusting for reduced lung function and additional covariates. The associations of PM2.5 absorbance and CPM remained significant in models adjusted for FEV1/FVC, but the associations with PM10 and PM2.5 were not significant. The mediation analysis showed sig-nificant indirect effects of NO2 and NOx on CPM mediated through reduced FEV1 and FVC. The largest indirect effects were found for exposures to NO2 (HR =1.037; 95%CI: 1.005–1.070) and NOx (HR =1.028; 95%CI: 1.004–1.052) mediated through reduced FVC. The mediated proportion effect ranged from 13.9% to 19.6% in fully adjusted models. This study provides insights into the mechanism of reduced lung function in association between long- term air pollution exposure and CPM. The mediated effect was substantial for exposure to nitrogen oxides (NOx and NO2), but less pronounced for PM10 and PM2.5.

  • Název v anglickém jazyce

    The mediating role of lung function on air pollution-induced cardiopulmonary mortality in elderly women: The SALIA cohort study with 22-year mortality follow-up

  • Popis výsledku anglicky

    Air pollution exposure is associated with reduced lung function and increased cardio-pulmonary mortality (CPM). Objectives: We analyzed the potential mediating effect of reduced lung function on the association between air pollution exposure and CPM. Methods: We used data from the German SALIA cohort including 2527 elderly women (aged 51–56 years at baseline 1985–1994) with 22-year follow-up to CPM. Exposures to PM10, PM2.5, PM2.5 absorbance, NO2 and NOx were assessed by land-use regression modelling and back-extrapolated to estimate exposures at baseline. Lung function (FVC, FEV1) was measured by spirometry and transformed to GLI z-scores. Adjusted Cox proportional hazards and causal proportional hazards mediation analysis models were fitted. Results: The survival analysis showed that reduced lung function (z-scores of FVC or FEV1 below 5% predicted) reflected significantly lower survival probability from CPM (p <0.0001). Longterm exposures to NOx and NO2 were associated with increased risks of CPM (eg. HR =1.215; 95%CI: 1.017–1.452 for IQR increase in NOx and HR =1.209; 95%CI: 1.011–1.445 for IQR increase in NO2) after adjusting for reduced lung function and additional covariates. The associations of PM2.5 absorbance and CPM remained significant in models adjusted for FEV1/FVC, but the associations with PM10 and PM2.5 were not significant. The mediation analysis showed sig-nificant indirect effects of NO2 and NOx on CPM mediated through reduced FEV1 and FVC. The largest indirect effects were found for exposures to NO2 (HR =1.037; 95%CI: 1.005–1.070) and NOx (HR =1.028; 95%CI: 1.004–1.052) mediated through reduced FVC. The mediated proportion effect ranged from 13.9% to 19.6% in fully adjusted models. This study provides insights into the mechanism of reduced lung function in association between long- term air pollution exposure and CPM. The mediated effect was substantial for exposure to nitrogen oxides (NOx and NO2), but less pronounced for PM10 and PM2.5.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30302 - Epidemiology

Návaznosti výsledku

  • Projekt

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2021

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH

  • ISSN

    1438-4639

  • e-ISSN

    1618-131X

  • Svazek periodika

  • Číslo periodika v rámci svazku

    233

  • Stát vydavatele periodika

    DE - Spolková republika Německo

  • Počet stran výsledku

    8

  • Strana od-do

    113705

  • Kód UT WoS článku

    000632393400008

  • EID výsledku v databázi Scopus

    2-s2.0-85100745600