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Respiratory risks of microplastics and nanoplastics: Where? What? How?
Summary
Researchers systematically reviewed experimental and epidemiological evidence linking inhaled microplastics and nanoplastics to pulmonary disorders including COPD, asthma, and fibrosis, identifying oxidative stress as the dominant initiating mechanism that cascades into mitochondrial dysfunction, inflammation, barrier disruption, and multiple forms of cell death.
Microplastics (MPs) and nanoplastics (NPs) are pervasive and persistent environmental pollutants raising growing concerns regarding their potential hazards to human respiratory health. This review systematically summarizes current epidemiological evidence and experimental findings concerning the respiratory toxicity of MPs and NPs. Exposure to these particles is associated with various pulmonary disorders, including pneumonia, chronic obstructive pulmonary disease, asthma, and other pathological lung injury. At the molecular level, MP- and NP-induced toxicity primarily involves oxidative stress, leading to mitochondrial dysfunction and endoplasmic reticulum stress. This oxidative damage triggers diverse forms of cell death, such as apoptosis, pyroptosis, ferroptosis, and autophagy. Furthermore, MPs and NPs induce pulmonary inflammation, disrupt the integrity of the alveolar-capillary barrier, promote pulmonary fibrosis, and cause DNA damage, mainly via oxidative stress pathways. This review also identifies critical directions for future research on the respiratory toxicity of MPs and NPs. Overall, this review highlights the respiratory health risks associated with MPs and NPs, emphasizing mechanisms involving oxidative stress, inflammation, and fibrosis, and underscores the urgent need for further investigation. It provides essential toxicological evidence and insights that could inform the development of effective protective strategies.