Exploring microplastic impact on whole blood clotting dynamics utilizing thromboelastography, 2023, Christodoulides et al.

[SNT Gatchaman]

Exploring microplastic impact on whole blood clotting dynamics utilizing thromboelastography
Christodoulides, Alexei; Hall, Abigail; Alves, Nathan J.

This study investigates the influence of microplastics on blood clotting. It addresses the lack of comprehensive research on the effects of microplastic size and surface modification on clotting dynamics in human whole blood. Thromboelastography was used to examine aminated (aPS), carboxylated (cPS), and non-functionalized (nPS) polystyrene particles with sizes of 50, 100, and 500  nm. Results show that cPS consistently activated the clotting cascade, demonstrating increased fibrin polymerization rates, and enhanced clot strength in a size and concentration-dependent manner. nPS had minimal effects on clotting dynamics except for 50  nm particles at the lowest concentration. The clotting effects of aPS (100  nm particles) resembled those of cPS but were diminished in the 500  nm aPS group. These findings emphasize the importance of microplastic surface modification, size, concentration, and surface area on in-vitro whole blood clotting dynamics.

Link | PDF (Frontiers in Public Health)

 

[Hutan]

On whether microplastics get into blood: (yes, they do)

Translocation of microplastics, particularly submicron particles (i.e., nanoparticles), into systemic circulation has been documented, and is well-summarized by Lett et al. (5). Of 22 volunteers tested in the Netherlands, 17 had quantifiable levels of microplastics in whole blood samples with polyethylene terephthalate and polystyrene being the most common plastics (6). Of note, the size cutoff in the Leslie et al. study was ≥700 nm particles, thus excluding a large proportion of smaller particles that are known to translocate into the circulatory system.

 

[Hutan]

There were controls.

Prior to initiation of thromboelastography (TEG), 1.5 ml of WB was aliquoted from the stock and brought to room temperature. MPs were introduced into the WB aliquot in accordance with the necessary volume to achieve a desired final concentration, as outlined in section “Microplastic particle preparation and storage.” Of note, a 0 μg/ml condition was also included in our study which involved introducing 75 μl of PBS into the 1.5 ml

Thromboelastography - looks like there is a special machine to measure relevant blood clotting parameters. I'm not sure what temperature the blood is at when the microplastics are added and the evaluation is done. It could be interesting to compare ME/CFS, LC and control blood using this tool.

Samples were run in accordance with manufacture-provided protocols for the TEG-5000 instruments (Haemonetics, Boston, MA), with instrument eCalibration performed between each set of samples. TEG clotting parameters of interest included R-time (clotting cascade activation), K-time (time to initial fibrin polymerization), Maximum Amplitude (MA; clot strength), and Angle (rate of fibrin polymerization). Additional TEG parameters collected included Time to Maximum Amplitude, Clotting Index, and G

 

[Hutan]

Studying coagulation in a relatively low-shear environment such as TEG allows us to focus in on the true effects microplastics have on coagulation without having to account for the intricacies that flow and endothelial cells might introduce into the system. Most importantly, in performing our experiments over the course of just a few days in a simple, systematic, and replicable fashion, we can truly explore the interplay of size and surface modification of PS microplastics in a manner that has yet to be done in the literature.

They seem to present the 'relatively low-shear environment' and lack of endothelial cells of the TEG as a good thing for experimentation, but of course it is a limitation of the study (and would also be a limitation of any experimentation with ME/CFS blood) in terms of knowing what actually happens in vivo.

(They do acknowledge the limitation of the experimental environment later.)

 

[Hutan]

Across all the microplastics tested in our study, cPS most consistently induced a strong clotting response – regardless of size and/or concentration. Not only was it able to significantly reduce the speed of cascade initiation or fibrin deposition, cPS also allowed for the generation of clots with strengths at or above expected baselines.

There are a few typos in the paper. Unless I have misunderstood, I think this was the most consequential one I saw - the cPS reduced the time until cascade initiation or fibrin deposition, or it increased the speed of these things. See Figure 2

On the particle size:

In our study, we were able to begin seeing significant pro-coagulant effects starting at the 50 nm size cPS particles, although not to the effect of our larger cPS particles.

There's also a platelet activation effect

In addition to cPS’ strong pro-coagulant effects, cPS has also been shown to promote strong platelet activation (18). The high MA readouts on TEG were thus expected findings as clot strength is largely due to platelet activity and their ability to forcefully contract on constructed fibrin scaffolds (19).

Interactions of micro plastics with the immune system

Literature has demonstrated the notable impact of nanoparticles on the activation of the innate immune system with intricate pathways, such as the complement system and/or neutrophil extracellular trap formation – both of which can impact coagulation phenotypes and would ideally be accounted for (37, 38).

 

[SNT Gatchaman]

Literature has demonstrated the notable impact of nanoparticles on the activation of the innate immune system with intricate pathways

See also this mouse study (preprint) —

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung
Cameron R Bishop; Daniel J Rawle; Kexin Yan; Bing Tang; Thibaut Larcher; Andreas Suhrbier

Global microplastic (MP) pollution is now well recognized, with humans and animals consuming and inhaling MPs on a daily basis. Herein we described the effects of azide-free, 1 um polystyrene MP beads co-delivered into lungs with a SARS-CoV-2 omicron BA.5 inoculum using a mouse model of mild COVID-19. Lung virus titres and viral RNA levels were not significantly affected by MPs, with overt clinical or histopathological changes also not observed.

However, RNA-Seq of infected lungs revealed that MP exposure suppressed innate immune responses at 2 days post infection (dpi) and increased pro-inflammatory signatures at 6 dpi. The cytokine profile at 6 dpi showed a significant correlation with the cytokine release syndrome signature seen in some severe COVID-19 patients. This study adds to a growing body of literature suggesting that MPs can dysregulate inflammation in specific disease settings.

Link | PDF (Preprint: BioRxiv)

In summary, we provide herein evidence that MPs in the lung can dysregulate innate inflammatory transcriptional responses to SARS-CoV-2 in a mouse model of mild COVID-19 infection. However, the dysregulation did not result in overt changes in disease or histopathology, suggesting MP-mediated changes were generally mild. To what extent such changes might influence COVID-19 disease severity at a population level may warrant investigation by perhaps comparing matched populations exposed to high and low levels of airborne MP pollution, although separating the influence of MP from other factors would represent a formidable challenge.

 

[Midnattsol]

And with plastics, there is the additional factor of where it came from and if it has absorbed compounds from that environment before entering us. There was a student project where I studied where plastic collected from the sea was remade into keychains etc., and I couldn't get behind it since the plastic can absorb so much crap making those everyday items potentially problematic.