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The rise and rise of plastic pollution

The rise and rise of plastic pollution

Keshav Raj Paudel is a senior researcher working in the field of chronic respiratory disease exploring the disease progression and pharmacological activity of drug candidates on various lung diseases (asthma, airway remodeling, COPD, and lung cancer) in experimental models (in vitro, in vivo, and ex vivo) using molecular, immunological, and biochemical assay. He has an interest in exploring the cell signaling pathways of various inflammation-related disorders induced by environmental pollutants such as bushfire smoke/particulate matter, air pollutants (urban particulate matter, traffic pollutants), and microplastics. Here, he explains his work investigating the Impact of Microplastic Inhalation on Lung Health.

Plastic pollution has become a pressing global environmental and public health concern, including in Australia, where awareness of the potential health impacts of microplastics is steadily increasing. Microplastics are tiny particles (<5mm in size) generated throughout the plastic lifecycle from production to disposal are now recognised as pervasive contaminants capable of entering ecosystems, food chains, and ultimately the human body. While earlier research predominantly focused on the marine environment and ingestion pathways, growing evidence indicates that inhalation may be an equally, if not more, significant route of exposure. Because microplastics are lightweight, airborne, and able to circulate freely in indoor and outdoor air, they can be inhaled deeply into the respiratory tract, raising important questions about their effects on lung health.

In 2023, our team received funding from the Sydney Partnership for Health, Education, Research and Enterprise (SPHERE) – Triple I to investigate the acute and chronic impacts of microplastic inhalation using an in vivo mouse model. This project represents one of the first systematic efforts in Australia to examine how microplastic exposure through the air may influence respiratory function and lung pathology.

In our acute exposure model, mice were subjected to one week of intranasal microplastic administration. At this early stage, we observed a modest increase in total cells within the bronchoalveolar lavage fluid (BALF), predominantly driven by macrophages; however, lung histology remained largely unchanged. These findings suggest that short-term exposure may trigger an early immune response without yet causing structural damage to lung tissue.

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In contrast, the chronic exposure model revealed markedly different outcomes. After eight weeks of repeated microplastic inhalation designed to reflect the human equivalent of exposure levels in highly polluted environments, we observed significant increases in BALF inflammatory cells, including macrophages, neutrophils, and lymphocytes. These cellular changes were accompanied by elevated cytokine levels, indicating heightened inflammatory activity. Histological analysis demonstrated clear evidence of lung parenchymal inflammation, collagen deposition suggestive of early fibrotic processes, and an increase in mucus-secreting cells, all of which point toward sustained and potentially progressive lung injury.

Taken together, our findings indicate that prolonged microplastic inhalation at environmentally relevant concentrations is sufficient to induce substantial respiratory inflammation and tissue damage. These results underscore the urgent need for further research to identify the molecular mechanisms underlying microplastic-induced lung injury and to explore potential genetic and therapeutic targets that could mitigate or prevent these harmful effects.

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