Greener Neighborhoods, Cleaner Air, Lower Epilepsy Risk: A Study of Nearly 440,000 People

Could the amount of greenery outside your front door influence your risk of developing epilepsy? A large-scale prospective study drawing on the UK Biobank suggests it might. Researchers followed 437,526 adults for a median of nearly twelve years and found that people living in greener neighborhoods had a measurably lower risk of incident epilepsy, while those exposed to higher concentrations of air pollutants faced an elevated risk. The work, published in the Journal of Advanced Research, is the first investigation to link residential greenness with epilepsy incidence, and it goes further by probing how genetic susceptibility and air pollution shape that relationship—and how these environmental factors may affect how long people with epilepsy actually live.

Epilepsy is one of the most common neurological disorders worldwide, affecting roughly 50 million people with active disease and producing an incidence rate of about 48.86 cases per 100,000 person-years in high-income countries. The burden is substantial: in 2017 alone, the European region recorded 0.78 million disability-adjusted life-years attributable to epilepsy, and epilepsy-related deaths rose 53 percent compared with 1990. Perhaps most striking is how much remains unexplained—more than 40 percent of epilepsy cases in adults have no known cause. That gap has pushed researchers to search for modifiable environmental factors that could reduce disease burden, and the new study offers some of the most detailed evidence yet that the environments we inhabit may matter.

The research team, led by investigators including Feipeng Cui and Yaohua Tian, harnessed the UK Biobank, a cohort of more than 500,000 participants aged 37 to 73 recruited between 2006 and 2010. After excluding individuals with a history of brain injury, infection, brain tumors, or neurosurgery, those with missing exposure data, and people who already had epilepsy at baseline, 437,526 participants remained in the primary analysis. Incident epilepsy cases were identified through hospital inpatient and death records coded under ICD-9 and ICD-10, primary care records, and self-reported conditions, with participants followed until diagnosis, death, loss to follow-up, or the end of February 2021. During the follow-up period, 2,448 new epilepsy cases emerged.

To quantify greenness, the researchers used the normalized difference vegetation index, or NDVI, a satellite-derived measure calculated from the MODIS sensor at 250-meter resolution. NDVI exploits the fact that healthy vegetation absorbs red light via chlorophyll while reflecting near-infrared radiation; the formula (NIR minus RED) divided by (NIR plus RED) yields values from minus 1 to 1, with higher values indicating denser green vegetation. The team computed summer NDVI within buffers of 300, 500, 1,000, and 1,500 meters around each participant’s residential postcode, minimizing seasonal variability and excluding water bodies. Air pollution exposure was estimated using land-use regression models from the ESCAPE project, which incorporate traffic volume, land use, topography, and population density to predict annual average concentrations of nitrogen dioxide, nitrogen oxides, and fine and coarse particulate matter (PM2.5 and PM10) at each address, with cross-validation R-squared values between 77 and 88 percent.

The results were consistent across every buffer size: each interquartile-range increase in NDVI was associated with a 7 to 8 percent reduction in epilepsy risk after adjustment for age, sex, ethnicity, body mass index, education, employment, smoking, alcohol consumption, physical activity, and diet. Conversely, each interquartile-range increase in NO2, NOx, PM2.5, and PM10 was linked to a 5 to 9 percent increase in risk, with hazard ratios of 1.08, 1.05, 1.09, and 1.05 respectively. Trends across exposure quartiles were significant for all pollutants and greenness measures, and the associations proved robust across an extensive battery of sensitivity analyses, including time-varying exposure models, exclusion of early cases to guard against reverse causality, and adjustment for noise pollution and baseline chronic diseases. The population-attributable risk estimates suggested that, if the associations are causal, roughly 16 to 24 percent of incident epilepsy cases could potentially be prevented under lower exposure conditions.

Because greenness and air pollution were negatively correlated—correlation coefficients ranged from minus 0.47 to minus 0.65—the researchers used causal mediation analysis to ask whether cleaner air explains part of the greenness benefit. The findings pointed to PM2.5 as a plausible mediator: fine particulate matter appeared to account for approximately 38 to 48 percent of the association between greenness and epilepsy incidence, although the wide confidence intervals, which included the null, mean these mediation estimates should be interpreted cautiously. The team also detected small antagonistic interactions between greenness and NO2 or PM2.5, consistent with the idea that vegetation partially buffers the harm from pollution, for example by absorbing gaseous pollutants through leaf stomata and intercepting particles on leaf surfaces.

The biological plausibility of a pollution-epilepsy link rests on well-characterized mechanisms. Particulate and gaseous pollutants can enter the brain via the bloodstream or the olfactory nerve, triggering neuroinflammation driven by astrocytic and microglial activation and cytokine release, along with oxidative stress from reactive oxygen and nitrogen species. These inflammatory and oxidative responses can promote neuronal hyperexcitability, raising seizure susceptibility. Experimental work has further shown that high PM2.5 exposure may worsen seizure symptoms and cognitive dysfunction by disrupting iron metabolism and the Nrf2-mediated ferroptosis pathway. Greenspace, meanwhile, may confer additional benefits beyond air purification, including greater physical activity and reduced psychological stress, both of which could support neurological health.

Genetics emerged as a critical modifier. Using 21 independent risk variants from the largest genome-wide association study of epilepsy, the team computed polygenic risk scores and found that each unit increase in the score raised epilepsy risk by 68 percent, while participants in the highest genetic risk tertile faced a 30 percent higher risk than those in the lowest. Crucially, the joint analysis showed that people with low greenness and high genetic susceptibility had markedly elevated risk—up to 59 percent higher for the 300-meter NDVI buffer—compared with those enjoying high greenness and low genetic risk. Statistically significant antagonistic interactions between greenness and polygenic risk indicated that abundant vegetation partially offset the inherited risk, suggesting that individuals with high genetic susceptibility may benefit most from living in greener surroundings.

The study also quantified what these exposures mean for longevity. At age 45, people with epilepsy had a life expectancy of 36.89 years, compared with 41.39 years for those without the condition—a gap of 4.50 years. Yet among epileptics, those in the highest quartile of residential greenness gained between 2.15 and 2.67 years of life expectancy relative to those in the lowest quartile, and those with the lowest air pollution exposure gained 1.76 to 2.51 years compared with the most exposed. These estimates, derived from flexible parametric survival models, suggest that environmental conditions are not merely relevant to whether epilepsy develops, but also to how long people with the condition survive.

The authors are careful to note the limitations inherent in observational research. NDVI captures overall vegetation coverage but not vegetation type; pollutants such as carbon monoxide, ozone, and sulfur dioxide were unavailable; exposure was assessed at residential addresses without accounting for workplace or mobility patterns; and the UK Biobank population is predominantly white and high-income, limiting generalizability. The polygenic risk score captured only major common variants rather than the full genetic architecture of epilepsy. Even so, the E-value analyses indicated that unmeasured confounders were unlikely to fully explain the findings. If validated in more diverse populations and through quasi-experimental designs, the research points to a tangible public health opportunity: expanding urban greenery and tightening air quality standards could help prevent a portion of epilepsy cases and extend the lives of those already living with the disorder.

Subject of Research: Associations of residential greenness and air pollution with epilepsy incidence, genetic susceptibility, and life expectancy

Article Title: Residential greenness, air pollution, and epilepsy: Insight in genetic susceptibility and life expectancy

Article References: Cui, F., Wang, M., Tang, L., Ma, Y., Wang, J., Zheng, L., Xing, M., Xie, J., Han, L., & Tian, Y. (2026). Residential greenness, air pollution, and epilepsy: Insight in genetic susceptibility and life expectancy. Journal of Advanced Research, 88, 1045-1053. https://doi.org/10.1016/j.jare.2026.01.043

Image Credits: AI Generated

DOI: 10.1016/j.jare.2026.01.043

Keywords: epilepsy, greenness, NDVI, air pollution, PM2.5, UK Biobank, polygenic risk score, life expectancy, neurology, environmental health, cohort study, gene-environment interaction