Tiny plastics may harm gut and liver health, review finds
“Our aim was to start conversations between clinicians and their patients about this emerging risk,” Dr. Priyata Dutta explained.
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01/28/2026
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by Doug Brunk
A growing body of research suggests that microscopic plastic particles are not just an environmental concern but may also pose risks to gastrointestinal and liver health. A comprehensive review published in Clinical Gastroenterology and Hepatology brings together the latest evidence linking exposure to micro- and nanoplastics (MNPs) with inflammation, gut dysbiosis, liver disease, and possibly gastrointestinal cancers.
“While MNPs are not classified as carcinogens, they can transport toxic substances and heavy metals that increase cancer risk,” the study’s first author Priyata Dutta, MD, of the department of internal medicine at Trinity Health, Ann Arbor, Michigan, told GI & Hepatology News. “The relationship between MNP exposure and health outcomes remains unclear. As plastic pollution increases, understanding the biological effects of MNP is crucial for public health policies.”
The review examines how tiny plastic fragments, created as larger plastics break down, enter the human body through food, water, and air. Once ingested, these particles can accumulate in the gastrointestinal tract, where they interact with the gut lining, immune system, and microbiome. Microplastics are defined as particles smaller than 5 millimeters, while nanoplastics are even smaller, measured in billionths of a meter, making them difficult to detect and study.
For the narrative review, Dr. Dutta, senior author David A. Johnson, MD, chief of gastroenterology at Eastern Virginia School of Medicine, Norfolk, and colleagues screened 800 publications (from inception to February 2025) and evaluated 15 human studies, along with relevant animal and laboratory research, retrieved from PubMed, EMBASE, and Cochrane.
They analyzed data from fecal testing, tissue samples, occupational exposure studies, and experimental models to understand how MNPs may affect GI and liver health. In addition, the authors reviewed available methods used to detect these particles, noting wide variation and a lack of standardized testing. “Our aim was to start conversations between clinicians and their patients about this emerging risk,” Dr. Dutta explained.
According to the review, multiple human studies have identified microplastics in stool samples from healthy individuals, patients with IBD, and people with high occupational exposure to plastics. Several studies showed higher levels of microplastics in patients with IBD, with concentrations correlating with disease severity. The authors noted that these raise questions about whether plastic exposure contributes to inflammation or whether inflamed intestines retain more particles.
Animal and laboratory studies in the review suggest that microplastics can disrupt the gut microbiome, reducing beneficial bacteria and promoting inflammation. Some plastics may also carry harmful chemicals or heavy metals, potentially amplifying their effects. The review highlights evidence that these particles can damage the gut barrier, trigger immune responses, and increase oxidative stress — processes already known to play a role in chronic GI diseases.
The liver also appears particularly vulnerable. The authors summarize studies showing microplastic accumulation in liver tissue and associations with metabolic dysfunction–associated steatotic liver disease, fibrosis, and cirrhosis. In occupational settings, long-term exposure to certain plastics, such as polyvinyl chloride, has been linked to rare liver cancers, although these findings are based on historical cohorts and specific industrial exposures.
The review also explores emerging concerns about cancer risk, particularly colorectal cancer. While microplastics are not classified as carcinogens, the authors describe experimental data suggesting they may promote tumor growth indirectly by driving chronic inflammation, altering the microbiome, and impairing immune surveillance.
Drs. Dutta and Johnson, for the coauthors, acknowledged limitations of the review, including that most human data come from observational studies, detection methods differ widely, and there is little information on long-term exposure.
“While epidemiological evidence is strongly suggestive, further research employing environmentally relevant exposure levels, mechanistic animal studies as well as longitudinal clinical studies, appropriately balanced for risk assessment, is necessary to more precisely define the risk,” Dr. Dutta emphasized. “These findings underscore the urgent need for continued investigation, heightened awareness among healthcare providers and patients, and the development of strategies to mitigate plastic exposures and related adverse health impacts.”
Following discussions among the authors, emergent recommendations pending more conclusive evidence would be to begin with small, incremental steps, as outlined below:
Recognize that thermal extremes accelerate plastic degradation. This includes avoiding cooking and storing food products in heat (e.g. microwave or freezing).
Avoid or minimize single use plastic exposures (e.g. use reusable water bottles over plastics) as well as liquid commonly prepared with temperature variances (e.g. convenient plastic coffee modules as well as tea bags).
Avoid or minimize exposure to highly processed/convenience foods, stored for long term exposure within plastics.
“Too much beyond these recommendations will not be helpful for patients at present, and potentially harmful for concerns,” Dr. Dutta and her team said. “Our job as clinicians is to make the best recommendations based on current evidence.”
The authors reported having no financial disclosures.
Summary content
7 Key Takeaways
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Developed a paper-based colorimetric sensor array for chemical threat detection.
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Can detect 12 chemical agents, including industrial toxins.
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Production cost is under 20 cents per chip.
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Utilizes dye-loaded silica particles on self-adhesive paper.
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Provides rapid, simultaneous identification through image analysis.
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Inspired by the mammalian olfactory system for pattern recognition.
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Future developments include a machine learning-enabled reader device.
The guidelines emphasize four-hour gastric emptying studies over two-hour testing. How do you see this affecting diagnostic workflows in practice?
Dr. Staller: Moving to a four-hour solid-meal scintigraphy will actually simplify decision-making. The two-hour reads miss a meaningful proportion of delayed emptying; standardizing on four hours reduces false negatives and the “maybe gastroparesis” purgatory that leads to repeat testing. Practically, it means closer coordination with nuclear medicine (longer slots, consistent standardized meal), updating order sets to default to a four-hour protocol, and educating front-line teams so patients arrive appropriately prepped. The payoff is fewer equivocal studies and more confident treatment plans.
Metoclopramide and erythromycin are the only agents conditionally recommended for initial therapy. How does this align with what is being currently prescribed?
Dr. Staller: This largely mirrors real-world practice. Metoclopramide remains the only FDA-approved prokinetic for gastroparesis, and short “pulsed” erythromycin courses are familiar to many of us—recognizing tachyphylaxis limits durability. Our recommendation is “conditional” because the underlying evidence is modest and patient responses are heterogeneous, but it formalizes what many clinicians already do: start with metoclopramide (lowest effective dose, limited duration, counsel on neurologic adverse effects) and reserve erythromycin for targeted use (exacerbations, bridging).
Several agents, including domperidone and prucalopride, received recommendations against first-line use. How will that influence discussions with patients who ask about these therapies?
Dr. Staller: Two points I share with patients: evidence and access/safety. For domperidone, the data quality is mixed, and US access is through an FDA IND mechanism; you’re committing patients to EKG monitoring and a non-trivial administrative lift. For prucalopride, the gastroparesis-specific evidence isn’t strong enough yet to justify first-line use. So, our stance is not “never,” it’s just “not first.” If someone fails or cannot tolerate initial therapy, we can revisit these options through shared decision-making, setting expectations about benefit, monitoring, and off-label use. The guideline language helps clinicians have a transparent, evidence-based conversation at the first visit.
The guidelines suggest reserving procedures like G-POEM and gastric electrical stimulation for refractory cases. In your practice, how do you decide when a patient is “refractory” to medical therapy?
Dr. Staller: I define “refractory” with three anchors.
1. Adequate trials of foundational care: dietary optimization and glycemic control; an antiemetic; and at least one prokinetic at appropriate dose/duration (with intolerance documented if stopped early).
2. Persistent, function-limiting symptoms: ongoing nausea/vomiting, weight loss, dehydration, ER visits/hospitalizations, or malnutrition despite the above—ideally tracked with a validated instrument (e.g., GCSI) plus nutritional metrics.
3. Objective correlation: delayed emptying on a standardized 4-hour solid-meal study that aligns with the clinical picture (and medications that slow emptying addressed).
At that point, referral to a center with procedural expertise for G-POEM or consideration of gastric electrical stimulation becomes appropriate, with multidisciplinary evaluation (GI, nutrition, psychology, and, when needed, surgery).
What role do you see dietary modification and glycemic control playing alongside pharmacologic therapy in light of these recommendations?
Dr. Staller: They’re the bedrock. A small-particle, lower-fat, calorie-dense diet—often leaning on nutrient-rich liquids—can meaningfully reduce symptom burden. Partnering with dietitians early pays dividends. For diabetes, tighter glycemic control can improve gastric emptying and symptoms; I explicitly review medications that can slow emptying (e.g., opioids; consider timing/necessity of GLP-1 receptor agonists) and encourage continuous glucose monitor-informed adjustments. Pharmacotherapy sits on top of those pillars; without them, medications will likely underperform.
The guideline notes “considerable unmet need” in gastroparesis treatment. Where do you think future therapies or research are most urgently needed?
Dr. Staller: I see three major areas.
1. Truly durable prokinetics: agents that improve emptying and symptoms over months, with better safety than legacy options (e.g., next-gen motilin/ghrelin agonists, better-studied 5-HT4 strategies).
2. Endotyping and biomarkers: we need to stop treating all gastroparesis as one disease. Clinical, physiologic, and microbiome/omic signatures that predict who benefits from which therapy (drug vs G-POEM vs GES) would transform care.
3. Patient-centered trials: larger, longer RCTs that prioritize validated symptom and quality-of-life outcomes, include nutritional endpoints, and reflect real-world medication confounders.
Our guideline intentionally highlights these gaps to hopefully catalyze better trials and smarter referral pathways.
Dr. Staller is with the Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston.