Sorry, I don't mean to be your personal party pooper, but almost every word in your comment is incorrect or out of context.
Primarily breaking down clothing fibres.
The study found polyethylene (PE) and vinyl (PVC). Most synthetic fibers in clothing are polyester. Vinyl is not something that most people wear everyday. PVC may be prevalent in the environment, with mnp's (micro-nano-plastics) being a large concern, but there are many sources of pvc in objects we interact with daily, but clothing isn't one of them. The age group of people with atherosclerosis (ASO-arteriosclerosis obliterans) is not one that is likely to have had much vinyl clothing exposure.
That get into water, and propagate from there.
The vector of introduction for mnp's into the body needs study. Oral ingestion of environmental contaminant mnp's occurs, and translocation across bowel is likely (there are studies showing mnp's in bowel). But, translocation across the portal circulation and liver into the systemic circulation, versus vascular short circuit across porta-systemic collaterals - that's an open question. Your comment is partially correct and intriguing but overly simple as a pathogenic mechanism.
Notably this study also sets out to prove them harmful and fails
The study explicitly states : "Microplastics and nanoplastics (MNPs) are emerging as a potential risk factor for cardiovascular disease in preclinical studies. Direct evidence that this risk extends to humans is lacking." The authors are looking for evidence that there is an association, not to prove a specific pathogenic mechanism or cause and effect. And, they succeeded, showing a hazard ratio of 4.5 for death among those with and without mnp's in their system.
as OP notes: "The findings do not prove that plastic particles drive strokes and heart attacks"
Disease and pathology are complex multi-factorial non-linear dynamical systems, and that is especially true for chronic degenerative diseases such as ASO. No one factor by itself "drives strokes and heart attacks", but anyone knowledgeable about vascular pathology and medicine will immediately recognize the importance of this study and the histological findings and the study statistics. They do indeed prove that those with plastic in their plaques are at much greater risk of dying in the next three years.
I'm unaware of a single study to show actual link between microplastics and any harmful effect.
With countless fields of study, journals, and papers out there, ever increasing, no one person can ever be fully up to date. I too am unaware of a million things I know nothing about or have no engagement in that industry or discipline. If you are unaware of such studies, time to crack a book (or PubMed, or something ...).
This in spite half a decade of intensive research into finding any harmful effect.
The reason there is a notable upsurge in studies and reporting on this subject is because there is mounting evidence of problems. Elucidating pathogenic pathways are still early, but many people who know this subject are getting grants and doing research - because there is something of concern. Crack a book.
Everything we know about them suggests that they're too small to have a mechanical effect
Wrong. Pathology like this operates largely through mesenchymal defense cells called macrophages which are on the order of 5-10 microns. The size, shape, textures, and edges of materials have a profound influence on the behavior of mesenchymal cells, and that influences design and complications of certain implantable polymer devices. The particles they found are on the order of a micron or less, but that is relatively big compared to the cells, so they can indeed have an effect. If the microscope revealed mnp's directly associated with macrophages (mp's), it is because mp's are responding to them which is their job. A common "everyday" histologic feature in clinical medicine is the "foreign body giant cell", which is a syncytium of macrophages that respond to foreign materials, especially organic polymers. The ability of mp's to recognize them comes either from their chemistry, their shape and mechanics, or through an intermediary such as protein or platelet adhesion, and the mechanical causes at this scale are well documented over the past 60 years of polymer device development.
biologically inert so no chemical effect either.
If cells are responding and pathological lesions are arising, then they are not biologically inert. They are often considered chemically "inert" in the lab under human-habitable conditions, but when implanted devices cause inflammatory complications or extrude, the microscope shows a rich mix of materials degradation and cellular response.
And they're obviously no more radioactive than the source plastic, and if you're wearing meaningfully radioactive clothing, you have real problems.
?WTF
They're pervasive because they're so small that they can pass through cellular membranes
No. They cannot pass through cell membranes. Crossing a cell membrane happens in several ways - endocytosis, gate-regulated diffusion, gate-related active transport, membrane translocation, etc. We correlate mechanisms with chemistry and size, and size is usually expressed in molecular weight daltons, sometimes in angstroms. If PVC and PE fragments are small enough, let's say up to a 10^5 - 10^6 daltons perhaps allowing some intracellular material, we would be in a realm that we do not yet understand, and the authors would not have seen that under the microscope. But for the particles observed in this study, "jagged-edged foreign particles among plaque macrophages" they did not pass through membranes. They were extra-cellular, and MP's surrounded them.
and so chemically inert that nothing metabolizes them.
See comment above. They are being degraded by enzymes or cells, as we see under the microscope on explanted specimens.
So they are everywhere, and they persist.
On that point, mounting evidence indicates you are correct.
And apparently do nothing.
Crack a book.