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Microplastics Modulate the Structural Response of Cedar Pollen Allergen to Atmospheric Stressors: Spectroscopic Evidence from UV-NO2 Exposure
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Laboratory tests examined how tiny plastic particles (microplastics) affect the structure of cedar pollen proteins when exposed to pollutants like nitrogen dioxide and ultraviolet radiation. The microplastics changed how the proteins responded to these stressors, sometimes preventing certain types of damage depending on which pollutant was present. The findings suggest microplastics actively alter how allergen proteins behave in polluted air rather than simply carrying them passively.
The atmospheric co-occurrence of microplastics, reactive nitrogen species, and solar radiation represents an emerging, yet poorly characterized, exposure scenario for airborne allergens. Here, we investigated whether laboratory-aged polyethylene terephthalate (PET) microplastics modulate the structural fate of cedar pollen proteins under nitrogen dioxide (NO2), ultraviolet (UV) radiation, and combined NO2 + UV stress. Employing a multi-spectroscopic approach integrating UV-visible (UV-Vis) absorption, steady-state and synchronous fluorescence, Stern–Volmer quenching analysis, Parallel Factor Analysis (PARAFAC)-resolved excitation–emission matrices (EEMs), and Fourier-transform infrared (FTIR) spectroscopy with amide I deconvolution, we suggest that aged PET microplastics exert stressor-dependent and mechanistically distinct effects. Under nitrative stress, microplastics may selectively sequester structurally perturbed and oxidized protein species from the soluble phase, effectively biasing the remaining population toward native-like conformers. Under photolytic stress, microplastics attenuate UV-induced β-sheet loss, consistent with the selective partitioning of damaged species into the solid phase or restricted conformational mobility. Strikingly, under combined NO2 + UV stress, microplastics dramatically enhance protein–pollutant binding cooperativity (binding constant, Kb = 81.5 L·mol−1, Hill coefficient, n = 1.79), indicative of increased interaction complexity and ground-state complex formation at the PET–protein interface, an effect not observed under either stressor alone. Collectively, these findings provide evidence that aged PET microplastics are not passive carriers but active modulators of allergen stability and chemical modification, potentially functioning as adsorbents, reaction platforms, and selective filters that reshape the population distribution of protein species in the soluble atmospheric compartment. This work provides a mechanistic foundation for evaluating environmental fate and provides mechanistic insights that may guide future toxicological investigations of pollen allergens in microplastic-polluted urban atmospheres.
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