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Microplastics in the Lungs: Exposure Pathways, Pulmonary Deposition, Toxicological Effects, and Carcinogenic Potential

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This review summarizes existing research on tiny plastic particles found in human lungs after breathing them in. Lab studies on plastic particles showed inflammation, cell damage, and genetic damage, while human data remain limited but confirm microplastics are present in lungs, linked to inflammatory and fibrotic lung conditions.

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Microplastics (MPs) are recently discovered environmental pollutants that have been increasingly gaining importance due to their harmful effects on human health, especially via inhalation and deposition in the respiratory tract. We review the potential respiratory system exposures and pathways of inhaled microplastics as well as the evidence regarding the impact on pulmonary inflammation, fibrosis, cell damage, and carcinogenic pathways. PubMed, Scopus, and Google Scholar were used for the literature review of studies published within the last 10 years. The research studies that met inclusion criteria were reviewed, and abstracts and titles of the studies were retrieved. Many research studies have demonstrated that inhaled microplastics can bypass mucociliary clearance and end up in the distal airways and alveoli. Once localized, the microplastic can come with chronic inflammation, oxidative stress, genetic damage, and interaction with other air pollutants. In experimental studies, particles of polystyrene and polyethylene were found to be cytotoxic and genotoxic, but it is hard to apply the results to human exposure due to the fact that the concentrations used in the lab are often higher than those in the environment. Human data is indeed scarce; it is established that the lungs of human beings contain microplastics, and the associations with fibrotic and inflammatory lung disorders support the biological relevance of microplastics. A summary of the evidence available indicates that there are several ways in which the presence of microplastics could impact respiratory health. However, the interrelationship between oxidative stress, inflammation and fibrosis is less defined, as most of the evidence has been generated in experimental rather than real environments, and is not well established in the public domain. The evidence, both experimental and human, is present for potential research into microplastics' relation to lung cancer in humans, as well as reduction of exposure and regulation.

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