From exposure to infection: mechanisms linking emerging pollutants to increased viral susceptibility

Emerging pollutants (EPs) - including microplastics (MPs), nanoplastics (NPs), pesticides, antibiotics (ABX), particulate matter (PM), and heavy metals (HMs) - are pervasive environmental contaminants increasingly recognized as critical non-infectious co-factors in viral pathogenesis. While epidemiological evidence links chronic environmental exposure to EPs with heightened respiratory viral morbidity, the biological plausibility and cellular trajectories driving this susceptibility remain incompletely defined. This review synthesizes current epidemiological, toxicological, and immunological insights to bridge the gap between environmental exposure and clinical infection, illustrating how EPs facilitate the transition from exposure to infection by systematically compromising host defenses. We elucidate the disruption of three hierarchical layers: (1) physical barrier breach, where EPs degrade epithelial integrity and mucosal defenses to facilitate viral entry; (2) immune dysregulation, characterized by oxidative stress-driven inflammation and the suppression of innate and adaptive surveillance; and (3) microbiota-host axis perturbation, where EPs-induced dysbiosis dismantles metabolic networks essential for antiviral immunity. Furthermore, we highlight direct non-immune mechanisms, including the role of MPs as viral vectors and the pollutant-induced upregulation of viral receptors. Integrating these mechanisms is critical for refining environmental risk assessment models and informing targeted public health strategies within a "One Health" framework to mitigate the viral disease burden associated with environmental pollution.