Microplastics and our gut: what a new systematic review reveals about the microbiome and health risks

Microplastics (particles <5 mm) and even smaller nanoplastics are already ubiquitous, from water and food to the air in our homes. In recent years, they have been found in human lungs, placenta, faeces and blood. A logical next question is how these particles affect the gut microbiome, which is involved in immunity, metabolism and gut barrier protection. A new study in BMC Gastroenterology is the first to systematically collect human and “human-relevant” data on this topic, providing a comprehensive picture of how microbiota composition and function are disrupted by exposure to microplastics.

Background of the study

The production and accumulation of plastic waste has been increasing for decades, and its fragmentation leads to the formation of microplastics (particles <5 mm) and even smaller nanoplastics. These particles are persistent in the environment, capable of long-distance transport, and accumulate in organisms, including humans. The detection of microplastics and nanoplastics in air, water, food, and household products makes everyday exposure virtually inevitable. Moreover, the particles have been found in the lungs, placenta, faeces, and blood, increasing concerns about their biological impact.

Exposure routes and why water and food are important

Humans come into contact with microplastics through ingestion, inhalation and skin contact, but the oral route is considered the main one: particles are widely present in food chains and drinking water systems - both tap and bottled. Due to the large daily volume of water consumption, this channel becomes a “chronic” and difficult-to-avoid source of microplastic intake. Once ingested, particles interact with the gastrointestinal tract before being excreted and can modify the local environment, including the microbiome.

Why the Gut Microbiome is the Target

The intestinal microbiota is critical for immune homeostasis, metabolism, and epithelial integrity. Its enzymatic activity produces short-chain fatty acids (SCFA) and AhR ligands, metabolites that support barrier and anti-inflammatory cascades. Dysbiosis (sustained shift in composition/function) is associated with barrier dysfunction, chronic low-grade inflammation, and metabolic disorders. Therefore, any factors that distort microbial communities and their metabolites have systemic consequences.

What was known before this review

Until recently, the literature has focused primarily on the environment and animal models. Experiments in mammals and aquatic organisms have shown that polymers such as PS, PE, PVC, and PET accumulate in the gut, reduce microbiota diversity, increase inflammation, and worsen colitis. Shortening of the colon, decreased mucus secretion, and increased risk of colorectal carcinogenesis have been reported with microplastic exposure. This has led to a demand for a “human-relevant” synthesis: what microbial shifts and functional impairments are observed in humans and human-based models.

Proposed mechanisms of influence on microbiota

• Physicochemical irritation: high specific surface area and reactivity of particles (especially nanofractions) are capable of damaging the epithelium and changing local niches for bacteria.
• Carriers of pollutants and pathogens: Microplastics can adsorb toxicants and serve as a “raft” for microbes, disrupting the ecosystem balance in the intestinal lumen.
• Shifts in composition and metabolism: a change in the ratio of large “framework” communities (Firmicutes/Bacteroidetes) and depletion of SCFA producers leads to a drop in buterate/propionate and a weakening of the barrier and immunomodulatory functions.
• Gas metabolites and inflammation: Increased proportions of H₂S producers (eg, Desulfobacterota) are associated with diarrhea/constipation, IBS and maintenance of inflammation.

Heterogeneity of Exposures: Why 'Type, Size, Shape, and Dose' Matter

Biological effects vary depending on the polymer (PE, PS, PET, PVC, PLA, etc.), size (micro- vs. nano-), shape (spherules, fibers, fragments), and concentration. Smaller particles have greater penetrating power and different kinetics of interaction with cells and microbes. These parameters, together with the food/water matrix, determine the depth of dysbiosis and the severity of functional disorders.

Clinical significance and risk hypotheses

Given the role of microbiota, MP-induced dysbiosis is logically associated with gastrointestinal pathologies (IBD, IBS, colitis), metabolic disorders and systemic inflammation. At the hypothetical level, the contribution of microplastics as an environmental driver of early colorectal cancer growth through a combination of barrier defects, inflammation and possible cofactors (adsorbed xenobiotics) is discussed. Prospective cohorts are needed to quantify these relationships.

Methodological challenges of the field

• Exposure measurement: standardization of particle isolation/identification in human biological samples.
• Microbiome data comparability: sequencing and analytical protocols (α/β-diversity, taxonomy, metabolomics) vary widely.
• Study design: lack of longitudinal and interventional studies in humans; small samples and narrow geography.
• Dose-response assessment: need for safe exposure thresholds and consideration of particle properties in risk calculations.

Why the current systematic review was needed

Against the background of disparate “human” data, the authors conducted a PRISMA search to synthesize human-relevant results: taxonomic shifts, changes in diversity and metabolic functions (including SCFA), and dependence of the effect on particle properties. This approach forms the basis for risk assessment and further standardization of methods.

What exactly did the authors do?

We conducted a systematic search of Scopus and PubMed using the PRISMA protocol, identifying 12 primary studies (2021-May 2024) specifically related to humans: 5 observational (involving human participants) and 7 model studies using human samples (simulated gastrointestinal system, in vitro). The analysis included data on microbiota composition at the phylum/family/genus levels, α- and β-diversity, and metabolic pathways (e.g. short-chain fatty acid - SCFA production). The geography of the studies was narrow: mainly China, but also Spain, France, and Indonesia.

What polymers and exposure parameters were considered?

The sample included common polymers:

• polyethylene (PE), polystyrene (PS), polyethylene terephthalate (PET), polyvinyl chloride (PVC), polylactic acid (PLA);
• microplastic mixtures;
• The size, shape and concentration of the particles varied - all these properties had an impact on the severity of the effects.

Key Findings: What's Happening to the Microbiome

The overall picture points to dysbiosis - an unfavorable shift in microbial communities under the influence of microplastics. In a number of studies, the following were observed during exposure to PET and microplastic mixtures:

• an increase in the proportions of Firmicutes, Synergistetes, Desulfobacterota with a simultaneous decrease in Proteobacteria and Bacteroidetes;
• decreased overall diversity and altered Firmicutes/Bacteroidetes ratio, which has been associated with metabolic disorders in the literature;
• depletion of taxa - key producers of SCFA, which affects the barrier function and anti-inflammatory regulation of the intestine.

What changes in the metabolism of microbiota

In addition to the composition, the functions suffer:

• the production of SCFA (acetate, propionate, butyrate), necessary for the nutrition of colonocytes and the maintenance of tight epithelial junctions, decreases;
• pathways involved in immune modulation and detoxification are shifted;
• activation of pro-inflammatory cascades is possible (including through increased formation of hydrogen sulfide by reducing bacteria), which is associated with diarrhea/constipation, IBS and exacerbations of inflammatory bowel diseases.

Potential clinical implications

Although direct prospective studies in humans are still limited, the overall pattern of signals paints a clear risk profile:

• Intestinal diseases: association with dysbiosis in IBD, IBS, colitis;
• Metabolic syndrome: F/B imbalance and SCFA decline support insulin resistance and chronic low-grade inflammation;
• Early colorectal cancer: The authors note the hypothesis of the involvement of microplastics as an environmental risk factor that increases inflammation and disrupts the barrier.

What is important to understand about “dose” and particle properties

The effect depends on the polymer type, size, shape and concentration. Smaller particles have a larger specific surface area and are likely to penetrate deeper, and can also carry adsorbed toxicants and pathogens - all of which enhance dysbiotic shifts. In other words, "which microplastic" and "how much" has practical implications for risk.

Viewing Limitations

The authors highlight several limitations:

• Lack of direct clinical data: The predominance of in vitro models limits extrapolation to real life.
• Heterogeneity of methods: different protocols for microplastic isolation/identification and microbiota sequencing confound meta-analysis.
• Narrow geography and samples: most works are from a few countries and have a small volume.

What does this mean for policy and practice?

1. Standards are needed: uniform protocols for measuring microplastics in human samples and profiling the microbiome;
2. Dose-response assessment: determine safe exposure levels and threshold effects;
3. Prevention at the environmental level: reduce sources of microplastics (packaging, synthetic fibers, abrasives), increase filtration of drinking water and control of industrial emissions;
4. Monitoring in vulnerable groups: children, pregnant women, patients with IBD/IBS and metabolic disorders.

What you can do now (sensible steps to reduce contact)

• Drinking water: use high-quality filters if possible; do not heat water in plastic containers.
• Food and cooking: Use glass/metal when storing and heating food, if possible; avoid scratched plastic utensils.
• Textiles and laundry: reduce microfibres from synthetics (full loads, gentle cycles, catch bags/filters).
• Household habits: ventilation/wet cleaning reduces airborne microplastics indoors.

Conclusion

A systematic review forms a consensus: microplastics are a plausible environmental driver of human dysbiosis, with disruptions in both microbiota composition and function (including a decline in SCFA), mechanistically linking exposure to intestinal and systemic inflammation, metabolic syndrome, and potentially cancer risks. The scientific community now needs standards, clinical cohorts, and prospective studies to define safe levels and target protective measures. At the level of everyday life and policy, it already makes sense to act on the precautionary principle.

Source: Systematic review in BMC Gastroenterology from August 13, 2025 (“Impact of microplastics on the human gut microbiome: a systematic review of microbial composition, diversity, and metabolic disruptions”). DOI: https://doi.org/10.1186/s12876-025-04140-2