Allowing the good in and keeping the bad out

We live in a world shaped by plastic. A material that has become inseparable from modern life. It wraps our food, carries our water, and lines the products we depend on every day.

As those plastic products fragment into smaller and smaller, eventually microscopic, pieces. They may become invisible to the naked eye but they continue to persist. They drift. They settle. They enter us.

Microplastics are now found in the food we eat, the air we breathe, and the water we drink. They’ve been detected in every human fluid, tissue, and organ tested to date. And while the idea of “plastic inside us” can sound abstract, one place where these particles have their first and deepest impact is in the gut.

Over the last few years, over 50 studies across humans, animals, and advanced gut models have converged on a common pattern. And while there is noise in that pattern, it’s not random. It’s a measurable, and repeatable shift in the gut microbiome that researchers are seeing emerge again and again.

Here’s how the pattern looks with what we know today.

A predictable change in our gut’s good bacteria

Microplastics don’t create random disruption. They consistently reshape the gut ecosystem in the same direction, across studies, particle sizes, and models.

Loss of good bacteria → bloom of opportunists

The same families of “good” bacteria repeatedly collapse, including:

1. Lactobacillaceae and Bifidobacteriaceae, which support our gut lining;
2. Akkermansiaceae, which helps maintain the gut’s protective mucus lining;
3. Bacteroidaceae, which support carbohydrate and fiber fermentation;
4. Muribaculaceae, which produce short-change fatty acids like butyrate; and
5. Erysipelotrichaceae and Tannerallaceae, which support our metabolism and gut lining.

When these families decline, the gut loses its natural resilience. Fermentation weakens. The mucus layer thins. And it becomes more difficult for our gut to do what it does best, allow the good in and keep the bad out.

A rise in opportunists

Nature typically does not leave empty space. When one species fades, another steps in.

The bacterial families that consistently bloom during microplastic exposure are not random bystanders. Groups like Enterobacteriaceae, Eggerthallaceae, Oscillospiraceae, and Pseudomonadaceae) show up again and again across in vitro, rodent, and emerging human studies. These microbial families are often associated with inflammatory bowel disease, metabolic syndrome, cardiovascular risk, oxidative stress, gut barrier dysfunction, and sensitivity to environmental toxins.

That overlap is meaningful. It suggests that microplastics shift the gut ecosystem in a pattern that mirrors other well-characterized biological stressors, from chemical pollutants to chronic inflammation to high-fat Western diets. The “signature” is familiar: loss of beneficial, fiber-loving bacteria and a rise in opportunistic, inflammation-associated bacteria.

It is worth noting here the distinction between correlation and causation matters. These studies don’t prove that micro- or nanoplastics directly cause chronic diseases. That level of evidence requires years of mechanistic work and longitudinal, human clinical studies.

But the consistency of the pattern tells us something important:

• Microplastics nudge the gut in the same direction that other disease-linked exposures do.
• Microplastics may not initiate disease on their own, but they may add biological friction. An additional stressor layered on top of everything else the gut is managing.
• In people already vulnerable due to genetics, diet, or environment, microplastics could be one of many factors that push their gut toward dysfunction.

In other words, microplastics might not be the sole cause, but they increasingly look like contributors. And in health, especially gut health, pressure matters.

Size matters: nanoplastics hit even harder

While fewer studies focus specifically on nanoplastics, the evidence we do have gives us a glimpse at another consistent story: the smaller the particle, the deeper the impact. Nanoplastics tend to trigger more severe microbiome disruption than their microplastic counterparts.

Across models, nanoplastics drive a sharper collapse in key beneficial families like: Lactobacillaceae, Akkermansiaceae, Erysipelotrichaceae, Ruminococcaceae, and Lachnospiraceae. These are the groups typically associated with gut barrier integrity, fiber metabolism, immune balance, and short-chain fatty acid production. Their decline is one of the strongest hallmarks of dysbiosis.

At the same time, nanoplastics cause an even stronger bloom of inflammation-associated bacteria, including: Enterobacteriaceae, Pseudomonadaceae, Campylobacteraceae, and Desulfovibrionceae.

This tilt from “protective” to “inflammatory” mirrors the association seen with microplastic exposure, but with even more significant impacts when nanoplastics are involved.

Why the difference? Because size changes biology.

Nanoplastics are small enough not only to interact with the gut lining but to penetrate it more readily than microplastics. And emerging mechanistic studies show they can go a step further: they can enter microbial cells themselves.

Scientists have visualized this directly by tagging nanoplastics with fluorescent markers. Under the microscope, they’ve been able to identify which microbes internalize the particles most easily, and unfortunately, many of the most susceptible species are our beneficial, health-promoting ones [14].

The takeaway: Microplastics disrupt the gut. Nanoplastics can penetrate deeper and disrupt it even more.

Lost friends, toxic new neighbors

The issue isn’t just that the microbiome “shifts.” It’s which microbes are disappearing, which are taking their place, and what that swap does to the gut ecosystem.

When beneficial bacteria decline, we lose the essential services they normally provide. These microbes are the metabolic workhorses that help maintain gut stability. Their loss leads to:

• lower butyrate production, reducing the fuel that nourishes colon cells and calms inflammation;
• weaker mucus maintenance, thinning one of the gut’s main physical defense layers;
• slower epithelial repair, impairing the gut lining’s ability to recover from daily wear;
• looser tight junctions, weakening the seams between cells, increasing permeability; and
• elevated inflammation markers, shifting the immune system into a more reactive state.

On the other hand, when harmful or opportunistic families bloom, they bring their own forms of stress:

• more lipopolysaccharide (LPS) endotoxin, which is a known driver of systemic inflammation;
• more hydrogen sulfide (H2S), which at high levels damages epithelial cells and impairs mucus production;
• more oxidative stress, which directly injures the gut lining; and
• faster inflammatory escalation, which pushes the system toward chronic activation.

Microplastics contribute to this shift in several ways. Particles that lodge in the mucus or embed in the intestinal folds become physical scaffolds where certain microbes can hide, cling, and grow, often favoring the very species linked to inflammation and disease. These tiny “plastic shelters” distort the competition for space and nutrients, giving pathogenic or stress-associated bacteria an advantage.

At the same time, as mucus weakens and tight junctions begin to falter, the gut becomes more vulnerable. More microbial fragments cross the epithelial barrier, the immune system is activated more frequently, and a cycle of irritation and dysbiosis takes hold.

The result is not one catastrophic event, but a steady unraveling: a gut with fewer allies, more irritants, and a barrier under pressure.

What all this means for human health

Across the reviewed publications, microplastics produce the same outcome:

• a predictable ecological collapse of the gut microbiome;
• a weakening of the gut’s defenses; and
• a swap of protective microbes for inflammatory ones.

And because exposure is daily and unavoidable, in our homes, our food, our water, this shift happens quietly over years.

Bad plastics in → Good bacteria out

Why Winnow matters in this landscape

Winnow was built for this modern exposure, where our guts face daily contact with microscopic plastic particles. It will take a lot of work before science catches up with the full implications of plastic exposure. Winnow is ready to help reduce the impacts starting today.

Our approach is grounded, conservative, and evidence-aware. Winnow is first and foremost an exceptional daily probiotic. Clean strains. Thoughtful formulation. Rigorous testing.

Second, it includes targeted strains supported by strong preclinical evidence of binding micro- and nanoplastics. Packed with Lactobacillus, Lactococcus, and Bifidobacterium, three of the families hit the hardest by micro- and nanoplastic exposure. We’re restoring the bacteria that plastics hit the hardest and adding in bacteria that hit back.

Winnow can’t remove the plastics that have already passed through your gut barrier. But we can offer something practical, grounded, and meaningful:

A daily probiotic that supports the very system microplastics erode. And includes strains with promising preclinical plastic-binding activity.

A small act of quiet defense in a world that keeps adding plastic into the mix.

Let’s flip the script together.

Good in. Bad out.

Every day.

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A snapshot of the data

The arrows reflect the consistency of the effect rather than its magnitude. ↓↓ strongly consistent decrease; ↓ consistent decrease; ↑↑ strongly consistent increase; ↑ consistent increase; ↕ mixed or context-dependent; - not enough data

Family	PS	PE	PP	PET	PVC	Functional generalizations
Bacteroidaceae	↓↓	↓↓	↓↓	↓↓	↓	Carbohydrate degraders; loss reduces SCFAs and digestion efficiency
Akkermansiaceae	↓↓	↓↓	↓↓	↓↓	↓↓	Critical for mucus layer integrity; loss weakens gut barrier
Lactobacillaceae	↓↓	↓↓	↓	↓	-	Beneficial probiotics; loss increases inflammation and susceptibility to pathogens
Bifidobacteriaceae	↓↓	↓↓	↓	↓	↓	Essential early-life taxa; maintain immune tolerance and mucosal health
Muribaculaceae	↓↓	↓↓	↓	↓	-	Major fiber-fermenting family; loss reduces butyrate and metabolic resilience
Tannerellaceae	↓↓	↓↓	↓	↓	↓	Involved in bile acid balance and mucosal homeostasis
Erysipelotrichaceae	↓↓	↓↓	↓	↓	↓	Linked to lipid metabolism; declines associated with inflammation
Streptococcaceae	↓	↓	↓	↓	-	Early fermenters; decline alters carbohydrate breakdown
Lactococcaceae	↓	↓	↓	↓	-	Important for lactate metabolism and pH balance
Odoribacteraceae	↓	↓	↓	↓	-	Butyrate-producers; loss weakens anti-inflammatory signaling
Atopobiaceae	↓	↓	↓	↓	-	Involved in bile acid and steroid metabolism
Fusobacteriaceae	↓	↓	↓	↕	-	Opportunistic pathogens; shifts reflect mucosal disturbance
Verrucomicrobiaceae	↓	↓	↓	↓	↓	Includes mucin specialists; loss correlates with thinning mucus
Enterobacteriaceae	↑↑	↑↑	↑↑	↑↑	↑↑	LPS-producing pathobionts; bloom signals inflammation and barrier leakiness
Eggerthellaceae	↑↑	↑↑	↑↑	↑↑	↑	Potent bile acid modifiers; expansion increases toxic metabolites
Oscillospiraceae	↑↑	↑↑	↑↑	↑↑	-	Stress-adapted anaerobes; growth reflects disrupted fermentation niches
Pseudomonadaceae	↑↑	↑↑	↑↑	↑↑	↑	Aerobic stress-resistant taxa; increase indicates oxidative gut environment
Melainabacteraceae	↑↑	↑↑	↑↑	↑↑	-	Primitive anaerobes; expansion linked to inflammation and energy stress
Veillonellaceae	↑	↑	↑	↑	-	Lactate-utilizers; increase reflects dysbiosis and altered pH
Clostridiaceae	↑	↑	↑	↑	↕	Some species pathogenic; expansion tracks inflammation
Barnesiellaceae	↑	↑	↑	↑	-	Immune-modulating taxa; shifts indicate mucosal stress
Moraxellaceae	↑	↑	↑	↑	-	Opportunistic aerobes; bloom signals oxidative shifts
Aeromonadaceae	↑	↑	↑	↑	-	Environmental opportunists; increase suggests weakened defenses
Vibrionaceae	↑	↑	↑	↑	-	Marine-associated pathogens; enrichment shows barrier compromise
Desulfovibrionaceae	↑	↑	↑	↑	-	H2S producers; high levels damage epithelial cells
Synergistaceae	↑	↑	↑	↑	-	Thrive in inflamed mucosa; expansion increases toxin load
Pyramidobacteraceae	↑	↑	↑	↑	-	Associated with periodontal and gut inflammation
Mycoplasmataceae	↑	↑	↑	↑	-	Mucosal invaders; increase reflects epithelial vulnerability
Campylobacteraceae	↑	↑	↑	↑	-	Pathogenic; bloom indicates oxygen leak and inflammation
Lachnospiraceae	↕	↕	↕	↕	↕	Key butyrate-producers; mixed responses reflect diet- and model-dependence
Ruminococcaceae	↕	↕	↕	↕	↕	Critical SCFA producers; mixed effects tied to energy availability
Prevotellaceae	↕	↕	↕	↕	↕	Fiber degraders; strongly diet-dependent responses
Desulfobacteraceae	↕	↕	↕	↕	-	Sulfate reducers; variable but important in inflammation
Burkholderiaceae	↓	↓	↕	↕	-	Environmental bacteria; shifts reflect redox changes
Saccharimonadaceae	↕	↕	↕	↕	-	CPR group; fluctuates with ecological stress

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References

[1] Chen, X. et al. Polyvinyl chloride microplastics induced gut barrier dysfunction, microbiota dysbiosis and metabolism disorder in adult mice. Ecotoxicol. Environ. Saf. 241, 113809 (2022).

[2] Chen, W. et al. Cyanidin-3-O-glucoside impacts fecal discharge of polystyrene microplastics in mice: Potential role of microbiota-derived metabolites. Toxicol. Appl. Pharmacol. 453, 116212 (2022).

[3] Chen, Y. et al. Polystyrene microplastics aggravate radiation-induced intestinal injury in mice. Ecotoxicol. Environ. Saf. 283, 116834 (2024).

[4] Chen, J. et al. Multiomics Reveals Nonphagocytosable Microplastics Induce Colon Inflammatory Injury via Bile Acid-Gut Microbiota Interactions and Barrier Dysfunction. ACS Appl. Mater. Interfaces 17, 44138–44159 (2025).

[5] Chen, D. et al. Microbial diversity and metabolomics analysis of colon contents exposed to cadmium and polystyrene microplastics. Ecotoxicol. Environ. Saf. 290, 117585 (2025).

[6] Chi, J. et al. Metabolic Reprogramming in Gut Microbiota Exposed to Polystyrene Microplastics. Biomedicines 13, 446 (2025).

[7] Choi, Y. S. et al. Dysbiosis of gut microbiota in C57BL/6-Lepem1hwl/Korl mice during microplastics-caused hepatic metabolism disruption. PLOS One 20, e0336627 (2025).

[8] Deng, Y. et al. Microplastics release phthalate esters and cause aggravated adverse effects in the mouse gut. Environ. Int. 143, 105916 (2020).

[9] Gan, H.-J. et al. Simulated Microplastic Release from Cutting Boards and Evaluation of Intestinal Inflammation and Gut Microbiota in Mice. Environ. Heal. Perspect. 133, 047004 (2025).

[10] Gao, B. et al. Size-dependent effects of polystyrene microplastics on gut metagenome and antibiotic resistance in C57BL/6 mice. Ecotoxicol. Environ. Saf. 254, 114737 (2023).

[11] Gao, B. et al. Mixture Effects of Polystyrene Microplastics on the Gut Microbiota in C57BL/6 Mice. ACS Omega 10, 7597–7608 (2025).

[12] Gao, B. et al. Association between microplastics and the functionalities of human gut microbiome. Ecotoxicol. Environ. Saf. 290, 117497 (2025).

[13] Hasegawa, Y. et al. Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice. Front. Immunol. 15, 1407936 (2024).

[14] Hsu, W.-H. et al. Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs. Nat. Commun. 16, 5026 (2025).

[15] Huang, W. et al. Influence of the co-exposure of microplastics and tetrabromobisphenol A on human gut: Simulation in vitro with human cell Caco-2 and gut microbiota. Sci. Total Environ. 778, 146264 (2021).

[16] Huang, H.-J. et al. Polystyrene Microplastics Can Aggravate the Damage of the Intestinal Microenvironment Caused by Okadaic Acid: A Prevalent Algal Toxin. Mar. Drugs 23, 129 (2025).

[17] Hwangbo, H. et al. Polystyrene Accelerates Aging Related-Gut Microbiome Dysbiosis and -Metabolites in Old-Aged Mouse. J. Microbiol. Biotechnol. 35, 1–11 (2025).

[18] Jeong, B. et al. Maternal nanoplastic ingestion induces an increase in offspring body weight through altered lipid species and microbiota. Environ. Int. 185, 108522 (2024).

[19] Jiménez-Arroyo, C. et al. Simulated gastrointestinal digestion of polylactic acid (PLA) biodegradable microplastics and their interaction with the gut microbiota. Sci. Total Environ. 902, 166003 (2023).

[20] Jin, Y., Lu, L., Tu, W., Luo, T. & Fu, Z. Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice. Sci. Total Environ. 649, 308–317 (2019).

[21] Kaluç, N. et al. Gut-lung microbiota dynamics in mice exposed to Nanoplastics. NanoImpact 36, 100531 (2024).

[22] Ke, D. et al. Occurrence of microplastics and disturbance of gut microbiota: a pilot study of preschool children in Xiamen, China. eBioMedicine 97, 104828 (2023).

[23] Kim, K. J. et al. In vivo exposure of mixed microplastic particles in mice and its impacts on the murine gut microbiome and metabolome. bioRxiv 2025.07.15.664901 (2025) doi:10.1101/2025.07.15.664901.

[24] Kuai, Y. et al. Long-term exposure to polystyrene microplastics reduces macrophages and affects the microbiota–gut–brain axis in mice. Toxicology 509, 153951 (2024).

[25] Li, B. et al. Polyethylene microplastics affect the distribution of gut microbiota and inflammation development in mice. Chemosphere 244, 125492 (2020).

[26] Li, H. et al. Polystyrene microplastics exposure: Disruption of intestinal barrier integrity and hepatic function in infant mice. Ecotoxicol. Environ. Saf. 288, 117357 (2024).

[27] Li, Z., Li, Y., Cao, F., Huang, J. & Gao, X. Gut microbiota and metabolic health risks from chronic low-dose microplastic exposure with focus on Desulfovibrio spp. Ecotoxicol. Environ. Saf. 302, 118721 (2025).

[28] Li, Y. et al. Combined exposure to microplastics and tetracycline leads to impaired skeletal development in young mice by the microbiota-gut-bone axis. Ecotoxicol. Environ. Saf. 306, 119308 (2025).

[29] Li, M. et al. Short-term microplastic exposure: A double whammy to lung metabolism and fecal microflora in diabetic SD rats. Ecotoxicol. Environ. Saf. 297, 118229 (2025).

[30] Li, X., Jing, K., Song, P. & Yu, J. Aged polystyrene microplastics exacerbate cadmium-induced hepatotoxicity in zebrafish through gut-liver axis metabolic dysregulation. Environ. Chem. Ecotoxicol. 7, 859–871 (2025).

[31] Liang, X., Wang, Y., Andrikopoulos, N., Ke, P. C. & Li, Y. Dysfunctional digestive tract highlights the metabolic hallmarks of nanoplastic-exacerbated Parkinson’s pathology. npj Park.’s Dis. 11, 300 (2025).

[32] Lu, L., Wan, Z., Luo, T., Fu, Z. & Jin, Y. Polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice. Sci. Total Environ. 631, 449–458 (2018).

[33] Lu, T. et al. Chronic exposure to polyethylene terephthalate microplastics induces gut microbiota dysbiosis and disordered hepatic lipid metabolism in mice. Ecotoxicol. Environ. Saf. 298, 118330 (2025).

[34] Marana, M. H. et al. Plastic nanoparticles cause mild inflammation, disrupt metabolic pathways, change the gut microbiota and affect reproduction in zebrafish: A full generation multi-omics study. J. Hazard. Mater. 424, 127705 (2022).

[35] Nissen, L. et al. Single exposure of food-derived polyethylene and polystyrene microplastics profoundly affects gut microbiome in an in vitro colon model. Environ. Int. 190, 108884 (2024).

[36] Nugrahapraja, H. et al. Effects of Microplastic on Human Gut Microbiome: Detection of Plastic-Degrading Genes in Human Gut Exposed to Microplastics—Preliminary Study. Environments 9, 140 (2022).

[37] Qiao, J. et al. Perturbation of gut microbiota plays an important role in micro/nanoplastics-induced gut barrier dysfunction. Nanoscale 13, 8806–8816 (2021).

[38] Rehman, A. et al. Impacts of polystyrene nanoplastics on zebrafish gut microbiota and mechanistic insights. Ecotoxicol. Environ. Saf. 299, 118332 (2025).

[39] Shen, W. et al. Sex-Specific Effects of Polystyrene Microplastic and Lead(II) Co-Exposure on the Gut Microbiome and Fecal Metabolome in C57BL/6 Mice. Metabolites 14, 189 (2024).

[40] Su, Q.-L. et al. The impact of microplastics polystyrene on the microscopic structure of mouse intestine, tight junction genes and gut microbiota. PLOS ONE 19, e0304686 (2024).

[41] Sun, H., Chen, N., Yang, X., Xia, Y. & Wu, D. Effects induced by polyethylene microplastics oral exposure on colon mucin release, inflammation, gut microflora composition and metabolism in mice. Ecotoxicol. Environ. Saf. 220, 112340 (2021).

[42] Sun, X. et al. Polyethylene terephthalate microplastics affect gut microbiota distribution and intestinal damage in mice. Ecotoxicol. Environ. Saf. 294, 118119 (2025).

[43] Tamargo, A. et al. PET microplastics affect human gut microbiota communities during simulated gastrointestinal digestion, first evidence of plausible polymer biodegradation during human digestion. Sci. Rep. 12, 528 (2022).

[44] Tilves, C. et al. Associations of Plastic Bottle Exposure with Infant Growth, Fecal Microbiota, and Short-Chain Fatty Acids. Microorganisms 11, 2924 (2023).

[45] Tu, P. et al. Deciphering Gut Microbiome Responses upon Microplastic Exposure via Integrating Metagenomics and Activity-Based Metabolomics. Metabolites 13, 530 (2023).

[46] Wang, Z. et al. Transfer toxicity of polystyrene microplastics in vivo: Multi-organ crosstalk. Environ. Int. 202, 109604 (2025).

[47] Wang, S. et al. The influence of microplastics on hypertension-associated cardiovascular injury via the modulation of gut microbiota. Environ. Pollut. 368, 125760 (2025).

[48] Wang, Z. et al. Polystyrene microplastics induce potential toxicity through the gut-mammary axis. npj Sci. Food 9, 139 (2025).

[49] Wei, G. et al. Low-dose polystyrene microplastics exposure increases susceptibility to obesity-induced MASLD via disrupting intestinal barrier integrity and gut microbiota homeostasis. Ecotoxicol. Environ. Saf. 299, 118310 (2025).

[50] Xia, Y. et al. Effects of microplastics and tetracycline induced intestinal damage, intestinal microbiota dysbiosis, and antibiotic resistome: metagenomic analysis in young mice. Environ. Int. 199, 109512 (2025).

[51] Xie, L. et al. Intestinal flora variation reflects the short-term damage of microplastic to the intestinal tract in mice. Ecotoxicol. Environ. Saf. 246, 114194 (2022).

[52] Xu, M. et al. Impact of Microplastic Exposure on Blood Glucose Levels and Gut Microbiota: Differential Effects under Normal or High-Fat Diet Conditions. Metabolites 14, 504 (2024).

[53] Yang, Y.-K.-X. et al. Effects of Polyvinyl Chloride Microplastics on the Reproductive System, Intestinal Structure, and Microflora in Male and Female Mice. Vet. Sci. 11, 488 (2024).

[54] Zhai, Z., Yang, Y., Chen, S. & Wu, Z. Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet–Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis. Environ. Heal. Perspect. 132, 097002 (2024).

[55] Zhang, Z. et al. Continuous oral exposure to micro- and nanoplastics induced gut microbiota dysbiosis, intestinal barrier and immune dysfunction in adult mice. Environ. Int. 182, 108353 (2023).

[56] Zhou, Y. et al. Gut microbiota combined with metabolome dissects long-term nanoplastics exposure-induced disturbed spermatogenesis. Ecotoxicol. Environ. Saf. 267, 115626 (2023).

[57] Agrawal, M. et al. Micro- and nano-plastics, intestinal inflammation, and inflammatory bowel disease: A review of the literature. Sci. Total Environ. 953, 176228 (2024).

[58] Ali, N. et al. The potential impacts of micro-and-nano plastics on various organ systems in humans. eBioMedicine 99, 104901 (2024).

[59] Bora, S. S. et al. Microplastics and human health: unveiling the gut microbiome disruption and chronic disease risks. Front. Cell. Infect. Microbiol. 14, 1492759 (2024).

[60] Chen, X. et al. Adverse health effects of emerging contaminants on inflammatory bowel disease. Front. Public Heal. 11, 1140786 (2023).

[61] Covello, C., Vincenzo, F. D., Cammarota, G. & Pizzoferrato, M. Micro(nano)plastics and Their Potential Impact on Human Gut Health: A Narrative Review. Curr. Issues Mol. Biol. 46, 2658–2677 (2024).

[62] Demarquoy, J. Microplastics and microbiota: Unraveling the hidden environmental challenge. World J. Gastroenterol. 30, 2191–2194 (2024).

[63] Duan, J., Liu, C., Bai, X., Zhao, X. & Jiang, T. Global trends and hotspots of gastrointestinal microbiome and toxicity based on bibliometrics. Front. Microbiol. 14, 1231372 (2023).

[64] Eichinger, J., Tretola, M., Seifert, J. & Brugger, D. Review: interactions between microplastics and the gastrointestinal microbiome. Ital. J. Anim. Sci. 23, 1044–1056 (2024).

[65] Fournier, E. et al. Microplastics in the human digestive environment: A focus on the potential and challenges facing in vitro gut model development. J. Hazard. Mater. 415, 125632 (2021).

[66] Garrido-Romero, M. et al. Relevance of gut microbiome research in food safety assessment. Gut Microbes 16, 2410476 (2024).

[67] Hirt, N. & Body-Malapel, M. Immunotoxicity and intestinal effects of nano- and microplastics: a review of the literature. Part. Fibre Toxicol. 17, 57 (2020).

[68] Huang, Z., Weng, Y., Shen, Q., Zhao, Y. & Jin, Y. Microplastic: A potential threat to human and animal health by interfering with the intestinal barrier function and changing the intestinal microenvironment. Sci. Total Environ. 785, 147365 (2021).

[69] Jiménez-Arroyo, C., Tamargo, A., Molinero, N. & Moreno-Arribas, M. V. The gut microbiota, a key to understanding the health implications of micro(nano)plastics and their biodegradation. Microb. Biotechnol. 16, 34–53 (2023).

[70] Mauliasari, I. R. et al. Benzo(a)pyrene and Gut Microbiome Crosstalk: Health Risk Implications. Toxics 12, 938 (2024).

[71] Mishra, S. K. et al. Microplastics as emerging carcinogens: from environmental pollutants to oncogenic drivers. Mol. Cancer 24, 248 (2025).

[72] Osman, A. I. et al. Microplastic sources, formation, toxicity and remediation: a review. Environ. Chem. Lett. 21, 2129–2169 (2023).

[73] Pacher-Deutsch, C. et al. The microplastic-crisis: Role of bacteria in fighting microplastic-effects in the digestive system. Environ. Pollut. 366, 125437 (2025).

[74] Pan, I. & Umapathy, S. Probiotics an emerging therapeutic approach towards gut-brain-axis oriented chronic health issues induced by microplastics: A comprehensive review. Heliyon 10, e32004 (2024).

[75] Romeo, M. et al. Exploring the Classic and Novel Pathogenetic Insights of Plastic Exposure in the Genesis and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). Livers 5, 21 (2025).

[76] Sinha, P., Saini, V., Varshney, N., Pandey, R. K. & Jha, H. C. The infiltration of microplastics in human systems: Gastrointestinal accumulation and pathogenic impacts. Heliyon 11, e42606 (2025).

[77] Souza-Silva, T. G. de et al. Impact of microplastics on the intestinal microbiota: A systematic review of preclinical evidence. Life Sci. 294, 120366 (2022).

[78] Thin, Z. S., Chew, J., Ong, T. Y. Y., Ali, R. A. R. & Gew, L. T. Impact of microplastics on the human gut microbiome: a systematic review of microbial composition, diversity, and metabolic disruptions. BMC Gastroenterol. 25, 583 (2025).

[79] Zolotova, N. et al. Microplastic effects on mouse colon in normal and colitis conditions: A literature review. PeerJ 13, e18880 (2025).