
6 Recent Studies on Environmental Risk Factors and Neurological Disease
Key Takeaways
- Long-term PM2.5 exposure increases incident Alzheimer disease risk in older adults, with slightly stronger associations after prior stroke and minimal mediation by hypertension, depression, or stroke.
- Epidemiologic syntheses link ambient air pollution to ischemic stroke, plausibly via gut- and lung-barrier effects on immunity and microbiome composition, supporting exposure-reduction strategies.
In recognition of National Public Health Week, held April 6-12, NeurologyLive summarizes recent literature showing that environmental exposures are associated with increased risk of neurologic disorders.
Environmental exposures are increasingly being recognized as contributors to neurologic disease risk across the lifespan. For example, recent evidence suggests that conditions such as
Air Pollution Exposure and Alzheimer Disease Risk
A 2026 nationwide cohort study, published in PLoS Medicine, examined the association between long-term exposure to fine particulate matter (PM2.5) and AD. Led by Yanling Deng, PhD, postdoctoral research fellow in the Gangarosa Department of Environmental Health at Emory University Rollins School of Public Health, the study used administrative health data with modeled air pollution exposure estimates to assess incident AD over time.1
The study included 27.8 million US Medicare beneficiaries aged 65 years and older from 2000 to 2018, with approximately 3.0 million incident AD cases identified. Higher exposure to PM2.5 was associated with an increased risk of AD (hazard ratio [HR] per interquartile range [3.8 µg/m³] increase, 1.085; 95% CI, 1.078–1.091), with a slightly stronger association observed among individuals with prior stroke (HR, 1.105; 95% CI, 1.096–1.114).
Additional findings showed that PM2.5 exposure was also associated with increased risks of hypertension, depression, and stroke; however, mediation analyses suggested these factors accounted for only a small proportion of the observed association with AD. These findings support air pollution as a potentially modifiable environmental risk factor for neurodegeneration and reinforced the need for population-level exposure reduction strategies to mitigate dementia risk.
Ambient Air Pollution and Stroke Risk
A 2024 review of epidemiologic studies, published in Cells, examined the relationship between ambient air pollution exposure and stroke incidence.2 Conducted by coauthors Alexandria Ruggles, MSc, and Corinne Benakis, PhD, both researchers of the Institute for Stroke and Dementia Research at the University Hospital of the LMU Munich in Germany, the analysis synthesized data from multiple cohort and case-control studies, using standardized exposure metrics and statistical pooling methods to assess risk across populations.
Findings suggested that environmental toxins, absorbed through the gastrointestinal tract or inhaled via the lungs, may influence immune responses and the microbiome at key barrier sites, potentially contributing to stroke risk. Exposure to fine particulate matter and other pollutants was consistently associated with increased risk of ischemic stroke, with some evidence of a dose-response relationship. Overall, the results support air pollution as a potential environmental risk factor for cerebrovascular disease and highlight the importance of strategies aimed at reducing exposure.
The authors noted that strategies to reduce the impact of fine particulate matter exposure may include further research on the systemic effects of environmental toxins, particularly at the gut and lung interfaces, and their role in stroke onset. For example, dietary approaches, such as increased intake of fiber and polyphenol-rich foods, have been associated with reduced bioavailability of xenobiotics by limiting their absorption. Further characterization of gut and lung microbiomes in relation to immune responses may also help inform therapeutic strategies targeting microbiome–host interactions
Environmental Pesticide Exposure and Neurodevelopmental Disorders
A 2024 published population-based cohort study investigated the association between environmental pesticide exposure and neurodevelopmental outcomes in pediatric patients.3 Conducted by senior author Rubén Trigueros, PhD, professor in the Department of Psychology at the University of Almeria in Spain, the study utilized geospatial data to estimate pesticide exposure levels in residential areas and linked these data to pediatric health records to identify diagnoses of neurodevelopmental disorders.
The cohort included 4,830 pediatric patients who followed over 11 years in a population of 119,897 across areas with high, medium, and low greenhouse gas concentrations. Findings showed that chromosomal abnormalities were the most common prenatal condition (28.6%), whereas intrauterine physical factors were least frequent (0.5%). Among perinatal diagnoses, gestational age less than 32 weeks was most prevalent (25%), whereas hyperbilirubinemia requiring exchange transfusion and birth complications were least common (0.4%). In the postnatal period, brain injury was the most frequently identified condition (36.7%), whereas unspecified abnormalities were least common (3.1%).
Overall, the findings demonstrate that regions with higher greenhouse concentrations were associated with increased rates of neurodevelopmental disorders, particularly among boys, as well as a younger age at referral. In addition, etiologic patterns varied by timing of diagnosis, with chromosomal abnormalities more common in prenatal cases, gestational age less than 32 weeks in perinatal cases, and brain injury in postnatal cases. Authors noted that further research is warranted to evaluate the relationship between pesticide exposure and neurodevelopmental disorders.
Prenatal Environmental Factors and Autism Spectrum Disorder Risk
A 2026 prospective cohort study, published in Pediatric Research, examined the role of prenatal environmental exposures and birth-related factors in autism spectrum disorder (autism) risk.4 Led by Lada Holland, PhD, project assistant at the Florey Institute of Neuroscience and Mental Health at The University of Melbourne, the study followed pregnant individuals and their offspring, collecting detailed data on environmental exposures, birth outcomes, and developmental assessments over time.
Factors associated with an increased likelihood of autism included maternal health factors such as higher prepregnancy body mass index (P = 0.005), preexisting mental health conditions, and selective serotonin reuptake inhibitor use, as well as environmental exposures including passive tobacco smoke (P = 0.003) and vinyl flooring (P = 0.008). Demographic factors, including socioeconomic disadvantage, were also associated with increased likelihood. In contrast, factors associated with a decreased likelihood of autism included maternal dietary factors, such as higher intake of folic acid, magnesium, and iron, and adherence to established dietary guidelines.
These findings support a multifactorial model of autism etiology, in which environmental and biological factors interact to influence neurodevelopment, and emphasize the importance of prenatal care and exposure reduction strategies. Authors noted that further studies should explore the composite effects of these prenatal and birth factors on autism outcomes via shared biological pathways, such as inflammation, and oxidative stress, in concert with genetic predisposition.
Gut Microbiome and Environmental Neurotoxicity
A 2026 review of recent studies, published in Frontiers Microbiology, explored how environmental pollutants, including air pollutants, heavy metals, persistent organic pollutants, and emerging contaminants, influence neurological health through alterations in the gut microbiome.5 Conducted by senior author Yi Huang, PhD, professor at Chengdu University of Technology, findings showed that exposure to these agents was associated with alterations in microbial composition, metabolic activity, and host–microbe signaling.
Additional results demonstrated that changes in microbial-derived metabolites, such as short-chain fatty acids, bile acids, and tryptophan derivatives, were linked to impaired intestinal barrier integrity and disrupted immune homeostasis. These microbiota-mediated disturbances were associated with oxidative stress, chronic inflammation, and neuroendocrine dysregulation, which may contribute to metabolic disorders, immune imbalance, neurotoxicity, and carcinogenesis.
Authors noted that mechanistically, pathways involving redox imbalance, activation of Toll-like receptor 4 (TLR4)/NF-κB and NOD-like receptor family pyrin domain-containing 3 (NLRP3), and dysregulation of aryl hydrocarbon receptor (AhR) signaling were identified as key links between environmental exposures and disease. Overall, the review highlights the gut microbiota as a potential target for interventions aimed at mitigating the health effects of environmental pollution and supporting disease prevention strategies.
Environmental Neurogenomics and Disease Susceptibility
A 2026 published review examined current knowledge on how environmental exposures interact with genetic susceptibility to influence neurological disease risk. Led by Mia Yang Ang, PhD, senior lecturer in the Department of Biomedical Sciences at Sunway University in Malaysia, the study synthesized findings from molecular, epidemiological, and epigenetic studies to describe how environmental factors can modify gene expression and contribute to disease pathogenesis.
In the review, studies showed that advancements in environmental neurogenomics have clarified how lifelong environmental exposures interact with genetic susceptibility to influence the onset and progression of disorders such as AD and PD. Authors noted that these findings support a shift from a gene-centric model to a more comprehensive framework that considers the interplay between genetic and environmental factors. Authors also identified several priorities to advance environmental neurogenomics toward translational application.
These include the development of large-scale, longitudinal exposome cohorts that integrate genomic and multiomics data with detailed environmental exposure assessments. Additional efforts may involve identifying and validating molecular and epigenetic biomarkers of cumulative neurotoxic exposure, incorporating gene-environment interactions into risk prediction models, and translating research findings into clinical decision-support tools. These insights emphasize the importance of integrating environmental exposure data into precision medicine approaches to better predict and prevent neurological disease.
Public Health Implications
Combing through the recent updates in literature, research clearly shows that environmental exposures are modifiable risk factors that may influence neurologic health at both individual and population levels. Studies suggest that reductions in exposures such as air pollution, pesticides, and other neurotoxic agents could possibly decrease the risk of neurologic disease and improved long-term outcomes. Overall, these data support the consideration of environmental factors in clinical assessment and management, as well as the development of public health policies aimed at reducing harmful exposures.

















