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Exposure to ozone (O 3) and nitrogen dioxide (NO 2) are related to pulmonary dysfunctions and various lung diseases, but the underlying biochemical mechanisms remain uncertain. Herein, the effect of inhalable oxidizing gas pollutants on the pulmonary surfactant (PS, extracted from porcine lungs), a mixture of active lipids and proteins that plays an important role in maintaining normal respiratory mechanics, is investigated in terms of the interfacial chemistry using in-vitro experiments; and the oxidative stress induced by oxidizing gases in the simulated lung fluid (SLF) supplemented with the PS is explored. The results showed that O 3 and NO 2 individually increased the surface tension of the PS and reduced its foaming ability; this was accompanied by the surface pressure-area isotherms of the PS monolayers shifting toward lower molecular areas, with O 3 exhibiting more severe effects than NO 2. Moreover, both O 3 and NO 2 produced reactive oxygen species (ROS) resulting in lipid peroxidation and protein damage to the PS. The formation of superoxide radicals (O 2 •–) was correlated with the decomposition of O 3 and the reactions of O 3 and NO 2 with antioxidants in the SLF. These radicals, in the presence of antioxidants, led to the formation of hydrogen peroxide and hydroxyl radicals (•OH). Additionally, the direct oxidation of unsaturated lipids by O 3 and NO 2 further caused an increase in the ROS content. This change in the ROS chemistry and increased •OH production tentatively explain how inhalable oxidizing gases lead to oxidative stress and adverse health effects. In summary, our results indicated that inhaled O 3 and NO 2 exposure can significantly alter the interfacial properties of the PS, oxidize its active ingredients, and induce ROS formation in the SLF. The results of this study provide a basis for the elucidation of the potential hazards of inhaled oxidizing gas pollutants in the human respiratory system. [Display omitted] • Oxidizing gases impacted the surface tension, phase behavior, and foaming ability of the PS. • Lipid peroxidation and protein damage of the PS were induced by oxidizing gas-phase air pollutants. • O 3 exhibited stronger adverse effects to the PS in comparison to NO 2. • Both ROS and oxidizing gas air pollutants contributed to oxidative damage of the PS. [ABSTRACT FROM AUTHOR]

The relationship between microplastics (MPs) and human respiratory health has garnered significant attention since inhalation constitutes the primary pathway for atmospheric MP exposure. While recent studies have revealed respiratory risks associated with MPs, virgin MPs used as plastic surrogates in these experiments did not represent the MPs that occur naturally and that undergo aging effects. Thus, the effects of aged MPs on respiratory health remain unknown. We herein analyzed the interaction between inhalable aged MPs with lung surfactant (LS) extracted from porcine lungs vis-à-vis interfacial chemistry employing in-vitro experiments, and explored oxidative damage induced by aged MPs in simulated lung fluid (SLF) and the underlying mechanisms of action. Our results showed that aged MPs significantly increased the surface tension of the LS, accompanied by a diminution in its foaming ability. The stronger adsorptive capacity of the aged MPs toward the phospholipids of LS appeared to produce increased surface tension, while the change in foaming ability might have resulted from a variation in the protein secondary structure and the adsorption of proteins onto MPs. The adsorption of phospholipid and protein components then led to the aggregation of MPs in SLF, where the aged MPs exhibited smaller hydrodynamic diameters in comparison with the unaged MPs, likely interacting with biomolecules in bodily fluids to exacerbate health hazards. Persistent free radicals were also formed on aged MPs, inducing the formation of reactive oxygen species such as superoxide radicals (O 2 •–), hydrogen peroxide (HOOH), and hydroxyl radicals (•OH); this would lead to LS lipid peroxidation and protein damage and increase the risk of respiratory disease. Our investigation was the first-ever to reveal a potential toxic effect of aged MPs and their actions on the human respiratory system, of great significance in understanding the risk of inhaled MPs on lung health. [Display omitted] • The differences in potential health risks between aged and unaged MPs were explored. • Aged MPs exerted a greater impact on the interfacial properties of lung surfactant relative to unaged MPs. • The adsorption of phospholipids and proteins promoted agglomeration of MPs. • The higher toxicity of aged MPs stems from the environmentally persistent free radicals that are formed. [ABSTRACT FROM AUTHOR]