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The Effects ofMicroplastics and Nanoplastics (MNPs)on Chronic Airway Inflammation
Summary
This review pulls together lab and animal research suggesting that when we breathe in tiny plastic particles, common in polluted city air and certain workplaces, they may trigger inflammation, stress cells, and disrupt the natural bacteria living in our airways, potentially worsening conditions like asthma and COPD. While the evidence so far comes mostly from cells and animals rather than large human studies, it highlights a growing concern that everyday exposure to microplastics floating in the air could quietly affect lung health over time.
Abstract Over the past decades, vast amounts of plastic waste have been generated, leading to a substantial environmental burden and consequently to significant human exposure to microplastics and nanoplastics. Yet, the effects of micro-nanoplastics (MNPs) on health have only recently begun to be recognized. An increasing body of evidence may suggest that these particles can cause growth inhibition, organ damage, reproductive toxicity, and disruption of the microbiota and metabolic pathways. Inhalation represents a major route of exposure, especially in urban and occupational settings. Inhaled MNPs may contribute to asthma pathogenesis and exacerbation through oxidative stress, mitochondrial dysfunction, epithelial barrier damage, T-helper 2 inflammation, and activation of inflammasome pathways. Likewise, preclinical data suggest that these particles may promote cell injury resembling chronic obstructive pulmonary disease, involving oxidative stress, ferroptosis, endoplasmic reticulum stress, and protease–antiprotease imbalance. Beyond direct effects on lung parenchymal cells, MNPs may disrupt the nasal and lung microbiota, potentially contributing to dysbiosis that may amplify inflammatory responses and epithelial dysfunction. This concise translational review aims to integrate molecular and cellular evidence from recent up-to-date in vitro and animal studies, together with emerging human data, to explore potential mechanisms through which MNP exposure may contribute to chronic airway inflammation.