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Chronic lung tissue deposition of inhaled polyethylene microplastics may lead to fibrotic lesions
Summary
In a mouse study, inhaled polyethylene microplastics accumulated in lung tissue over 90 days of repeated exposure, causing chronic inflammation, immune changes, and early signs of lung scarring (fibrosis). Even at the lowest doses, the microplastics triggered inflammatory cell buildup and thickening of lung walls. These findings suggest that long-term breathing of airborne microplastics could lead to permanent lung damage, which is concerning given rising levels of plastic particles in indoor and outdoor air.
Given the expected increase in exposure to airborne microplastics, we here aimed to assess the acute and subchronic toxicity of inhaled polyethylene microplastics (PE-MPs). At 24 h post-exposure (0, 125, 250, and 500 μg/lung), PE-MPs were found within alveolar macrophages in the lungs of PE-MP-treated mice, along with an increase in the total number of pulmonary cells and higher pulmonary levels of LDH, CXCL-1, and CCL-2. Similarly, when exposed twice for 14 days (weekly, 0, 125, 250, and 500 μg/lung), the total number of pulmonary cells and the levels of pulmonary chemokines and blood IgE were elevated, whereas the expression of surface proteins related to cell-to-cell interactions was inhibited on the pulmonary cells of mice exposed to PE-MPs. After 90 days of repeated intratracheal instillation (0, 5, 25, and 50 μg/lung), PE-MPs deposited in the lung tissues and increased dose-dependently both the total number of pulmonary cells and inflammatory cytokine levels. Furthermore, infiltration of inflammatory cells, formation of multinucleated giant cells, and thickening of the alveolar wall were noted in the lung tissues of PE-MP-treated male and female mice. While the production of IgA and IgG was inhibited in male and female mice following exposure to PE-MPs, the levels of IgE and IgM tended to increase. In addition, the expression of fibrillar collagens was enhanced in the lung tissues of PE-MP-treated mice. Taken together, we suggest that chronic pulmonary exposure to PE-MPs may cause immune dysregulation by impairing the antigen-presenting function of alveolar macrophages and that PE-MP-induced chronic inflammation may be linked to fibrotic lesions. In addition, we believe that these hypotheses will be clarified by further study of the effects of chronic exposure to PE-MPs on lung function.