Mapping microplastics in the human body

When you follow the microplastics literature for a while, you start to notice a specific kind of study that shows up more and more often. Someone gets a tissue sample from a human being, such as a brain, a placenta, an artery, a chunk of testis, a vial of cerebrospinal fluid, and asks a question that sounds almost silly until you sit with it. “Is there plastic in this?”

Five years ago there were maybe half a dozen such studies. Today the list is more than twenty distinct tissues, fluids, and compartments, spanning almost every major organ system. That growth is the product of researchers, in labs around the world, working to understand the scope of the problem.

Why “detection” is not the same as “danger”

Finding a plastic particle in a tissue is not the same as showing that particle is causing harm. Those are two different questions and they demand two different kinds of study. A detection paper asks, “is it there?” A mechanism paper asks, “how does it work in the lab?” A causation paper asks, “does it matter?” We are much further along on the first and second questions than the second, because it is much easier to run a spectrometer or challenge a culture or animal model than it is to run a decade-long cohort study.

That does not make the detection and mechanism work irrelevant. It sets a floor. If a substance is not in a tissue, we do not need to argue about whether it does anything there. Once it is in a tissue — repeatedly, across labs, across countries — the harm question stops being hypothetical and becomes worth asking.

How researchers know it is plastic

Because this is the point where a lot of skepticism lives, a short primer.

There are many techniques for measurement plastic particles, but there are three techniques doing most of the work.

• Fourier-transform infrared spectroscopy (FTIR). You shine a broad band of infrared light at a suspect particle. Different chemical bonds (for example, the C=O in polyethylene terephthalate, the C-Cl in PVC) absorb specific frequencies. The absorbance pattern is a fingerprint that gets matched against a library. This is how most tissue-microplastic work identified polymer type until recently.
• Raman spectroscopy. Similar idea, different physics: you shine a laser and read the light scattered back. Raman is more sensitive at very small particle sizes, which is why the newer nanoplastic papers lean on it. It is slower and finickier than FTIR but it can find particles FTIR would miss.
• Pyrolysis gas chromatography-mass spectrometry (pyr-GC/MS). You take a whole tissue sample, heat it in a controlled way, and analyze the vapors coming off. If the sample contained polymer, the vapor has telltale monomer signatures. Pyr-GC/MS gives you mass of plastic per gram of tissue, a real quantitative number, where FTIR/Raman mostly give you counts of particles. This is how the 2025 Nihart et al. paper reported concentrations in brain, liver, and kidney.

The dominant methodological worry across all three is contamination. Plastic is everywhere. It is in lab dust, in reagents, in the plastic bags samples get shipped in. That makes sense because today’s world is literally built on plastic. Many studies build blanks into every batch, work in filtered clean-air hoods, and subtract background so aggressively that anything left over is very likely real. The field’s blanks are much better than they were five years ago, but not all research has been done with the same diligence.

None of this is perfect. Some early papers had contamination issues. Some polymers are still hard to distinguish from natural biomolecules. Very small nanoparticles are still at the edge of what can be reliably called. But the honest read is that the detections in the map below have generally been made with the methods and blanks they need. When I say “found in brain tissue,” I mean identified by FTIR or Raman or pyr-GC/MS, in samples that were run against contamination controls.

If you’re interested in reading more about these challenges, check out our companion piece: The challenge of measuring plastics in humans.

The interactive map

The graphic below is a working map of peer-reviewed studies with direct detection of plastic in a human tissue. Click any dot for the finding, the study, and a direct link to the paper. Switch between systems to filter.

Twenty-two entries. Fifteen distinct organ systems. Every dot is a peer-reviewed paper. This isn’t a 100% complete list of papers for each area, but a comprehensive sweep of bodily systems.

The tour, by system

The central nervous system

The brain finding is the one that has done the most work in public conversation, so it is worth starting there. In a 2025 Nature Medicine paper, Nihart and colleagues measured microplastic mass by pyr-GC/MS in frontal cortex, liver, and kidney from the same postmortem donors. Cortex loads were substantially higher than liver or kidney, and concentrations were rising year over year across the sample window ^[1]. The polymers were dominantly polyethylene.

That paper alone would be striking. Two other CNS-adjacent findings raise the stakes. In 2024, Amato-Lourenço et al. identified synthetic polymer particles in human olfactory bulb tissue — the nerve tissue at the top of the nasal passage that projects directly into the brain ^[2]. This matters because the olfactory route is one of the few ways an inhaled particle could reach the CNS without crossing the blood-brain barrier. And in 2025, He et al. reported detection of polypropylene, PVC, polyethylene, and polystyrene in human cerebrospinal fluid, with associations to Alzheimer's-related pathology ^[3].

Three separate labs, three different sample types, all pointing at the same compartment. That is the pattern the field is watching most closely.

The cardiovascular system

Arterial plaque. In 2024, Marfella and colleagues published the study that changed a lot of people’s heart on this issue. Among 257 patients undergoing carotid endarterectomy, those with detectable polyethylene or PVC in their plaque had roughly a 4.5-fold higher hazard of heart attack, stroke, or death over 34 months ^[4]. About 58% of the plaques contained polyethylene. This is an association, not a mechanism, but it is the closest the field has to a hard human outcome signal.

Blood. In 2022, Leslie et al. published the first quantification of plastic particles in human blood: PET and polystyrene were most common, detected in 17 of 22 healthy adult donors at averages around 1.6 µg/mL ^[5]. That paper alone reframed the field. Once plastic is in blood, it can go anywhere blood goes.

Heart tissue. Yang et al. in 2023 found microplastics directly in atrial appendage, pericardium, and pericardial fluid from patients undergoing cardiac surgery ^[6].

Thrombi. Two studies found microplastics inside clots. Wu et al. (2023) identified 87 particles across cardiac thrombi from 26 patients ^[7]. Wang et al. (2024) found microplastics in 80% of 30 thrombi from cerebral arteries, coronary arteries, and deep veins, with concentrations that tracked ischemic stroke severity ^[8].

Once you look at these together, the vasculature is not a passing-through space for these particles. It is an accumulation space.

The respiratory system

Jenner et al. (2022) identified microplastic fibers and fragments in 11 of 13 surgical lung samples recovered across upper, middle, and lower lobes ^[9]. Qiu et al. (2023) then reported particles in bronchoalveolar lavage fluid from never-smokers, confirming that the airways themselves carry plastic, not just resected tissue ^[10]. Two independent labs, two different sample modalities, converging.

The digestive and excretory systems

Liver. Cirrhotic liver tissue carried significantly higher microplastic loads than healthy liver in Horvatits et al. (2022) ^[11]; the Nihart 2025 pyr-GC/MS analysis also detected polymer in postmortem livers ^[1].

Spleen. Detected at autopsy ^[11]. The spleen is the body’s primary immune-filtration organ, where circulating particles and worn cells get pulled out of blood. Finding plastic there is, mechanistically, exactly where a systemic exposure model would predict.

Kidney. Detected in postmortem tissue in Nihart 2025, at lower concentrations than brain or liver but consistently across donors ^[1].

Stool. Schwabl et al. (2019) found microplastics in every participant’s stool across an eight-country pilot. The median was ~20 particles per 10 g across nine polymer types ^[12]. Liu et al. (2023) found ~54 particles per gram in meconium from twelve newborns, a striking finding because meconium accumulates in utero and confirms transplacental transfer of particles to the fetus before birth ^[13].

Saliva and urine. Abbasi et al. (2021) identified 645 particles across saliva samples from a 2,000-person cohort, framing the mouth as one of the highest-flux plastic entry points ^[14]. Pironti et al. (2023) directly detected microplastics in human urine, suggesting a fraction of ingested plastic reaches systemic circulation and is renally cleared ^[15].

The reproductive system

Female. Amereh et al. (2022) found microplastics in all thirteen placentas from intrauterine growth restriction cases, with inverse associations to birth weight, length, and Apgar scores ^[16]. Xu et al. (2024) reported higher concentrations in uterine fibroid tissue than in adjacent healthy uterus — one of the first findings to link tissue detection density to a specific pathology ^[17].

Male. Hu et al. (2024) detected microplastics in 100% of twenty-three human testis samples; polyethylene dominated at ~329 µg/g ^[18]. Codrington et al. (2024) found particles in penile tissue from five of six patients undergoing prosthesis surgery — PET (~48%) and polypropylene (~35%) dominant ^[19]. Zhao et al. (2023) detected particles in both testis and semen samples ^[20].

Breast milk. Ragusa et al. (2022) detected polyethylene, PVC, and polypropylene in 26 of 34 samples analyzed within a week of childbirth ^[21].

The skeletal system

Yang et al. (2025) is the first study to characterize microplastic deposition in bone marrow, cartilage, and intervertebral discs. Particles reach these tissues through blood circulation, and inflammatory markers are elevated where they land ^[23].

The external interface

Hair and skin. The Abbasi 2021 cohort measured surface deposition on both — ~7,500 particles across 2,000 hair samples, ~4,000 particles each on face and hand surfaces ^[14]. These are external findings, not internal exposures, but they set an environmental baseline: the surface load reflects the air you breathe and the dust you sit in.

Eye. In 2025, Zhang et al. detected five polymer types in human aqueous humor sampled during cataract and IOL surgery — with abundance patterns that varied by age and sex ^[22].

What the diagram actually shows

Now zoom back out.

The pattern is not that microplastics are concentrated in any one organ. It is that they have been detected in essentially every organ system anyone has looked in carefully. That includes the compartments most protected by the body’s barriers — the placenta, the blood-brain-barrier-adjacent olfactory tissue, the tightly filtered aqueous humor, the vascular endothelium. It also includes the excretory outputs, which is important the other way: it means some of what enters is leaving.

Three specific things the diagram does support:

• One. Human exposure is systemic, not just gastrointestinal. Once particles are small enough to cross the gut, they distribute the way anything else in blood distributes.
• Two. The compartments where particles have been found do correlate with the routes we would predict from basic physiology. Blood goes everywhere; so does plastic. Filtration organs (spleen, liver, kidney) get more of it than others. Barriers can be crossed but they slow things down. The diagram has an underlying logic.
• Three. Not all plastic in the body is inert bystander material. Marfella's plaque paper, Wang's thrombus paper, and Amereh’s IUGR placenta paper all showed a dose-linked association to a real clinical variable. Those are association studies, not causation. But they are the first ones that let researchers start asking the harm question with human numbers.

What the diagram does not show

Being equally honest about the ceiling.

The diagram does not show that everyday exposure causes disease. Marfella is one carotid cohort, not a general-population study. The tissue-detection papers report on tens to hundreds of samples, not millions. The dose-response question of “how much particle load corresponds to how much clinical risk?” is still open.

The diagram does not resolve nano vs. micro. Most detection studies quantify the microplastic-sized fraction because that is what the instruments can see clearly. The nano fraction is likely the biologically active one, and it is systematically under-counted in almost every paper cited above. We wrote about that biology in more detail in nano vs micro: where the biology fundamentally changes.

The diagram does not tell you what to do. It tells you that the exposure is real and systemic. What follows from that — for policy, for personal choices, for supplement design — is a separate conversation and involves values, not just measurements.

Where I read the evidence today

The diagram has moved fast enough over five years that whatever it looks like in 2031 will likely make the 2026 version look sparse. That trajectory is what I pay attention to, more than any single paper.

What I do with it, day to day, is be as proactive as makes sense for my life. I filter my water, try to reduce plastic when reasonable, ventilate my enclosed spaces where I can, reach daily fiber goals, and I take Winnow. These are small, steady interventions that I can handle that help reduce the exposure for me and my family.

That is the lens I look through, and the diagram is one of the reasons why I do those things.