BACKGROUND: Neurodegenerative disease has a great adverse impact on population's death and disability worldwide. However, the association of air pollution and residential greenness with neurodegenerative disease and their potential mechanisms still remain uncertain.
METHODS: We used data from a population-based prospective cohort in Ningbo, China. Exposure to PM, PMand NOwere assessed by land-use regression (LUR) models and residential greenness was estimated by Normalized Difference Vegetation Index (NDVI). Our primary outcomes were all neurodegenerative diseases, Parkinson's disease (PD) and Alzheimer's disease (AD). Cox proportional hazards regression models were used to examine the association of air pollution and residential greenness with risk of incident neurodegenerative disease. Furthermore, we also explored the potential mediation relationship and effect modification between greenness and air pollutants. 2.5 10 2
RESULTS: During the follow-up period, we identified a total of 617 incident neurodegenerative diseases, 301 PD and 182 AD. In single-exposure models, PMwas positively associated with all outcomes (e.g. AD hazard ratio (HR): 1.41, 95 % confidence interval (CI): 1.09-1.84, per interquartile range (IQR) increment), whereas residential greenness showed protective effects (e.g. neurodegenerative disease, HR: 0.82, 95%CI: 0.75-0.90, per IQR increment for NDVI in 1000 m buffer). NOwas positively associated with risk of neurodegenerative disease and PMwas associated with neurodegenerative disease and AD. In two-exposure models, after adjustment for PM, the association for greenness generally attenuated towards null. Moreover, we identified the significant modification effect of greenness on PM2.5 on additive and multiplicative scales. 2.5 2 10 2.5
CONCLUSION: In this prospective study, we found that exposure to higher residential greenness and lower concentrations of particulate matter were associated with lower risk of neurodegenerative disease, PD and AD. Residential greenness could modify the association of PMwith neurodegenerative disease. 2.5
