Bioaccumulation of microplastics in decedent human brains, 2025, Nihart et al

forestglip

forestglip

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Bioaccumulation of microplastics in decedent human brains

Alexander J. Nihart, Marcus A. Garcia, Eliane El Hayek, Rui Liu, Marian Olewine, Josiah D. Kingston, Eliseo F. Castillo, Rama R. Gullapalli, Tamara Howard, Barry Bleske, Justin Scott, Jorge Gonzalez-Estrella, Jessica M. Gross, Michael Spilde, Natalie L. Adolphi, Daniel F. Gallego, Heather S. Jarrell, Gabrielle Dvorscak, Maria E. Zuluaga-Ruiz, Andrew B. West, Matthew J. Campen

(Line breaks added)

Abstract
Rising global concentrations of environmental microplastics and nanoplastics (MNPs) drive concerns for human exposure and health outcomes.

Complementary methods for the robust detection of tissue MNPs, including pyrolysis gas chromatography–mass spectrometry, attenuated total reflectance–Fourier transform infrared spectroscopy and electron microscopy with energy-dispersive spectroscopy, confirm the presence of MNPs in human kidney, liver and brain.

MNPs in these organs primarily consist of polyethylene, with lesser but significant concentrations of other polymers. Brain tissues harbor higher proportions of polyethylene compared to the composition of the plastics in liver or kidney, and electron microscopy verified the nature of the isolated brain MNPs, which present largely as nanoscale shard-like fragments.

Plastic concentrations in these decedent tissues were not influenced by age, sex, race/ethnicity or cause of death; the time of death (2016 versus 2024) was a significant factor, with increasing MNP concentrations over time in both liver and brain samples (P = 0.01). Finally, even greater accumulation of MNPs was observed in a cohort of decedent brains with documented dementia diagnosis, with notable deposition in cerebrovascular walls and immune cells.

These results highlight a critical need to better understand the routes of exposure, uptake and clearance pathways and potential health consequences of plastics in human tissues, particularly in the brain.

Link | PDF (Nature Medicine) [Open Access]
 
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Decedent means deceased, in case anyone else didn't know.

Concentration of total plastic (top) and only polyethylene (bottom) in 2016 and 2024 organs. Higher in 2024 in brain and liver, but not kidney. I wonder why the spread of the values for the brain seems too get much more condensed in 2024.
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Age, sex, race/ethnicity and cause of death having no association with plastic concentration in the brain is interesting.
In the full multiple linear regression models, none of the independent variables were significantly associated with either measure of polymer concentration in decedent brains (Table S8). Additionally, neither model’s F-statistic was significant, indicating that the model was no better at predicting the dependent variable than chance alone (LogTotal: F(8, 41)=1.355, p=0.24, and LogPE:F(8, 41)=1.499,p=0.19). This lack of significance among independent variables may be due to the small sample size (n = 52) paired with the relatively large number of independent variables included in the models (n = 6). The backward elimination process revealed that the best-fit model included only one independent variable: date of death (Table S8). Specifically, death in 2024 was associated with a 0.24 unit increase in LogTotal relative to death in 2016 (p=0.02). Similarly, LogPE concentrations were 0.24 units higher in decedents who died in 2024 relative to those who died in 2016 (p=0.01).

Given the heteroscedasticity of residuals in the multiple linear regression models, we also conducted robust linear regressions using the log-transformed and non-transformed dependent variables. This method is comparatively robust to the violations of the assumptions of linear regression listed above. The results from the robust linear models were the same in terms of significance for date of death regardless of whether the dependent variable was log-transformed or not; across all full models (prior to backwards elimination), none of the six independent variables were significantly associated with the dependent variables, and the best-fit models consistently included only the date of death.
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Regarding brains from people with dementia having higher plastic concentration, they say that's expected for several reasons that are not plastic being causal for dementia:
Py-GC/MS analysis revealed total plastics concentrations in dementia samples (median = 26,076 µg g−1; Fig. 1d and Supplementary Table 1) that were higher than in any normal frontal cortex cohort (P < 0.0001 by two-sided t test). Atrophy of brain tissue, impaired blood–brain barrier integrity and poor clearance mechanisms are hallmarks of dementia and would be anticipated to increase MNP concentrations; thus, no causality is assumed from these findings.
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I wonder how robust the storage is where they can compare brains from eight years ago to recently deceased people's brains. Is it not possible that the mass of the brain possibly increases in 8 years from absorbing the formaldehyde or something, which would show up as lower plastic concentration? I don't know anything about tissue storage, so maybe this has all been figured out.
 
How would that affect the measurements?
If you take the weight or volume of the piece you check and divide it by the total mass or volume of the brain, the proportions are constant regardless of expansion.

If they store the pieces over a long period of time, I assume they measure and log the original proportions when they divide it in the first place?
 
Utsikt said:
How would that affect the measurements?
If you take the weight or volume of the piece you check and divide it by the total mass or volume of the brain, the proportions are constant regardless of expansion.

If they store the pieces over a long period of time, I assume they measure and log the original proportions when they divide it in the first place?
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Maybe I'm not understanding, but the concentration is in micrograms of plastic per gram of tissue. I don't see them say they use historical tissue measurements. So if the brain absorbed some formalin over time and increased its mass, then the concentration of plastic would go down.
 
On PR there was mention of a paper which found that the microplastics were found in the myelin sheaths. I didn't check the validity of the findings. The paper in this thread seemed unclear as to where the particles were found: they were assuming that they weren't all in the vascular space.
 
forestglip said:
Where do they assume that? And what would be the significance if that was the case?
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I don't feel like calling up the paper again, but I did see somewhere in it that they were assuming that the particles were not only in the vascular space. When I first read an article about finding microplastics in the brain, my first thought was "Did they check whether the particles were just in the plumbing?" I could imagine finding stuff in the vascular space without getting past the BBB.

If the particles are getting lodged in the myelin sheaths, that could affect signal transmission. As I understand it, the sheaths are frequently stripped off and replaced (in new configurations) as the neural pathway changes function (a memory strengthens, a pain signal gets reduced, etc). However, since that process is adaptive, maybe it would adapt to microplastics altering sheath properties.
 
Creekside said:
When I first read an article about finding microplastics in the brain, my first thought was "Did they check whether the particles were just in the plumbing?" I could imagine finding stuff in the vascular space without getting past the BBB.
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If this was the case, wouldn't plastic levels be similar in all three organs? Instead, it's about ten times higher in the brain than in the liver or kidneys in this paper.

Edit: Oh, that's what they said too:
While blood was not cleared from the decedent’s organs during autopsy, it is unlikely that the nanoplastics in the brain are selectively contained in the vascular compartment, as the kidneys and livers would also have comparable blood volumes.
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expert reaction to a study investigating the accumulation of microplastics in human organs

Some snippets:

Prof Oliver Jones, Professor of Chemistry, RMIT University
Only data from two years – 2016 and 2024 are presented. It is not explained why only these two years were studied, but regardless, you simply can’t make a trend from data from just two years. Data from 2017-2023 would be needed to say if there was an actual trend or if it was just a random variation.
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The concentrations of microplastics in brain samples from 2024 have much less variation than any of the other data. This does not seem likely to me, but it is not explained. Similarly, in 2016, the kidney samples seemed to contain a more diverse range of plastics than liver samples, but in 2024, the liver had a more diverse range. The brain samples are consistent at both time points. This also seems odd but is not discussed.
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The main analytical method used in this study was pyrolysis gas chromatography-mass spectrometry. This method can give false results when used to measure plastics because fats (which the brain is mainly made of) give the same pyrolysis products as polyethylene (the main plastic reported) [1]. The authors did try to address this concern but I am not certain they were able to account for everything.
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It is also challenging to properly account for potential contamination while handling or analysing samples in microplastic studies. This paper says that the findings are not likely to be lab contamination because samples were consistently handled and processed. I don’t think this is necessarily true. After all, consistent protocols could potentially result in consistent contamination. Even standard lab equipment, such as disposable lab gloves, can give false microplastic readings [2]. We also don’t know what happened to the samples during the original autopsy (bodybags are made of polyethylene, for example). There is also the issue of background contamination in any laboratory that needs to be controlled for [3]. Plastic contamination is almost everywhere, so how can we be confident that any particles found are evidence that plastic is crossing membranes in the human body or if it is just contamination from plastic in the clothes or lab equipment or background contamination in the air, etc?
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Prof Theodore B. Henry, Professor of Environmental Toxicology from the School of Energy, Geoscience, Infrastructure and Society at Heriot-Watt University
Another challenge of interpretation of these results is the difficulty in finding suitable control tissues, or tissues that have not been exposed to plastics, for which presence of polymers does not occur and the presence in the tissues can be compared (essentially all tissues had plastic polymers, which does suggest that there could be artifacts or analytical issues that are affecting the analyses that are not accounted for).
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The reported presence of plastic particles in histological sections of tissues by polarised wave microscopy should be verified independently and could readily be done within existing banks of preserved human tissue sections held at many institutions. Given the levels of particles that are reported in the present study it is surprising that similar particles have not been detected in other studies or examinations of the same tissues that have applied the same techniques. The authors of this article correctly note in their conclusion that their results of detection of plastic polymers in tissues are associative and not linked to any negative health outcome.
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