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Air pollution and microplastic as modifiers of epithelial injury and repair in models of acute, chronic, and allergic airway inflammation
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Scientists exposed lab-grown human airway cells to air pollution particles and microplastic fibers, and found the combo was more damaging when the cells were already stressed—whether from allergies, smoking-related damage, or infection. This suggests that people with existing lung conditions like asthma or COPD may be especially vulnerable to the health effects of breathing in pollution and microplastics, since their airway cells have a harder time repairing themselves under this "double hit."
The toxic effects of air pollutants on the airway epithelium are associated with oxidative stress, a pro-inflammatory response, and impaired innate immune responses. The chronic exposure to noxious factors leads to cumulative damage to the alveolar compartment, reduced diffusion capacity, and impaired lung function. This study aimed to investigate the biological responses of bronchial epithelial cells exposed to PM and microplastic, following prior induction of acute, chronic, and allergic epithelial injury. Primary, normal bronchial epithelial cells were cultivated in air-liquid interface (ALI) in models of normal, acute (lipopolysaccharide (LPS) treated), chronic (cigarette smoke extract (CSE) treated for 14 days), and allergic (house dust mite (HDM) + IL-13 treated for 3 days). Simultaneously, cells were divided into two groups: uninjured or physically injured by a scratch. Cells were then stimulated with microplastic fibres (200 μg/cm) and PM (50 μg per insert) applied to the top of the epithelial cell layer for 48 h. Combined exposure to PM and microplastics induced profound cytotoxic effects across all models. Mechanical injury modulated inflammatory responses in a model-dependent manner, with the most pronounced dysregulation observed in allergically primed epithelial cells. In control and LPS-stimulated cultures, co-exposure to PM and microplastics significantly disrupted epithelial barrier integrity. PM and microplastic exposure were associated with increased TGF-β and EGFR expression across several injury models, with a tendency toward enhanced TGF-β signalling in secretory epithelial cells under chronic and allergic conditions, largely independent of mechanical injury. Overall, pollutant-induced responses varied according to the underlying epithelial injury state. Atmospheric pollutants influenced epithelial immune response, contributing to airway epithelial injury and affecting regenerative capacity, particularly when cellular biology was additionally compromised by bacterial, tobacco or allergic stimuli.
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Researchers exposed nasal lining cells from healthy people, asthma patients, and COPD patients to polyamide microplastic fibers and found that diseased airways responded very differently than healthy ones. Asthma cells showed changes in cholesterol metabolism and stress responses, while COPD cells showed altered immune cell movement and signaling. This suggests that people with existing respiratory conditions are more vulnerable to the harmful effects of inhaled microplastic fibers.
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Lab tests on airway cells found that fine air pollution particles (PM2.5) push healthy cells' energy-producing "engines" (mitochondria) to work harder without breaking down, but in cells from people with asthma, those same engines couldn't keep up—leaving them more stressed and vulnerable to damage. Microplastic fibers had a different, mixed effect: they boosted energy production in some asthma-related conditions but also caused cells to weaken over time when combined with certain triggers. This suggests people with asthma may be more biologically vulnerable to air pollution and microplastic exposure, highlighting why reducing
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Tiny plastic particles floating in the air we breathe may be doing more damage to our lungs than we realized. This review of existing research found that when these microplastics land in our airways, they can trigger cell stress, inflammation, and damage to the protective lining of our lungs—potentially making respiratory problems worse over time. While scientists still need more long-term studies to fully understand the risks, this research is an early warning sign that the plastic pollution in our air isn't just an environmental issue—it could be a health issue too.
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Scientists exposed lab-grown human airway cells to tiny nanoplastic particles (like those found in breathing air polluted with plastic waste) and found the particles weakened the protective barrier these cells normally form, while also triggering inflammation-related signals. This suggests nanoplastics could make airways more vulnerable, especially in people whose lung lining is already damaged or still developing—though this was shown in a lab model, not in humans breathing polluted air, so more research is needed to confirm real-world impact.
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