Galileo and COVID
mikefortunWe're still doing this Galileo schtick? Absolutely the worst model for the science-authority relationship, but scientists (well, at least physical scientists) still love it. More to come...
We're still doing this Galileo schtick? Absolutely the worst model for the science-authority relationship, but scientists (well, at least physical scientists) still love it. More to come...
First: Another list on another google doc and just looking at it https://docs.google.com/document/u/0/d/1UTQvW_OytC37IatMNR5qJK7qKfSylNpI2fT3pdteVZA/mobilebasic gets me started: we're all barely keeping up and just trying to direct the firehose into some readily available container like a google doc because we can't drink any more and it's the easiest thing to hand. I'm happy with the dangerous "we": all we humanists and all them scientists are trying to do kaelidoscopics at speed, saving the excess for future analysis while trying to do the analysis right now and get something in print right now which is aleready too late. "They" have better containers (infrastructure) and that matters, but I think it's important to note the shared space of urgency and excess and ask about the effects these have on analysis, ours and theirs and: ours.
It has to be hurried, the only take worth anything these days is the hot take, for scientists, science journalists, science analysts. An exaggeration, but I'm rushed. We know that air pollution (two words harboring such complexity and excess on its own: PM2.5, ozone, NOX, etc.etc.) impacts health in numerous ways, in and beyond our repiratory system; we know that those physiological logics are compounded by cultural logics, in their complexity and excess: race poverty geolocation healthcare access nutritional needs etc. etc. A kaleidoscopic intersectional analysis that, to get good reliable outcomes, takes time.
A need for generosity.
So as I make my way down the list in the google doc and read that some group or some lab shows the COVID-19 intersects with air pollution and makes for worse outcomes for African Americans I'm predisposed toward belief, for many good reasons, compounded by the rush. And the data and the correlations between, say, increased mortality in areas of northern Italy where there are higher levels of airpollution is certainly believable, compelling -- for NO2
https://www.sciencedirect.com/science/article/pii/S0048969720321215?via%3Dihub
and air pollution generally
https://www.sciencedirect.com/science/article/pii/S0269749120320601
That kind of crunching of large data sets seems believable -- and has been stamped as peer reviewed. So what do we do with this article in The Conversation
critical of a Harvard School of Public Health study available as a preprint on medrxiv --
https://www.medrxiv.org/content/10.1101/2020.04.05.20054502v2
-- that concludes that "an increase of only 1 μg/m3 in PM2.5 is associated with an 8% increase in the COVID-19 death rate (95% confidence interval [CI]: 2%, 15%)"? The Canadian researchers in The Conversation are not convinced:
"It is almost impossible to try to adjust for the influence of all these factors, as this study tried to do, because the interactions between these variable are so complex. Accounting for these factors could only be done in studies using information from individual-level information."
"Proper peer review must not be bypassed — and the onus for respecting its role falls not just on journalists but also on scientists to communicate the correct information accurately."
I'm suspicious -- and if I had more time I would be more suspicious of my suspicions -- for two reasons: one, a lot of those studies on the google docs list are preprints. But more importantly, the call for "individual-level information." What does this mean? I don;t think anyone is working with "individual level information" in all of these studies, so why does this one become a target?
1. Because it's Harvard PH, of Six Cities study fame, first linking air pollution to increased mortality and the key reference point for US air pollution regulation. There's a long history of the oil industry and their scientists just trying to pick holes and cast doubt on these studies out of Harvard.
2. The criticism smacks of the most recent devious strategy of the air regulation opponents, which is to call for individiual level data in epidemiological to be released in the name of "transparency." Which can't be done.
So who are these Canadian guys and are they up to something more than "just raising questions and being good scientific skeptics"?
UPDATE 1 HOUR LATER:
So I looked them up: Mark Goldberg was a member of the Reanalysis Team of the Health Effects Institute that validated the Six Cities Study:
https://theasthmafiles.org/content/hei-validation-six-cities-study
Unlikely, then, that he is some undustry beard...
I situate my research at the crossroads of history, philosophy, sociology and anthropology of science. In the past, I have focused on epigenetics, environmental research, empirical bioethics and environmental justice, within and outside the academia, as you can read here, or here. Now I am focusing on antibiotic resistance, and I use it as a lens to interpret the contradictions of the last century derived by industrial production, environmental degradation and biomedical cultures.
What interests me is the (at that time) new epistemic discourse that since the Forties has been produced to explain morphological changes of organisms produce when they experience new environmental conditions or perturbations. Through an important experiment at the base of the so-called concept of genetic assimilation, Conrad H. Waddington showed that a thermic shock can produce changes in wings’ veins of fruit flies, changes that can eventually be inherited across generations, without the environmental trigger that caused them.
This focus on production and (genetic) storage of biological differences elicited by the environment is nowadays coupled with the knowledge produced through microbiome research that explains the phenotypic patterns that recur across generations.
In a thought-provoking twist, with microbiome research, the focus shifts from production and inheritance of biological differences to production and inheritance of biological similarities. Microbiome research shows that some phenotypic patterns are allowed by ecological communities of microorganisms composing all animals. Bacteria allow the development and functioning of our bodies within an epistemic framework that is now key to understand biology. The network of vessels composing mammals’ stomach is formed through cellular differentiation and expression of genes coordinated by bacteria. The same is true for our immune system that is coordinated by gut bacteria. Food, which is an important aspect of our lives also impacts on this microecology and mediates between our biological functions and functioning of means of production whose parts dedicated to food production have immense importance for our biology and our internal and external ecologies. Antibiotic resistance is one of the crossroads where culture, biology, history and the Anthropocene meet. Indeed, Antibiotic resistance shows that means of production of our societies have an even more widespread, deep and allegedly unexpected impact on the biology of animals and plants. The microorganism can indeed adapt to resist the selective toxicity of antibiotics. Moreover, bacteria can transfer their genetic code horizontally, by touch, so that we can acquire antibiotic resistance by eating food that functions as a vector, by hosting lice on our heads and many other contacts. Bacteria that are resistant to antibiotics that have been used as growth factors in animal husbandry and to prevent diseases in livestock and aquaculture, spread in natural ecosystems and can be found in wild species. Rivers and estuarine waters are places hosting antibiotic resistance.
Searching on PubMed (the search engine for biomedical literature) titles of articles containing the terms ‘antimicrobial’ and ‘Louisiana’ I retrieved just one twelve-years-old article. No results with terms such as 'Mississippi' or 'New Orleans'. The authors collected and analysed Oysters from both waters of Louisiana Gulf and in restaurants and food retailers in Baton Rouge. In most of the samples gathered, scientists recognised the presence of bacteria (Vibrio parahaemolyticus and Vibrio vulnificus) resistant to specific antimicrobials. Food production is indeed the first factor in terms of the quantity of antibiotics used. This use and related antibiotic resistance impact all the living beings present in a specific area, and can easily travel around the globe through many channels. As Littman & Viens have highlighted, a sustainable future is a future without antibiotics as “there may be no truly sustainable way of using antibiotics in the long-run, as microorganisms have shown to be almost infinitely adaptable since the first introduction of antibiotics” (Littman & Viens 2015). But in the meanwhile, we need to use them and antibiotic resistance is a phenomenon that can be better studied through environmental research, by analysing wild species and emissions nearby livestock, for instance.
The study that I retrieved focuses on Oysters. But what about antibiotic resistance conveyed through food that is consumed by the most?
What about exposures of communities that are living in highly polluted areas?
And what is the additive value on antibiotic resistance for individuals who experience the presence of industrial pollutants and that live in areas where cancer epidemics are registered?
In this respect, there is a strategy to cope with the issue of antibiotic resistance promoted by the Center for Disease Control and Prevention. The document doesn’t mention any action to monitor and regulate the production and usage of antibiotics in livestock. Nevertheless, the CDC wants to scrutinise, through genome sequencing, “Listeria, Salmonella, Campylobacter, and E. coli and uploads sequence data into PulseNet for nationwide monitoring of outbreaks and trends.” Moreover, the document reports that “In Fiscal Year 2019, Louisiana will begin simultaneously monitoring these isolates for resistance genes. When outbreaks are detected, local CDC-supported epidemiologists investigate the cases to stop spread.”
The questions that I would like to ask (to local ppl, activists, researchers, practitioners..) are:
What could be the epidemiologic characteristics (socioeconomic status, gender, residence..) of the populations more vulnerable to antibiotic resistance?
What is the additive role of antibiotic resistance for people living in highly polluted areas?
What is the impact of antibiotic resistance for people and patients living in areas where cancer incidence is high?
And on the long run I am interested in imagining possible strategies to not only living with the problem but also to tackle the problem itself, which means to develop strategies to answer the questions:
Why antibiotic resistance, which is known since a century, it’s a problem on the rise?
What is the role and interest of capitalism, in terms of profit-making of corporations, knowledge production and environmental degradation, in not being able to resolve antibiotic resistance?
What can be strategies of local communities to tackle the problem and to promote environmental justice in terms of alliances with ecologists, doctors, epidemiologists and other activists?