The Guardian's front page is currently promoting a story that says antibiotic resistance is associated with air pollution—in particular, with small particulates called PM2.5, which are produced mostly by fossil fuels in richer countries and by dust and residential coal burning in poorer ones. Unfortunately, when I clicked through to the study this was based on, I found this:
The misuse and overuse of antibiotics are the main drivers of antibiotic resistance...
This is perfectly reasonable. It's surely the modern, industrial-scale use of broad-spectrum antibiotics that are both the first and main cause of increasing antibiotic resistance. But later on there was this:
We found that the magnitude of the contribution of PM2·5 to aggregate antibiotic resistance is greater than that of antibiotic use...
Now they're saying that air pollution is the primary cause of antibiotic resistance. So which is it?
Data in the study strongly supports the PM2.5 hypothesis. In fact, they report that PM2.5 contributes 10.9% of variation in antibiotic resistance, compared to only 2.4% for antibiotic use.
That's four times as much, which makes this whole result seems unlikely—especially since the study doesn't even hint at an underlying mechanism for the hypothesized PM2.5 dynamic. I'd take this one with a grain of salt for now.
That study (https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(23)00135-3/fulltext#%20) is just garbage. They found some correlation, so it must be causation.
Note that it is on the The Lancet web-site, but the actual journal is "The Lancet Planetary Health", which an author-pay journal.
All Lancet journals have peer review.
From their instructions for authors:
Peer review
• The Lancet Planetary Health operates a single-anonymised peerreview process
• Every Article and Meta-analysis published in The Lancet Planetary
Health has been peer reviewed. Occasional contributions (eg,
Commentaries) are accepted without peer review
• On submission to The Lancet Planetary Health, your report will
first be read by one or more of the journal’s staff of physicians
and scientists. This is an important feature of our selection
process and many papers are turned away on the basis of
in-house assessment alone. That decision will be
communicated quickly
• Research papers are followed by peer review by at least three
reviewers. You will receive notification of which editor is
handling the peer review of your paper.
That is what they arite. Doesn't tell you much about the quality of the peer-review.
How thorough the review is will always depend on the assigned reviewers no matter the journal. The point is that this is a serious journal and not some quack pay journal where all you have to do to get published is pay a large fee.
How do you know that?
"So which is it?"
The first sentence is in the introduction where they are explaining the current understanding of the field
The latter is when they are explaining the results of their own study.
"That's four times as much, which makes this whole result seems unlikely—especially since the study doesn't even hint at an underlying mechanism for the hypothesized PM2.5 dynamic"
Did you actually read the paper Kevin? Because they do explain it.
"The major air pollutant, in the form of particulate matter (PM)2·5, has been shown to contain diverse antibiotic-resistant bacteria and antibiotic-resistance genes, which are transferred between environments and directly inhaled by humans, causing respiratory-tract injury and infection.7, 8, 9 PM2·5 could also increase cell-membrane permeability to enhance the efficiency of horizontal gene transfer, accelerating the evolution and exchange of antibiotic-resistance elements in bacterial pathogens.10, 11"
"PM2·5 contains a high abundance of antibiotic resistance-determinant genes and the abundance of these genes in urban PM2·5 is higher than in sediment, soil, rivers, and some engineering-treatment systems.7 Antibiotic-resistance elements carried by air pollutants could be directly exposed to humans, which is a substantial risk as the daily intake of antibiotic-resistance genes through inhalation exceeds intake of antibiotic-resistance genes through drinking water.8, 9 Antibiotic-resistance elements in PM2·5 can be replenished from the natural environment and anthropogenic settings (eg, hospitals, farms, and sewage-treatment facilities) through wind action, water evaporation, dust transport, and wet or dry settlement spread over long distances and across regions.24 "
The mechanism and results explained are the equivalent of lighting a fire in a forest. The initial fire is the result of the match or lighter (antibiotic overuse), but the spread of that fire to wider regions is driven primarily by environmental factors like the wind, temperature, and dryness of the forest (PM2.5, soil, and water carrying antibiotic resistance bacteria and then affecting others even if they have never been subjected to antibiotic overuse directly).
"PM2·5 contains a high abundance of antibiotic resistance-determinant genes and the abundance of these genes in urban PM2·5 is higher than in sediment, soil, rivers, and some engineering-treatment systems.7 "
The "7" in the end is a refernce here:
https://pubs.acs.org/doi/abs/10.1021/acs.est.8b04630
And this refers to _fine aerosol_ rather than _particulate matter_, but calling it PM2.5.
Reference 8 also about aerosol.
I thought taht particulate matter refres to solid particle, but apparently not:
https://en.wikipedia.org/wiki/Particulates
The wikipedia entry starts:
"Particulates or atmospheric particulate matter (see below for other names) are microscopic particles of solid or liquid matter suspended in the air."
Which sounds like it would include water droplets, but reading the rest of the entry they clearly don't mean that.
PM2.5 are considered aerosols. so what the heck are you arguing about?
I am commenting on the wikipedia entry.
Wikipedia is a site on the internet with entries that describe various things.
""The major air pollutant, in the form of particulate matter (PM)2·5, has been shown to contain diverse antibiotic-resistant bacteria and antibiotic-resistance genes, which are transferred between environments and directly inhaled by humans, causing respiratory-tract injury and infection.7, 8, 9 PM2·5 could also increase cell-membrane permeability to enhance the efficiency of horizontal gene transfer, accelerating the evolution and exchange of antibiotic-resistance elements in bacterial pathogens."
Don't know whose fault it is, but this seems to be playing REALLY fast and loose with language.
Talking about "air pollution" but what they actually seem to mean is not smoke and suchlike, but sneezing from sick people?
Which is reasonable in terms of biology (constant stream of low level horizontal transfer of bacterial DNA).
But the framing language seems almost deliberately chosen to be unhelpful. If the problem you want to solve is people sneezing, or perhaps wind blowing over sewage treatment pools, using language that immediately suggests smoke, cars, and indoor cooking seems absolutely perverse!
I think they were somewhat sloppy in their language. I think they were trying to express that antibiotic overuse is still the root cause, and that this paper is highlighting an important transmission mechanism.
Yes. The authors talk about development of antibiotic resistance, driven by overuse of antibiotics, and the spread of resistance, driven in part by particulates. Kevin is conflating those. Note, the spread also includes gene swapping among different bacteria.
But the study is still observational, so a grain of salt is warranted, though in this case, only a small one. We still have to see if it holds up.
They explictly write in the "Findings":
" Antibiotic resistance derived from PM2·5 caused an estimated 0·48 (95% CI 0·34–0·60) million premature ..."
So the authors themselves confuse between resistance _spread by_ pM2.5 and _derived from_ it.
Maybe just a misuse the word "derived" by the authors, but a serious review should have caught it. "resistance derived from PM2-5" really stands out as a non-sensical concept.
When talking about infections, that is referring to spread of resistance to people. All that says is that people picked up their antibiotic resistance bugs from particulate matter, not that the particulate matter caused the gene for the resistance to develop.
Seems to me you could easily test this by looking at antibiotic resistance rates in areas that have been subjected to wild fire smoke. That smoke is filled with PM2.5 particles.
Antibiotic resistance is not easily measured. It is only detected by complicated processing of lots of data. The data on wildfire influence may have already been included in the data in the study.
It's saying that bacteria are just as subject to damage from PM 2.5 as your lungs are and those that survive are less easily damaged by things that would poison them, like antibiotics, and in that way the smoke from forest fires spreads the antibiotic resistance.
Cute theory, but uh, unlikely.
PM 2.5 particles are about 2.5µ in size.
Bacteria vary in size but 1µ radius is a reasonable approximation. This is much smaller than eukaryotic cells.
So essentially what you're saying is like saying that people can be damaged by walking past very large boulders that, somehow, managed to slide their way through the skin. I'm unaware of any mechanism by which PM2.5 seriously kills/damages bacteria, and such a mechanism seems unlikely given the physics and the evolutionary pressures.
"The misuse and overuse of antibiotics are the main drivers of antibiotic resistance"
This is wrong, as far as human use is concerned (setting aside the new study). The majority of antibiotic use is for real infections. Resistance is inevitable with antibiotic use, period.
Overuse and misuse should be reduced but if they are eliminated there would still be development of resistance. The real problem is that not enough money and effort are directed to development of new antibiotics. A new antibiotic is not a real blockbuster money maker, because it would have to compete with cheap non-patented antibiotics which will be as efficient in most cases.
As for this study, let's see if it is reproduced. It is an observational study which could be subject to many problems. It does not explain why (PM)2·5 particles contain antibiotic-resistant bacteria and antibiotic-resistance genes, which I suppose is what Kevin refers to. Does that claim involve another study which should be scrutinized and reproduced?
(PM)2·5 particles are probably not going to be eliminated any more than antibiotic overuse, so this doesn't change the need for new antibiotic development. Good luck getting everyone to wear masks all the time.
Evidently Japanese commonly use (PM)2·5 masks so in principle they would be less susceptible to developing antibiotic resistance from this source, but isolating such an effect would probably be difficult.
I would agree with those that say that the study is badly written. But the gist of it is that bacteria do stick to particulate matter or aerosol droplets and that some of these bacteria are resistant to antibiotics (this does not by any means imply that they are more robust overall BTW) plus that they are likely to swap resistance genes while traveling with the small particles.
In other words air pollution contributes to the spread of bacterial infections, including resistant infections. The headline suggests that air pollution CAUSES resistance. The text of the article does not claim that nor prove it. It is just that air pollution helps spread resistant strains which is dangerous by itself.
If the article were written in proper English these misunderstandings would not happen.
It seems like their data set is country by country, but I wish they could segment it by rural vs urban sets. For example, I would assume that PM2.5 from the Port of Long Beach has 0 impact on antibiotic resistance where as the same type of pollution in Tulare County has a large impact.
It might even strengthen their conclusions.
The paper says "PM2·5 was one of the largest drivers of antibiotic resistance, contributing 10·9% (95% CI 4·3–17·4) of variation in aggregate resistance, followed by [current health expenditure] (10·1%, 2·8–17·3), drinking-water services (2·7%, 0·7–4·7), and antibiotic use (2·4%, 1·8–2·9)."
So neither PM2·5 nor antibiotic use was *the* main driver of resistance according to these results, by a long shot. How do the other variables correlate with either PM2·5 or antibiotic use? The authors say they tested for covariance, but still couldn't really identify a dominant driver. Why do so many people think that antibiotic overuse is the the main driver when total use is only a very small factor in this analysis? Are they all wrong, or is there something wrong with the identification of variables in this study?
What the study shows is correlation. They didn't show that "PM2·5 was one of the largest drivers of antibiotic resistance", they show it is one of the most correlated variables. That doesn't tell you much about causation.