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Effect of environmental pollutants particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (NO) and ground level ozone (O3) on epilepsy

BMC Neurology volume 25, Article number: 133 (2025) Cite this article

Abstract

Background

Epilepsy is a common condition that affects the brain and causes frequent seizures. Impaired brain biology is the world’s fastest-growing brain disorder, and exposure to environmental pollutants is the leading cause of mental health impairment. The growing literature suggests that air pollution is an emerging cause of neurological diseases. However, the existing evidence on air pollution and epilepsy is inadequate. This study aimed to investigate the effect of environmental pollutants particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (NO) and ground-level ozone (O3) on epilepsy.

Methods

This study recorded data on air pollutants and epilepsy using the electronic platforms Pub Med, Web of Science, Scopus, and Google Scholar. The keywords included for the literature search were based on two main aspects: exposure (air pollutants) and outcome (epilepsy). Initially, 78 articles and reports were identified, and after revising the abstracts and full articles, 06 studies were selected for a detailed analysis and discussion. The Odds Ratio (OR) and 95% confidence intervals (CIs) were extracted to investigate the impact between air pollutants and epilepsy. The effect of air pollution on epilepsy has been investigated through a compilation of six studies encompassing 371,515 individuals. The Cochrane chi-squared test (Chi2), fixed-effects design was used when I2 < 50% and P > 0.05; otherwise, a random-effects model was adopted.

Results

The results revealed that exposure to PM2.5 and NO2 were positively and significantly associated with epilepsy (RR = 1.00; 95% CI: 1.00-1.01; p = 0.03), NO2 (RR = 1.03; 95% CI: 1.02–1.03; p < 0.01). However, no association was identified between PM10, SO2, CO, and O3 with epilepsy. The results suggest a potential association between air pollution exposure and epilepsy.

Conclusions

Air pollutants PM2.5 and NO2 increase the risk of epilepsy. The findings suggest that reducing levels of these pollutants could be a strategic approach to mitigate neurological health risks in populations worldwide. Further research is warranted to elucidate the mechanisms and causal relationships between air pollutants and epilepsy. Public health initiatives aimed at reducing air pollution levels and targeted interventions to protect vulnerable populations hold promise for alleviating the burden of epilepsy associated with environmental exposures.

Peer Review reports

Introduction

The extensive damage caused by ambient air pollution on human health has been well-documented in the scientific literature. The initial investigations focused on respiratory, cardiovascular, and cerebrovascular systems [1,2,3]. However, recent studies have highlighted the deleterious impacts of air pollution on the neurological system, including impaired cognitive functions [4] and epilepsy [5].

Epilepsy is one of the most prevalent neurological diseases characterized by a predisposition to generate epileptic seizures. Epilepsy causes a sizable disease burden globally, regionally, and nationally [6, 7] and affects around 50 million people worldwide. Globally, approximately 5 million people are diagnosed with epilepsy each year, and 80% of the people with epilepsy are from low and middle-income countries [8].

Evidence suggests that air pollution induces neuroinflammation and oxidative stress in the central nervous system, contributing to the development of epilepsy [9, 10]. Particulate matter can enter the brain, triggering the release of pro-inflammatory cytokines and widespread neuroinflammation while activating astrocytes and microglia, which are detrimental to the CNS [9]. Furthermore, air pollutants, including SO2 and NO2, have been linked to toxic effects on nerve cell function in the CNS and cause protein oxidation, apoptosis in the hippocampus, and lipid peroxidation [11, 12].

The global literature has revealed a short-term association between air pollution and epilepsy, particularly among pollutants such as SO2 and NO2, indicating an elevated risk of epilepsy, especially among children [13–14]. However, the impact of air pollution on epilepsy remains incompletely understood due to inconsistent study designs, statistical approaches, and mixed findings between air pollutants and epilepsy. Therefore, this study “aimed to investigate the effect of environmental pollutants particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), carbon monoxide (NO), sulfur dioxide (SO2) and ground-level ozone (O3) on epilepsy”.

Materials and methods

Study design and settings

This study was conducted in the “Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia,” from December 1, 2023, to Jan 31, 2024.

Search strategy

The literature search was performed, and data were collected using electronic platforms such as PubMed, Embase, Google Scholar, Web of Science and Scopus to search the literature on the relationship between air pollutants and epilepsy. The keywords included a combination of two main items: exposure (air pollutants) and outcome (epilepsy). We filtered the data using the key terms “environmental pollution, air pollution, particulate matter, PM2.5, PM10, Nitrogen dioxide (NO2), Sulfur Dioxide (SO2), Carbon Monoxide (CO), Ozone (O3), seizures, epilepsy”. While initially using the term “environmental pollution and epilepsy,” 79 documents were identified; after screening and going through the abstracts, 06 cohort studies were finally selected for a detailed analysis and discussion (Fig. 1).

Inclusion and exclusion criteria

The inclusion criteria were set as follows: Studies with exposures to air pollution (PM2.5, PM10, NO2, SO2, CO, O3), and outcome was epilepsy with original research; the article language was written in English. However, the exclusion criteria include studies other than original articles, such as letters, editorials, brief communications, case reports, review articles or meta-analyses, were excluded. Moreover, studies with different outcomes that missed key information and had methodological flaws were excluded.

Fig. 1
figure 1

PRISMA flow diagram for the selection of documents

Full size image

Statistical analysis

The statistical analyses were performed using RStudio version 4.3.2 and package ‘meta.’ The risk ratio (RR), % change and odds ratio (OR) with 95% confidence intervals (CIs) were extracted from the included studies. We considered the odds ratio as equivalent to relative risk, similar to the meta-analysis done in another study [15]; percentage (%) change was converted to RR using the following formula [16]: RR = 1-(%change)/100. The RR were then pooled to investigate the relationship between air pollutants and epilepsy, using the Mantel-Haenszel method [17]. For studies that reported more than one value for RR, both values were used as separate data points. Sub-group analysis was performed for studies that included the required data for male and female genders. A p-value less than p < 0.05 was considered significant. The “Cochrane chi-squared test (Chi2) was used to evaluate heterogeneity among articles; a p-value < 0.05 indicates the existence of heterogeneity. To estimate the impact of heterogeneity on the analysis, the I2 value was calculated. I2 is a measure of heterogeneity and methods for calculating the associated 95% CI. I2 expresses the proportion of variability in a meta-analysis. I2 values ≥ 50% and p < 0.05 indicated a moderate to high degree of heterogeneity among pooled studies. A fixed-effects design was used when I2 < 50% and p > 0.05; otherwise, a random-effects model was adopted” [18]. Egger’s test was performed to evaluate publication bias, and the visual examination of the symmetry in funnel plots further assessed it. Leave-one-out sensitivity analysis was done to determine the reliability of this meta-analysis.

Risk of bias assessment

The existence of publication bias was assessed by Egger’s Regression test and funnel plot. Sensitivity analysis was done to evaluate the reliability of this analysis. RStudio version 4.3.2 was used to generate both.

Sensitivity analysis

A leave-one-out sensitivity analysis was conducted to assess the overall results’ robustness by determining each study’s influence. The outcomes were similar when individual studies were excluded for each pollutant, which indicates that the findings were not heavily dependent on one study. The sensitivity analysis on particulate matter (PM 2.5) shows moderate sensitivity to including specific studies. Excluding some studies leads to a non-significant pooled Odds Ratio (OR) with p-values up to 0.15. However, this does not drastically change the overall effect’s significance, indicating that the conclusion is not overly dependent on any single study.

Results

The impact of air pollution on epilepsy has been investigated through a compilation of six studies encompassing 371,515 individuals. Among these, approximately 60% were male and 40% were female. These studies originate from diverse geographical locations, with three conducted in China and one in Australia, Chile, and Iran. In the subsequent sections, we present each study’s outcomes and the effects observed for various pollutants. Detailed information regarding each study and its findings is outlined in Table 1.

Table 1 Air pollutants and their effect on epilepsy
Full size table

The impact of PM2.5 on epilepsy

In five studies focusing on the impact of PM2.5 on epilepsy, the Cochrane chi-squared test and I2 statistic indicated insignificant heterogeneity (Chi2 = 7.81, p = 0.17, I2 = 36%). Therefore, a fixed model was employed. The forest plot analysis demonstrated a significant association between PM2.5 pollutants and epilepsy (RR = 1.00; 95% CI: 1.00-1.01; p = 0.03) (Table 1; Fig. 2). The funnel plot suggested a small likelihood of publication bias, further confirmed by Egger’s test. Additionally, leave-one-out sensitivity analysis indicated that the meta-analysis findings were robust, as excluding any single study did not alter the outcomes.

Fig. 2
figure 2

Impact of PM2.5 on Epilepsy. *(A) and (B) are two RRs from within the same study and are used as separate data points

Full size image

Impact of PM10 on epilepsy

Six studies reported the impact of PM10 on epilepsy. The Cochrane chi-squared test and I2 statistic revealed a significant heterogeneity (Chi2 = 26.221, p < 0.01, I2 = 77%), so a random effect model was used. The forest plot analysis showed that the PM10 pollutant was positively but not significantly associated with epilepsy (RR = 1.01; 95% CI: 0.99–1.02; p = 0.35) (Table 1; Fig. 3). The funnel plot indicated a slight chance of publication bias, but Egger’s test showed no publication bias. Leave-one-out sensitivity analysis suggests that the meta-analysis findings were not heavily dependent on one study as the outcomes did not markedly differ when each study was excluded.

Fig. 3
figure 3

Impact of PM10 on Epilepsy. *(A) and (B) are two RRs from within the same study and are used as separate data points

Full size image

Impact of NO2 on epilepsy

Six studies reported the impact of NO2 on epilepsy. The Cochrane chi-squared test and I2 statistic revealed a significant heterogeneity (Chi2 = 6.21, p = 0.40, I2 = 3%), so a fixed effect model was used. The forest plot analysis showed that the NO2 pollutant was positively and significantly associated with epilepsy (RR = 1.03; 95% CI: 1.02–1.03; p < 0.01) (Table 1; Fig. 4). The funnel plot and Egger’s test showed no presence of publication bias. Leave-one-out sensitivity analysis indicates that the meta-analysis findings were not heavily dependent on one study, as the outcomes did not markedly differ when each study was excluded.

Fig. 4
figure 4

Impact of NO2 on Epilepsy. *(A) and (B) are two RR from within the same study and are used as separate data points

Full size image

Impact of sulfur dioxide (SO2) on epilepsy

Six studies reported the impact of SO2 on epilepsy. The Cochrane chi-squared test and I2 statistic revealed a significant heterogeneity (Chi2 = 34.07, p < 0.01, I2 = 82%), so a random effect model was used. The forest plot analysis showed that the SO2 pollutant was positively but not significantly associated with epilepsy (RR = 1.02; 95% CI: 0.99–1.05; p = 0.23) (Table 1; Fig. 5). The funnel plot showed some publication bias, and Egger’s test showed no presence of publication bias. Leave-one-out sensitivity analysis indicates that the meta-analysis findings were not heavily dependent on one study as the outcomes did not differ markedly when each study was excluded.

Fig. 5
figure 5

Impact of SO2 on Epilepsy

Full size image

Impact of carbon monoxide (CO) on epilepsy

Five studies reported the impact of CO on epilepsy. The Cochrane chi-squared test and I2 statistic revealed a significant heterogeneity (Chi2 = 23.83, p < 0.01, I2 = 83%), so a random effect model was used. The forest plot analysis showed that the CO pollutant was positively but not significantly associated with epilepsy (RR = 1.02; 95% CI: 0.96–1.09; p = 0.38) (Table 1; Fig. 6). The funnel plot showed some publication bias, and Egger’s test showed no publication bias. Leave-one-out sensitivity analysis indicates that the meta-analysis findings were not heavily dependent on one study, as the outcomes did not markedly differ when each study was excluded.

Fig. 6
figure 6

Impact of CO on Epilepsy

Full size image

Impact of ground-level ozone (O3) on epilepsy

Five studies reported the impact of O3 on epilepsy. The Cochrane chi-squared test and I2 statistic revealed a significant heterogeneity (Chi2 = 27.76, p < 0.01, I2 = 82%), so a random effect model was used. The forest plot analysis showed that the O3 pollutant was not significantly associated with epilepsy (RR = 1.00; 95% CI: 0.97–1.03; p < 0.01) (Table 1; Fig. 7). The funnel plot showed some publication bias, and Egger’s test showed no publication bias. Leave-one-out sensitivity analysis indicates that the meta-analysis findings were not heavily dependent on one study, as the outcomes did not markedly differ when each study was excluded.

Fig. 7
figure 7

Impact of Ground Level O3 on Epilepsy. * (A) and (B) are two RR from within the same study and are used as separate data points

Full size image

Discussion

The present study investigates the impact of environmental pollutants PM2.5, PM10, NO2, SO2, NO, and ground-level ozone (O3) on epilepsy. We found a significant link between air pollutants PM2.5 and NO2 and epilepsy. These pollutants, commonly found in urban areas due to vehicle emissions and industrial activities, are potent stressors affecting the central nervous system. This study’s findings emphasize the importance of considering environmental factors in understanding the pathophysiology of epilepsy. This insight leads to discussions about how these pollutants affect the brain, potential public health interventions, and the need for further research. It is crucial to place these findings in the context of existing knowledge and explore the direct and indirect pathways through which PM2.5 and NO2 impact epileptic seizures. The relationship between air pollution and neurological health, especially epilepsy, is a growing concern in environmental health. This discussion summarizes evidence from recent studies on the impact of specific air pollutants PM2.5, PM10, NO2, CO, SO2, and ground-level O3 on epilepsy incidence and seizure frequency.

The literature shows a significant link between PM2.5 and PM10 exposure and increased seizure risk in individuals with epilepsy. The delicate and coarse particulate matter may worsen respiratory conditions, leading to hypoxemia, a known seizure trigger. Additionally, the inflammatory response induced by particulate matter may contribute to neuronal excitability, facilitating seizures [25].

The NO2 exposure has been associated with a higher risk of epilepsy development, disrupting the blood-brain barrier and leading to neuroinflammation and increased seizure susceptibility, especially in urban areas with high vehicular emissions [26]. Although less researched about epilepsy, CO exposure has been linked to neurological damage that may predispose individuals to seizures. Acute CO poisoning can cause hypoxic injury, potentially triggering seizures in susceptible individuals [27].

The emerging evidence suggests that SO2 exposure may have neurotoxic effects that alter central nervous system functioning [28]. However, the exact pathways through which SO2 exposure might influence seizure activity remain fully elucidated. Inhalation of O3, a potent oxidant, causes oxidative stress and inflammation within the respiratory system, which could indirectly affect neurological health. While direct evidence linking O3 exposure to epilepsy is limited, the potential for O3 to exacerbate underlying conditions that trigger seizures warrants further investigation [29].

In our comprehensive analysis of the environmental factors influencing epilepsy, focusing on air pollutants like PM2.5 and NO2, we identified a correlation with epilepsy incidence. However, diverse viewpoints in the literature, such as the Xu et al. study [21], demonstrated a complex relationship between air pollution and epilepsy and suggested nuanced findings. For example, a 10 µg/m3 increase of NO2 and SO2 was linked to a 3.17% and 3.55% rise in outpatient visits for epilepsy. The NO2 and SO2 were positively related to outpatient visits for epilepsy. This indicates that the impact of air pollutants on epilepsy may vary based on the type of pollutant and other environmental or genetic factors.

Yang et al. [30] reported that PM2.5, PM10, and SO2 are common air pollutants that affect the occurrence of convulsions in children. PM2.5 and SO2 are risk factors; an increase in the level of PM2.5 could increase the occurrence of child convulsions. The highest incidence of convulsions was observed in children 1 to 2 years old, and it was higher in boys than in girls. Similarly, the present study identified PM2.5 and NO2 as central air pollutants that increase the risk of epilepsy.

Another study in Kerman, Iran, by Farahmandfard et al. (2022) [19] suggested that certain air pollutants could be risk factors for epilepsy and hospital admission, reinforcing the connection between air quality and neurological health. However, the roles of different pollutants and their mechanisms of action remain complex and not fully understood, as highlighted by Kawakami et al. [31] study on nitric oxide fractions in the epilepsy-prone mouse brain, which explored potential biochemical pathways in epileptogenesis.

The present study findings are significant in relation to the epidemiological data from the World Health Organization (WHO) to illustrate how even a small percentage (1%) increase in risk rate can have substantial implications for the global epidemiology of epilepsy. The epidemiological data from the WHO [8] demonstrates that 50 million people worldwide have epilepsy, and approximately 5 million new cases are diagnosed with epilepsy each year [8]. A 1% increase in risk, though statistically reasonable, would correspond to an estimated 500,000 additional cases globally and 50,000 new cases per annum. This 1% increase could exacerbate health inequities and strain already overburdened healthcare systems. The present study findings provide a better understanding of the impact of air pollution on epilepsy and public health significance, strengthening the epidemiological and clinical implications of the study findings. The findings emphasize the complexity of the relationship between air pollution and epilepsy, underscoring the need for further research to unravel air pollutants’ direct and indirect effects on neurological health. The divergent results and methodologies of these studies highlight the importance of a multifaceted approach to understanding the environmental determinants of epilepsy and informing public health interventions and policy.

Pathophysiological mechanisms

The exact mechanisms by which air pollution contributes to epilepsy are still being investigated. Several plausible pathways have been proposed, including neuroinflammation, oxidative stress, alteration of neurotransmitter systems, and neuronal damage. These pathophysiological conditions damage the cellular structures and disrupt normal neuronal function, potentially contributing to the development of epilepsy [32, 33]. At the same time, further research is needed to fully elucidate the relationship between air pollution and epilepsy. Air pollution continues to rise globally, and efforts to reduce emissions and mitigate the impact of pollution on human health are more critical than ever. Additionally, healthcare providers should be aware of the potential link between pollution and epilepsy when evaluating and managing patients with this condition. Addressing pollution at both individual and societal levels is essential to create a healthier environment and reduce the burden of neurological disorders such as epilepsy.

Study strengths and limitations

Similar to other studies, this study has some strengths and limitations. This study investigated and highlighted a critical topic: the impact of air pollutants on epilepsy. This is the first study to highlight the effects of air pollutants on epilepsy and provide a comprehensive understanding of the pathophysiological phenomenon, enhancing generalizability across different settings and conditions. We identified the publication bias by including a more balanced and unbiased estimate of the actual effect size. The limitations of this study include the limited availability of literature; hence, our analysis is based on the six studies. Despite the efforts to include published studies from leading science journals, publication bias remains a concern in analysis. Overall, in this study, we synthesized the evidence and interpreted the findings in the appropriate context.

Conclusion

The study findings emphasize the impact of air pollutants on epilepsy, highlighting the intricate mechanisms through which environmental factors contribute to the pathophysiology of seizures. These findings underscore the need for enhanced public health initiatives to reduce air pollution levels and further research to elucidate the complex interactions between air quality and neurological disorders. Addressing air pollution not only improves overall health but also offers a potential pathway to mitigate the burden of epilepsy, thereby improving the quality of life for those affected by this condition.

Data availability

The raw data supporting the conclusions of this article may be provided on reasonable request to the corresponding author.

Abbreviations

PM:

Particulate matter

NO2 :

Nitrogen dioxide

SO2 :

Sulfur dioxide

CO:

Carbon monoxide

O3 :

Ozone

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Acknowledgements

We thank the researchers supporting project number RSP 2025 R47, King Saud University, Riyadh, Saudi Arabia.

Funding

King Saud University, Riyadh, Saudi Arabia (RSP 2025 R47).

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Authors and Affiliations

  1. Department of Medicine (Neurology Unit), College of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia

    Bandar Nasser Aljafen

  2. College of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia

    Narmeen Shaikh & Joud Mohammed AlKhalifah

  3. Department of Physiology, College of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia

    Sultan Ayoub Meo

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Contributions

BNJ, NS, JAK: literature review, data collection and analysis, and review of the manuscript. SAM: conceptualization, literature review, writing and editing; all authors have read and approved to publish the manuscript.

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Correspondence to Sultan Ayoub Meo.

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Aljafen, B.N., Shaikh, N., AlKhalifah, J.M. et al. Effect of environmental pollutants particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (NO) and ground level ozone (O3) on epilepsy. BMC Neurol 25, 133 (2025). https://doi.org/10.1186/s12883-025-04142-3

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  • DOI: https://doi.org/10.1186/s12883-025-04142-3

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BMC Neurology

ISSN: 1471-2377

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