Yeager R, Riggs D, DeJarnett N, et al. Association between residential greenness and cardiovascular disease risk. J Am Heart Assoc. 2018;7(e009117).
To assess the impact of residential green space on markers of cardiovascular disease (CVD)
Design & Participants
This was a cross-sectional study of 408 participants (48% female, mean age 51.4±10.8) who were patients at the University of Louisville outpatient cardiovascular clinic between 2009 and 2014. All participants were recruited because of mild-to-moderate cardiovascular risk factors (eg, mean BMI 32.9, mean blood pressure 131/80) and/or history of past cardiac events.
Participants’ residential addresses were mapped using Geographic Information System (GIS) software and spatially correlated with current Normalized Difference Vegetation Index (NDVI) satellite data to rate the relative quantity of surrounding green space in 250 m- and 1 km-radius circles, using the standardized method from −0.1 (completely urban/no vegetation) to 0.9 (high-density forest).
Urinary and blood biomarker data was collected from each participant to assess levels of current cardiovascular risk, damage, and/or repair, as follows:
- Cardiovascular risk: urinary epinephrine, norepinephrine, dopamine, serotonin, normetanephrine, 3-methoxytyramine, metanephrine, 5-hydroxyindole-3-acetic acid, homovanillic acid, and vanillylmandelic acid concentrations, all markers of sympathetic neuroendocrine activation known to contribute to CVD.
- Cardiovascular damage: urinary F2-isoprostane, a marker of oxidative stress.
- Cardiovascular repair: serum circulating angiogenic cell (CAC) subtypes 1-15, reflecting vascular regrowth after damage.
All samples were collected between 1:00 pm and 4:00 pm, to minimize circadian variations. Urinary samples were standardized to creatinine levels.
Patient biomarker and NDVI data were analyzed using GIS spatial correlation software. All results were adjusted for multiple demographic, clinical, residential, and environmental factors, including age, sex, ethnicity, smoking status, BMI, statin use, median household income, area deprivation index, density of roadways within 50 m of the residence, and concentration of PM2.5 (particulate matter with a diameter <2.5 micrometers) air pollution outside the home for all statistical models.
After adjusting for all measured factors listed above, the data show significant inverse association of residential green space with all biomarker categories, including the following:
- Decrease of urinary epinephrine concentration with increasing residential green space (−6.9% per Δ 0.1 NDVI; 95% CI: −11.5% to −2.0%, P=0.006) within 250 m, with statistical significance holding at 1 km.
- Decrease of urinary F2-isoprostane concentration with increasing residential green space (−9.0% per Δ 0.1 NDVI; 95% CI: −15.1% to −2.5%, P=0.007) with 250 m, with statistical significance holding at 1 km.
- Decrease of relevant serum CAC concentrations with increasing residential green space within 250 m (effect sizes between −8.0% and −15.6%) and 1 km (effect sizes between −6.9% and −10.1%).
Data demonstrated even more pronounced associations for certain groups, including women, participants who were not using beta-blockers, and participants without a history of previous myocardial infarction.
This study is published in the Journal of the American Heart Association and demonstrates the increasing interest of the conventional medical system in the United States on topics of nature and health. Disciplines such as urban planning, public health, and parks and recreation have been researching the beneficial effects of green space for many years. It is nice to see more mainstream medical journals beginning to take interest in this topic.
The findings of the current study under review should not be surprising. Empirical studies have been reporting beneficial effects of exposure to green space for many decades.1 One of the first of these studies, published in The Lancet over a decade ago, showed significant reductions in cardiovascular mortality among individuals living in areas surrounded by greater amounts of green space using the entire British National Health Service dataset of 41 million people.2 Other studies have shown similar green space associations with coronary heart disease and stroke.3,4
As suggested by the biomarkers used in this study, the primary mechanism of action proposed is modulation of the psychophysiological stress response with resultant physical and mental health effects. This is sometimes referred to as “allostatic load.”5,6 Much recent research has demonstrated the relationship between neighborhood environmental factors and increases in allostatic load,7,8 and decades of research have explored the effect of acute exposure to green space on biomarkers of stress.9 This current study is one of the first to utilize neuroendocrine and vascular repair biomarkers in a residential green space study, expanding the evidence for a mechanism of action of the epidemiological cardiovascular outcomes mentioned above, based on reduction of psychophysiological stress and allostatic load.
As a cross-sectional study the data here can only demonstrate associations between residential green space and CVD biomarkers. It cannot establish causation, and because participants were not asked about how much time they spent at their residence, may not accurately reflect how duration of green space exposure affects these biomarker outcomes.
Of greater interest is why epinephrine is the only urinary neuroendocrine biomarker (of the 10 tested) that demonstrated an association. If residential green space has an impact on psychophysiological function as other studies have reported, why do these other biomarkers not reflect these changes? It may be that fluctuations in these markers are too transient to measure baseline effects from chronic residential exposures, in which case other markers such as cortisol may be more appropriate. Other studies have explored this approach with positive results.10
This study is published in the Journal of the American Heart Association and demonstrates the increasing interest of the conventional medical system in the United States on topics of nature and health.
In addition, it is interesting that a study designed to measure CVD risk did not utilize more conventional CVD biomarkers such as high-sensitivity C-reactive protein (hs-CRP) or fibrinogen, when such markers are known to respond to psychophysiological stress. All of the risk biomarkers in this study were collected via urine sample, but each participants’ blood was drawn to capture vascular repair capacity via CAC count, so collection of hs-CRP or fibrinogen was feasible. It may be that these latter markers reflect inflammatory immunological activity more than neuroendocrine stress. Regardless, future studies may want to expand their collection of various biomarkers to provide a more robust investigation of potential mechanisms.
Cardiovascular disease continues to be one of the major causes of morbidity and mortality. Evidence suggests that environmental factors such as proximity and exposure to restorative green spaces influence stimulatory, oxidative, and repair mechanisms that affect cardiovascular health. It may be clinically and economically beneficial to support maintenance and access to these green spaces as part of a holistic, preventive approach to reducing burdens of disease.