First report of micro/nano plastics in patients with atheroma and their link to worse clinical outcomes (composite of all-cause death, heart attack and stroke)
Wow this is staggering, but sounds right intuitively. I did a post on the Rutgers study recently finding way more nanoplastics than previously thought in bottled water. I agree that reducing bottled water use would be a low hanging, highly impactful, and environmentally sound priority for individuals and policy leaders.
In the meantime I use a countertop reverse osmosis filter for drinking water which theoretically “is designed to reduce impurities from the water down to 1/10,000 of a micron. That’s ten times smaller than a nanoparticle if my math is correct.” While RO membranes might introduce some nanoplastics in the end filtration product, I doubt this approaches the amount seen in the Rutgers study of typical bottled water people drink.
Thank you for posting, Eric. I'll have to read the paper when I have more time, but this is frightening. Unfortunately, my confidence that anything will be done to mitigate the problem globally is low, so it will be helpful to know if there's anything individuals can do.
So does this mean that microplastics cause inflammation and plaque buildup OR does this just mean that the microplastics get entombed by the plaque that would have formed anyway?
ALL of the study participants had plaque. (Recall that ALL of them had surgery to remove the plaque). So why didn't plastics get entombed in the plaque of the 42% who did not have plastics in their plaque? Not to mention, plastics are not just found in plaque, but have also been found in the gastrointestinal tract (colon, liver), lymph nodes and spleen, lung, placenta, and other places.
I read the article yesterday and agree it's highly concerning. However, many questions remain to be answered:
1. What is the mechanism for MNPs becoming embedded in plaque, since it must be transported from elsewhere in the body?
2. What is the mechanism for the observed differences in non-fatal MI and stroke between subjects who had MNPs in their plaque vs. those who didn't?
3. What was the cause of death for those who died? Unless I missed it, the authors didn't look into this. It's possible some participant passed from unrelated causes.
4. Carotid endarterectomy is done to lower the risk of stroke in patients with plaque. How much higher was the stroke risk in the subjects compared to a matched population of CEA patients?
5. Since MNPs were found in carotid plaque, it makes sense they may also be found in coronary arteries. This would be a fruitful avenue of investigation.
6. In the past, the decision to perform CEA was mostly based on the degree of luminal compromise on ultrasound, using velocity as a surrogate for stenosis. However, there is increasing focus on characterizing plaque morphology and vulnerability using sonography and related methods (such as contrast-enhanced ultrasound). I wonder if plaque with MNPs might have a different signature than other plaque.
Regardless of what further research shows, plastics are problematic. We often think of ubiquitous water bottles as the greatest threat, but there are so many other instances where plastic is used in food and drink containers.
If, as CDC suggests, we all have plastics in our bodies, why were they detected in only 58% of patients with plaques and why only polyethylene ? Let’s not confuse correlation with causation. It’s possible that patients with more aggressive forms of atherosclerosis create kinds of plaques that are prone to absorb polyethylene particles. That would explain the absence of other plastics
it wasn't just polyethylene. PVC too. I think your alternative explanation is a reach. If the findings are independently replicated, I will conclude it's cause and effect.
Replication prove association, not causation. The same alternative explanations would apply. The reason you see my alternative explanation as a reach is the strength of your prior (concern about the health effects of microplastics, admittedly not unreasonable). Treating replication as proof of causation is confirmation bias.
Wow this is staggering, but sounds right intuitively. I did a post on the Rutgers study recently finding way more nanoplastics than previously thought in bottled water. I agree that reducing bottled water use would be a low hanging, highly impactful, and environmentally sound priority for individuals and policy leaders.
In the meantime I use a countertop reverse osmosis filter for drinking water which theoretically “is designed to reduce impurities from the water down to 1/10,000 of a micron. That’s ten times smaller than a nanoparticle if my math is correct.” While RO membranes might introduce some nanoplastics in the end filtration product, I doubt this approaches the amount seen in the Rutgers study of typical bottled water people drink.
A complementary deep dive if desired:
https://mccormickmd.substack.com/p/surprising-levels-of-microplastics
And vote, vote, vote… and make our environment and planet the most important consideration among many others which stir up misplaced passion.
thanks Ryan
Thank you for posting, Eric. I'll have to read the paper when I have more time, but this is frightening. Unfortunately, my confidence that anything will be done to mitigate the problem globally is low, so it will be helpful to know if there's anything individuals can do.
it is frightening but there's so much that we can do --that we're not doing
Yikes!
that was my reaction, Michael!
I guess this should not be surprising, but it certainly is alarming. Thank you so much for bringing this to our attention.
I am sending this article to my doctor.
So does this mean that microplastics cause inflammation and plaque buildup OR does this just mean that the microplastics get entombed by the plaque that would have formed anyway?
ALL of the study participants had plaque. (Recall that ALL of them had surgery to remove the plaque). So why didn't plastics get entombed in the plaque of the 42% who did not have plastics in their plaque? Not to mention, plastics are not just found in plaque, but have also been found in the gastrointestinal tract (colon, liver), lymph nodes and spleen, lung, placenta, and other places.
I read the article yesterday and agree it's highly concerning. However, many questions remain to be answered:
1. What is the mechanism for MNPs becoming embedded in plaque, since it must be transported from elsewhere in the body?
2. What is the mechanism for the observed differences in non-fatal MI and stroke between subjects who had MNPs in their plaque vs. those who didn't?
3. What was the cause of death for those who died? Unless I missed it, the authors didn't look into this. It's possible some participant passed from unrelated causes.
4. Carotid endarterectomy is done to lower the risk of stroke in patients with plaque. How much higher was the stroke risk in the subjects compared to a matched population of CEA patients?
5. Since MNPs were found in carotid plaque, it makes sense they may also be found in coronary arteries. This would be a fruitful avenue of investigation.
6. In the past, the decision to perform CEA was mostly based on the degree of luminal compromise on ultrasound, using velocity as a surrogate for stenosis. However, there is increasing focus on characterizing plaque morphology and vulnerability using sonography and related methods (such as contrast-enhanced ultrasound). I wonder if plaque with MNPs might have a different signature than other plaque.
Regardless of what further research shows, plastics are problematic. We often think of ubiquitous water bottles as the greatest threat, but there are so many other instances where plastic is used in food and drink containers.
Again, thanks for posting!
If, as CDC suggests, we all have plastics in our bodies, why were they detected in only 58% of patients with plaques and why only polyethylene ? Let’s not confuse correlation with causation. It’s possible that patients with more aggressive forms of atherosclerosis create kinds of plaques that are prone to absorb polyethylene particles. That would explain the absence of other plastics
it wasn't just polyethylene. PVC too. I think your alternative explanation is a reach. If the findings are independently replicated, I will conclude it's cause and effect.
Replication prove association, not causation. The same alternative explanations would apply. The reason you see my alternative explanation as a reach is the strength of your prior (concern about the health effects of microplastics, admittedly not unreasonable). Treating replication as proof of causation is confirmation bias.