This study showed significant relations between short-term exposure to air pollutants CO, NO2, PM10, PM2.5 and epilepsy admissions in Kerman, Iran.
In this study CO increased epilepsy admissions. Consistent with this study, Bao et al's study in China showed an association between CO and increased epilepsy hospitalization 1.1% (95% CI: 0.1%, 2.1%) (16). Also in Mexico, there was an association between ambient CO and epilepsy admissions RR = 1.098 (95% CI: 1.045–1.155) (17).
In this study, NO2 had a significant relation with epilepsy admission in total and several different age groups, and the strongest relation was observed in males. Automobile exhaust is one of the most important sources of nitrogen dioxide. Wang et al's study in China found a significant association between the NO2 of automobile exhaust and neurobehavioral function in school age children. In this study two primary schools were chosen. One school was located in a clear area and the other in a traffic dense and polluted area. NO2 had been monitored for traffic related air pollution on the school campuses and classrooms. Children participated in assisted neurobehavioral testing to assess neurobehavioral performance (18). A systematic review, in 2017 concluded that high concentrations of NO2 in polluted air significantly affects the central nervous system in children and adults, and represent a significant risk factor for human health (19). A study from China showed a significant relation between increasing concentration of NO2 with epilepsy attacks 2% (95% CI: 0.5% – 3.6%) (16). Also in Mexico, an ecological study showed a significant relation between nitrogen dioxide with epilepsy attacks RR = 1.083 (95% CI: 1.038–1.13) (17). In a cohort study in Denmark, the authors found that residential exposure to road traffic and air pollution is associated with a higher risk for febrile seizures IRR = 1.05, (95% CI: 1.02–1.07) (20). A study in southern Spain showed that even low level NO2 exposure and traffic related air pollution had adverse effects on children’s neurodevelopment (21). Xu et.al's study in China showed that the RR for epilepsy attacks was 3.17 (95% CI: 1.41–4.93) per 10 µg/m3 increase of NO2 (11). However, in the US, the authors showed a protective effect for N2O in epilepsy IRR = 0.85 (95% CI: 0.74–0.97) (9). N2O is a different compound and is derived mainly from agricultural fertilizers and natural sources, but NO2 is mainly produced by vehicles.
Another pollutant evaluated in this study was PM10, which had a significant relation with epilepsy admission in total and several subgroups, and the strongest relation was found in the under 18 year's subgroup. Several studies have shown relations between ambient PM10 and epilepsy attacks (17, 22, 23). Consistent with this study, Cakmak et al. in Mexico showed an association between PM10 and hospital admission for epilepsy RR = 1.083 (95% CI: 1.038–1.13) (17). A study in six cities in Italy found positive associations between PM10 exposure and total emergency calls from 2002 to 2006 (24). Also, increased emergency calls for epilepsy attacks were observed with exposure to PM10 in China, RR = 1.5 (95% CI: 1.1–2.0) (22). Radmanesh et al's study in Iran, showed that hospital admissions for patients with cerebral ischemic attack, epilepsy, and different types of headaches on dusty days increased significantly compared to clean days. Also hospital admissions of these patients significantly increased with increased concentrations of ambient PM10 (23). Another study from Iran showed that exposure to PM10 increased oxidative stress and the expression of inducible nitric oxide synthase (iNOS) messenger RNA levels and reduced the concentrations of antioxidant enzymes (25).
In this study PM2.5 had a significant relation with epilepsy admission in total and several subgroups, and the strongest relation was found in the above 59 years subgroup. Consistent with this study, a significant association observed between PM2.5 and epilepsy attacks in Mexico RR = 1.065 (95% CI: 1.002–1.132) (17). Prenatal exposure to pollutants may cause permanent changes in neurotransmitters and altered brain development resulting in long term deficits in one or more memory systems (26). Other studies have shown that oxidative stress, neuro inflammation, glial activation, and cerebrovascular damage are the primary pathways for inducing brain pathology by air pollution (27). Oxidative stress, changes in autonomous function and progression of atherosclerosis can be exacerbated by exposure to ambient PM (28).
In this study O3 and SO2 were inversely related with epilepsy admission. In an ecological study in China, Xu et al. also reported negative associations between ambient O3 and epilepsy attacks − 0.84% (95%Cl: -1.58%, 0.09%) (11). An interventional study showed that ozone can be protective against pentylenetetrazole (PTZ) induced epilepsy attacks (29). But in another study conducted in Mexico, a significant direct association was observed between O3 and hospital admission for epilepsy attacks RR = 1.100 (95% CI: 1.025–1.181) (17). In Fluegge et al's study in the USA, no significant relation was observed between O3 and epilepsy attacks (9). In the current study the average concentration of O3 was 30.21 ± 11.19ppb, which is less that Xu et al's study (mean = 100 ppb ± 63) (11) which showed a negative association, and Cakmak et al's study (mean = 93.26 ppb) (17). More research is needed to clarify the effect of ozone exposure on epilepsy.
Some of the strengths of this study was including about 12 years air pollution and epilepsy admission data, and using Generalized Additive Models (GAM) to adjust for nonlinear confounder variables. However, given the ecological nature of this study, results cannot be easily inferred to the individual level.