The Association of Air Pollution with New-onset Epilepsy
Abstract number :
2.074
Submission category :
16. Epidemiology
Year :
2024
Submission ID :
776
Source :
www.aesnet.org
Presentation date :
12/8/2024 12:00:00 AM
Published date :
Authors :
Presenting Author: Tresah Antaya, MPH – Western University
Lixia Zhang, PhD – ICES Western
Britney Le, MSc – ICES Western
Tor Oiamo, PhD – Toronto Metropolitan University
Piotr Wilk, PhD – Western University
Kathy Speechley, PhD – Western University
Jorge Burneo, MD, MSPH, FAAN, FAES, FRCPC – Western University, London Ontario Canada
Rationale: Air pollution has been associated with certain neurological disorders, but its association with epilepsy has been insufficiently explored. Our primary objective was to estimate the association of long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) with new-onset epilepsy among adults in Ontario, Canada. Our secondary objective was to assess whether age, sex, immigration status, and health conditions associated with seizures and epilepsy modify these associations.
Methods: We used a nested case-control study design and individually linked health administrative and environmental databases. We included Ontario residents aged 18 to 80 on January 1, 2010, excluding those with prior diagnoses of seizures or epilepsy. We identified as cases those who developed epilepsy within six years and matched each case with up to five controls using risk-set sampling, defining the epilepsy diagnosis date as the index date for cases and their matched controls. The air pollutants were measured as the average of the annual average concentrations at participants’ postal codes over the three years before their index date. To address our primary objective, we used conditional logistic regression models to estimate the risk of new-onset epilepsy for an interquartile range increase in the concentration of each pollutant individually and in a multi-pollutant model. To address the secondary objective, we included interaction terms between each pollutant and potential effect modifier in the multi-pollutant model.
Results: We included 24,761 cases and 118,692 controls. The median [IQR] pollutant concentrations were 7.9 [1.3] µg/m3 for PM2.5, 9.6 [9.2] ppb for NO2, and 42.7 [5.4] ppb for O3. In the individual pollutant models, we observed significant associations between epilepsy onset and PM2.5 (OR=1.055 95% CI: 1.034, 1.076), NO2 (OR=0.938, 95% CI: 0.903, 0.974), and O3 (OR=1.096, 95% CI: 1.074, 1.119). In the multi-pollutant model, NO2 (OR=0.928, 95% CI: 0.891, 0.965) and O3 (OR=1.090, 95% CI: 1.060, 1.121) remained statistically significant. We also observed significant interactions with PM2.5 for immigration status and cancer, with NO2 for age, cancer, and stroke, and with O3 for age and stroke (Figure 1).
Conclusions: We observed a significant negative association between epilepsy onset and NO2 and a significant positive association for O3 in the individual and multi-pollutant models, and a positive association with PM2.5 in the individual pollutant model. Additionally, several characteristics modified the associations of all three air pollutants with new-onset epilepsy. The negative association observed between NO2 and epilepsy may be a result of residual confounding. Future research should continue to explore the associations between specific air pollutants and epilepsy onset.
Funding: Ontario Ministry of Health (MOH) and Ministry of Long-Term Care (MLTC), Lawson Health Research Institute’s Internal Research Fund, Jack Cowin Endowed Chair in Epilepsy Research at Western University (Burneo), Ontario Graduate Scholarship, and Western Graduate Research Scholarship (Antaya).
Epidemiology