Environmental Pollution and Related Redox Pathways Contributing to Retinal Diseases.
- 1Department of Ophthalmology, University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, 55131 Mainz, Germany.
- 2Vista Alpina Eye Clinic, Bahnhofplatz 1A, 3930 Visp, Switzerland.
Abstract
Environmental pollution, a detrimental consequence of industrialization and globalization, is increasingly recognized as a potential risk factor for a wide range of human diseases, including retinal disorders. The retina is particularly vulnerable to environmental stressors, including particulate matter, nitrogen oxides, carbon monoxide, traffic-related noise, and extreme environmental conditions such as elevated temperatures. Epidemiological and experimental evidence suggests that these exposures may contribute to the development and progression of retinal diseases through mechanisms involving oxidative stress, chronic inflammation, immune dysregulation, and vascular dysfunction. These processes may ultimately contribute to retinal vasculopathies and degenerative disorders. Consequently, the pathophysiological mechanisms linking environmental exposures to retinal injury have received increasing attention in recent years. This review provides a disease-centered perspective on the relationship between environmental pollution and retinal diseases, integrating epidemiological evidence with experimental findings across specific retinal disorders. Among the environmental pollutants investigated to date, fine particulate matter (PM2.5) and nitrogen dioxide (NO₂) have the most consistent epidemiological evidence for adverse effects on retinal health, particularly in relation to age-related macular degeneration (AMD). The review also discusses the methodological limitations and heterogeneity of the available evidence, as well as current knowledge gaps and future research perspectives.
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BibTeX
@article{zhang2026environmental,
title = {{Environmental Pollution and Related Redox Pathways Contributing to Retinal Diseases.}},
author = {Liyu Zhang and Qi Tang and Elsa Wilma Böhm and Felix Mathias Wagner and Adrian Gericke},
journal = {Antioxidants (Basel, Switzerland)},
year = {2026},
month = oct,
doi = {10.3390/antiox15101258},
url = {https://europepmc.org/article/MED/42939831},
note = {CC BY},
}
RIS
TY - JOUR
TI - Environmental Pollution and Related Redox Pathways Contributing to Retinal Diseases.
AU - Liyu Zhang
AU - Qi Tang
AU - Elsa Wilma Böhm
AU - Felix Mathias Wagner
AU - Adrian Gericke
PY - 2026
DA - 2026/10/01
JO - Antioxidants (Basel, Switzerland)
DO - 10.3390/antiox15101258
UR - https://europepmc.org/article/MED/42939831
AB - Environmental pollution, a detrimental consequence of industrialization and globalization, is increasingly recognized as a potential risk factor for a wide range of human diseases, including retinal disorders. The retina is particularly vulnerable to environmental stressors, including particulate matter, nitrogen oxides, carbon monoxide, traffic-related noise, and extreme environmental conditions such as elevated temperatures. Epidemiological and experimental evidence suggests that these exposures may contribute to the development and progression of retinal diseases through mechanisms involving oxidative stress, chronic inflammation, immune dysregulation, and vascular dysfunction. These processes may ultimately contribute to retinal vasculopathies and degenerative disorders. Consequently, the pathophysiological mechanisms linking environmental exposures to retinal injury have received increasing attention in recent years. This review provides a disease-centered perspective on the relationship between environmental pollution and retinal diseases, integrating epidemiological evidence with experimental findings across specific retinal disorders. Among the environmental pollutants investigated to date, fine particulate matter (PM2.5) and nitrogen dioxide (NO₂) have the most consistent epidemiological evidence for adverse effects on retinal health, particularly in relation to age-related macular degeneration (AMD). The review also discusses the methodological limitations and heterogeneity of the available evidence, as well as current knowledge gaps and future research perspectives.
SN - 2076-3921
ER -