Article Text
Abstract
Background/aim Cardiovascular disease (CVD) causes more than a quarter of deaths in the UK each year. A beneficial association of greenspace and CVD has previously been observed, however the underlying mechanisms require further investigation. We aim to assess the contribution of an environmental pathway-specific exposure – air pollution – that is proposed to partially drive associations of greenspace and CVD.
Methods A hybrid air pollution model was developed using output from a dispersion model within a land-use regression (LUR) model to estimate long-term nitrogen dioxide (NO2) concentrations for Greater London. LUR variables offered to the model included building volume, household census data, land use and high-resolution vegetation data in multiple buffer sizes (range: 25 m–5000 m). London Air Quality Network monitoring sites with sufficiently complete data (n=54) were used to develop the model. Model validation was via grouped (leave-25%-out) cross-validation. The regression coefficient of the vegetation cover variable was multiplied by the 10th minus 90th percentile to estimate the reduction in NO2 concentration at sites with the lowest compared to the highest vegetation cover area.
Results The hybrid model for NO2 yielded an adjusted R2 of. 82 for modelled versus monitored NO2. Grouped cross-validation R2 was. 82. The dispersion model output explained a large portion of the variance in NO2 concentrations – 55%. The building volume and vegetation cover variables added 25% and 2% explained variance, respectively. Despite a small increase in R2, contrasts in vegetation cover area at sites (10th-90th percentile) resulted in a substantial reduction in NO2 concentration of 10.75 μg/m3. The estimated reduction of NO2 attributed to vegetation cover was not in excess of the difference in average concentrations at roadside compared to background monitoring sites – 23.51 μg/m3 – indicating a feasible contribution.
Conclusion Vegetation cover on average reduced ambient NO2 at London monitoring sites by 5.09 μg/m3, suggesting the environmental pathway is a plausible mechanism by which greenspace influences cardiovascular health. Further assessment of the mediating role of air pollution in greenspace and CVD morbidity/mortality associations in the London-based UK Biobank population (~60,000) is underway.