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Micro and nanoplastics meet lung surfactant: interaction mechanisms across in vivo, in vitro, and in silico studies
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This review summarizes existing research on how tiny inhaled plastic particles affect lung surfactant, a fluid that helps keep air sacs open. Studies in animals, lab cells, and computer models found that these particles can interfere with how surfactant spreads and functions, which may contribute to inflammation and worsen lung disease.
Micro- and nanoplastics (MNPs) are emerging contaminants found throughout the environment, with growing concern over their potential health impacts, particularly on the respiratory system, as inhalation is a major route for these particles into the internal physiology. This review integrates in vivo, in vitro and in silico evidence on how inhaled micro and nanoplastics interact with lung surfactant (LS), a lipid protein system that stabilizes alveoli by lowering surface tension. Across models, MNP exposure has been linked to reduced surfactant adsorption and spreading, altered film compressibility, collapse behavior, disrupted lipid and protein organization, which together may promote inflammation and worsen pre-existing lung disease. By aligning outcomes across experimental scales, we identify gaps that currently limit risk interpretation like inconsistent reporting of particle size, shape, weathering, and dose metrics relevant to inhalation; simplified LS formulations and assays that do not reproduce breathing like compression expansion, humidity, and the air liquid interface; limited linkage between molecular interactions and functional endpoints such as oxygenation, mechanics, and clearance; and insufficient integration of simulations with experimentally constrained parameters. We conclude with methodological priorities for harmonized study designs and cross-validation to better predict respiratory hazards from airborne MNPs.
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Scientists found that micro and nanoplastics from common products like foam packaging, lunch boxes, and water bottles can impair the function of pulmonary surfactant, the crucial substance that keeps our lungs from collapsing. Polystyrene foam particles caused the most damage, both in lab tests and in mice, where they triggered lung inflammation. The nanoplastic fraction, though a small part of the total mass, appeared to drive most of the harm by forming clumps with the surfactant at the air-liquid surface in the lungs.
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Researchers used molecular simulation to study how microplastics in indoor dust interact with lung-lining lipid molecules, finding that MP surfaces adsorb lung surfactant components in ways that could impair pulmonary surfactant function and increase inflammatory signaling after inhalation.
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Researchers investigated how oligomeric plastic particles interact with lung surfactant bilayers to understand inhalation risks, proposing that as plastics break down to oligomeric sizes through environmental degradation they may penetrate and disrupt the protective surfactant layer lining the lungs.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.