Gut microbiome alterations associated with microplastics: Underestimated risk from tiny particle

Micro/nanoplastics (MNPs) have emerged as environmental pollutants, with their presence documented in marine, freshwater, and terrestrial ecosystems.1 MNPs originate from a variety of sources, including food packaging, industrial processes, clothing, cosmetics and construction materials, most of which are linked to human activities.2 They have been detected in a wide range of animals and plants, posing a substantial threat to numerous living organisms.3 These particles can enter the human body via different routes, such as food, inhalation and even intravenous injection.4 They have been detected in a range of human organs and body fluids, including gut, liver, lung, brain, testis, blood, semen, skeletal tissues and placenta.5 Gut microbiota are associated with a variety of diseases and disorders.6–10 Alterations in gut microbial composition induced by microplastics (MP) and nanoplastics (NP) can exacerbate some gut diseases, such as inflammatory bowel disease.11 MNP exposure may influence the gut microbiota, resulting in elevated susceptibility to infectious diseases. For instance, ingestion of polystyrene (PS) MP was found to alter the gut microbiota of silkworm, which potentially contributed to increased susceptibility to Bombyx mori nucleopolyhedrovirus.12 MNP‑induced gut microbiota dysbiosis may compromise colonization resistance and facilitate enteric infections, which deserves further investigation. MNP exposure disturbs the gut microbiota in various vertebrate animals. For instance, in the gut of silver carp exposed to polyethylene (PE) MP, the abundance of Cetobacterium, Clostridium_sensu_stricto_1 and norank_o_PeM15 decreased, whereas Cyanobium PCC-6307 and norank_o_Chloroplast increased.13 In murine models, polylactic acid (PLA) MP significantly enriched Helicobacter, Lachnospiraceae_A2 and Lachnospiraceae_NK4A136_group, while PLA NP increased the abundance of Helicobacter, Lachnospiraceae_NK4A136_group and Roseburia.14 Similarly, in zebrafish, exposure to PE MP reduced unclassified Bdellovibrio, Actinomycetales and unclassified Actinobacteria, while exposure to polyester (PES) MP resulted in decreases in Plesiomonas and unclassified TM7.15 MNP exposure similarly disrupts the gut microbiota in invertebrates. For example, exposure to PS MP altered the gut microbial communities of honeybees, significantly reducing Lactobacillus and increasing Bartonella.16 Similarly, ingestion of PS MP decreased the abundance of Vibrionaceae, Bacteroidaceae and Nitriliruptoraceae in the gut of silkworms.12 Moreover, both PE and PS MP exposure led to enrichment of Citrobacter and Lactococcus in the gut of darkling beetles.17 In humans, higher levels of MP exposure are associated with gut microbial dysbiosis. For instance, abundances of Anaerostipes, Veillonella and Blautia were significantly greater in adults with high MP exposure than in a low-exposure cohort.18 Similarly, in preschool children, the low-exposure group exhibited lower abundances of Alistipes, Rikenellaceae, Streptococcus and Streptococcaceae than the high-exposure group.19 Furthermore, higher abundances of Butyricicoccus, Coprococcus, Dorea, Fusobacterium and Ruminococcus_torques_group were observed in the high-exposure individuals compared with their low-exposure counterparts.20 Gut microbial dysbiosis induced by MNPs extends beyond the intestinal tract. For instance, in female zebrafish, gut microbiota dysbiosis caused by PS MP has been shown to mediate reproductive impairments through immune-metabolic endocrine crosstalk.21 Similarly, both oxidized and unmodified PE MP disrupted the gut microbiota–gut–brain axis, leading to neurotoxicity in mice.22 Moreover, oral exposure to polyhydroxyalkanoates (PHA) or polypropylene (PP) MP both disturbed the gut microbiome–gut–liver axis in mice, with PP MP inducing greater hepatotoxicity than PHA MP.23 The fast and accurate detection of MNP continues to present significant challenges. Currently, over 20 analytical approaches, such as µ-Fourier transform infrared spectroscopy, µ-Raman, laser direct infrared spectroscopy, pyrolysis coupled with gas chromatography, mass spectrometry and surface-enhanced Raman spectroscopy, are available for the detection, identification and quantification of MNP. However, most of these methods are time consuming and require laboratory settings.24 Moreover, detecting MNP in complex sample metrics (eg, biological samples) typically involves extensive and labor-intensive pretreatment steps, which limits detection efficiency.25 Furthermore, the efficient collection of certain sample types (eg, airborne particulates in contaminated air) remains technically challenging for reliable MNP analysis.26 Collectively, these methodological limitations lead to an underestimation of MNP distribution and concentrations across diverse samples and environmental compartments. Alterations in gut microbiota induced by MNP exposure are closely linked to environmental MNP levels. MNPs exhibit considerable variation across different countries and areas because environmental concentrations are affected by multiple factors that are likely to change significantly with the widespread adoption of alternative plastic materials or the implementation of effective interventions to reduce environmental plastic pollution.27 Moreover, measured MNP concentrations at a given site or in a specific sample can vary depending on the analytical method used, as there is currently no universally accepted gold-standard quantification technique.28 Therefore, future studies on the effects of MNPs on gut microbiota should also employ experimentally appropriate doses, particularly for plastic types that are not yet in widespread use. Some alternative aspects also warrant consideration in further research. First, while existing studies have predominantly examined the toxic effects of common MNPs such as PS, PE, polyvinyl chloride, polyethylene terephthalate and PP,29 greater attention should be directed toward a wider range of alternative polymer types. Second, although MP have been extensively investigated, research on their NP counterparts remains relatively limited. Third, despite the development of certain preventive and interventional measures to mitigate the spread and toxicity of MNPs in the intestinal environment, there is a need for novel strategies that are both effective and free of potential risks. Fourth, the potential health risks of promising alternative materials intended to replace conventional plastics need to be thoroughly assessed before their widespread adoption.30 Additionally, more rapid, accurate and reliable methods for the qualification and quantification of diverse MNPs across varied sample types must be developed and implemented.