What question did this study set out to answer?

The study aims to evaluate how PM2.5 and microplastic exposure affects mitochondrial function in bronchial epithelial cells from healthy and asthmatic donors.

June 27, 2026Open Access

Distinct mitochondrial response patterns to PM2.5 and microplastic exposure in healthy and asthmatic bronchial epithelial cells: an exploratory pilot study

Key Points

The study aims to evaluate how PM2.5 and microplastic exposure affects mitochondrial function in bronchial epithelial cells from healthy and asthmatic donors.
Primary bronchial epithelial cells from healthy and asthmatic donors were cultured and exposed to PM2.5 and/or microplastics for 24 hours.
Mitochondrial activity and reactive oxygen species production were measured using Seahorse technology.
Cells were treated with control, lipopolysaccharide (LPS), cigarette smoke extract (CSE), and allergic stimuli (house dust mite + IL-13).
In healthy cells, PM2.5 exposure increased maximal mitochondrial respiration and ATP production with no exhaustion observed.
Asthmatic cells did not show increased mitochondrial activity despite elevated reactive oxygen species production, indicating impaired responses.
Microplastic exposure enhanced mitochondrial metabolism in certain conditions for asthmatic cells but reduced cell viability after 48 hours when exposed to LPS.

Abstract

Air pollution impairs mitochondrial biology through mechanisms driven by oxidative stress, excessive reactive oxygen species (ROS) production, apoptosis, and tissue injury. Specific components of air pollution—particularly PM 2.5 and microplastic fibers — disrupt mitochondrial function via multiple interconnected pathways. The study aimed to evaluate the mitochondrial function in bronchial epithelial cells from healthy and asthmatic donors following exposure to PM 2.5 and/or microplastics. Primary bronchial epithelial cells from healthy and asthma groups were cultured in control, lipopolysaccharide (LPS), cigarette smoke extract (CSE), and allergic (house dust mite HDM + IL-13)-treated models and stimulated with microplastic fibers and/or PM 2.5 for 24 h. The mitochondrial activity (Seahorse) and ROS production were measured. In healthy cells, 24-h exposure to PM 2.5 increased maximal mitochondrial respiration across all conditions and basal and ATP-dependent production in the CSE-stimulated group, with no signs of exhaustion. In asthma cells, however, ROS production was not matched by increased mitochondrial activity, suggesting impaired adaptive responses. PM 2.5 exposure partially attenuated the increase in maximal respiration induced by allergic stimulation in asthma cells. Microplastic exposure exhibited a distinct pattern: it did not increase ROS, but enhanced mitochondrial metabolism (basal respiration and ATP-dependent respiration) in LPS and CSE, and HDM/IL-13 (maximal respiration and ATP-dependent respiration) treated asthma cells, yet reduced cell viability after 48 h in LPS-treated asthma cells, suggesting early mitochondrial fatigue under this condition. PM 2.5 exposure alters mitochondrial activity via oxidative stress, imposing greater metabolic stress and potential harm to bronchial epithelial cells from individuals with asthma, while exerting lower negative effects on cells from healthy donors. Microplastic exposure had context-dependent effects in asthmatic bronchial epithelial cells.

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