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The impaired response of nasal epithelial cells to microplastic stimulation in asthma and COPD
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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.
Microplastic particles from the air are inhaled and accumulate in the lungs, potentially causing immunological reactions and airway tissue injury. This study aimed to evaluate the biological effects of polyamide fibres on nasal epithelium co-cultivated with macrophages in control, asthma, and COPD groups. Nasal epithelial cells alone or in co-culture with monocyte-derived macrophages were exposed to polyamide fibres for 48 h. We identified 8 differentially expressed genes (DEGs) in controls, 309 DEGs in asthma (including ANKRD36C, BCL2L15, FCGBP, and IL-19), and 22 DEGs in COPD (e.g., BCL2L15, IL-19, CAPN14, PGBD5, PTPRH), particularly in epithelial/moMφ co-cultures. Microplastic exposure induced inflammatory cytokine secretion only for IL-8 production in controls (epithelial/ moMφs co-culture) and asthmatic (monoculture) epithelial cells in contrast to PM, which was a strong inflammatory inducer. Gene Ontology analysis revealed that microplastic exposure affected sterol and cholesterol biosynthesis, secondary alcohol metabolism, and acetyl-CoA metabolism in asthma, and cell motility, chemokine signaling, leukocyte migration, and chemotaxis in COPD. Microplastic stimulation altered the response of airway epithelial cells in obstructive lung diseases differently than in controls, linking to Th2 inflammation, stress response modulation, and carcinogenesis. Asthmatic and COPD epithelial cells are more susceptible to damage from microplastic fibre exposure.
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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."
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Researchers exposed both healthy and asthmatic mice to airborne microplastics and found significant lung inflammation, immune activation, and increased mucus production in both groups. Microplastic particles were taken up by immune cells called macrophages, and gene analysis revealed changes in immune response, cellular stress, and cell death pathways. The study suggests that inhaling microplastics may worsen respiratory health in both normal and vulnerable populations.
Potential toxicity of micro- and nanoplastics in primary bronchial epithelial cells of patients with chronic obstructive pulmonary disease
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Researchers investigated how micro- and nanoplastics affect lung cells taken from patients with chronic obstructive pulmonary disease (COPD), a condition that already impairs breathing. The study aimed to determine whether plastic particle exposure poses additional toxic risk to people whose airways are already compromised.
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model
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Mouse experiments found that microplastic exposure worsened inflammatory responses in healthy lungs but did not further aggravate airway inflammation in mice with pre-existing asthma, suggesting the lung's response to microplastics depends on baseline immune state.
Distinct mitochondrial response patterns to PM2.5 and microplastic exposure in healthy and asthmatic bronchial epithelial cells: an exploratory pilot study
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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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