Modern environmental factors

Linking a person, @Cybergreen91, who argues that mold, VOCs, and/or nanoparticles, such as titanium dioxide, are likely environmental causes of ME/CFS and other chronic illnesses. No idea if his science is sound.

S4ME thread: The Role of Insoluble Nanoparticles and Other Environmental Triggers in Chronic Illness

Youtube channel

The main video explaining his theory, and his explanation in that thread, are very long, so here is an AI generated summary of just the scientific evidence in the video:

 

Potential links to cholinesterase-inhibiting chemicals in both gulf war illness and psychiatric disorders.

Acetylcholinesterase inhibitor exposures as an initiating factor in the development of Gulf War Illness, a chronic neuroimmune disorder in deployed veterans, Michalovicz et al, July 2020

Depressive symptoms and suicide attempts among farmers exposed to pesticides, Zheng et al, June 2024

 

Fluoroquinolone-induced serious, persistent, multisymptom adverse effects, Golomb et al, 2015

(Fluoroquinolones are a class of antibiotics. One example is ciprofloxacin.)

This study isn't about ME/CFS, it's just talking about a variety of symptoms from taking these drugs, but the delayed fatigue is possibly related.

Potentially similar mechanism to ME/CFS PEM?

I found this through a Google Scholar search I was trying:

Hoping to find case reports or studies where they are talking about some seemingly totally unrelated condition and maybe have never heard the term PEM, but where what they describe sounds a lot like PEM. I'm seeking connections to other conditions which might give clues.

The above seems to be the only relevant result for that specific search term though.

 

From Jarred Younger's weekly YouTube update, concerning pollution:

 

If it turns out risk of ME or some other chronic illness is increased by chemicals which circulate in the blood, then maybe some modern day bloodletting is in order:

Effect of Plasma and Blood Donations on Levels of Perfluoroalkyl and Polyfluoroalkyl Substances in Firefighters in Australia: A Randomized Clinical Trial
Gasiorowski et al
8 April 2022

Abstract

Importance Elevated levels of blood perfluoroalkyl and polyfluoroalkyl substances (PFASs) have been associated with a range of adverse health outcomes. Firefighters have been exposed to PFASs in firefighting foams and have previously been shown to have higher PFAS levels in blood samples than the general population. No interventions have been shown to reduce PFAS levels.

Objective To examine the effect of blood or plasma donations on PFAS levels in firefighters in Australia.

Design, Setting, and Participants This 52-week, open-label, randomized clinical trial enrolled participants from May 23 to August 23, 2019. Participants were 285 Fire Rescue Victoria staff or contractors with serum levels of perfluorooctane sulfonate (PFOS) of 5 ng/mL or more who were eligible to donate blood, had not donated blood in the 3 months prior to randomization, and were able to provide written informed consent. Analysis was performed on an intention-to-treat basis from May to July 2021.

Interventions Firefighters with baseline PFOS levels of 5 ng/mL or more were randomly assigned to donate plasma every 6 weeks for 12 months, donate blood every 12 weeks for 12 months, or be observed only.

Main Outcomes and Measures The primary end points were changes in the serum PFOS and perfluorohexane sulfonic acid (PFHxS) levels after 12 months of plasma or blood donations or after observation only. Secondary end points included changes in serum PFAS levels from week 52 to week 64, changes in other PFASs, and changes in complete blood count, biochemistry, thyroid function, and lipid profile from screening to week 52.

Results A total of 285 firefighters (279 men [97.9%]; mean [SD] age, 53.0 [8.4] years) were enrolled; 95 were randomly assigned to donate plasma, 95 were randomly assigned to donate blood, and 95 were randomly assigned to be observed. The mean level of PFOS at 12 months was significantly reduced by plasma donation (–2.9 ng/mL; 95% CI, –3.6 to –2.3 ng/mL; P < .001) and blood donation (–1.1 ng/mL; 95% CI, –1.5 to –0.7 ng/mL; P < .001) but was unchanged in the observation group. The mean level of PFHxS was significantly reduced by plasma donation (–1.1 ng/mL; 95% CI, –1.6 to –0.7 ng/mL; P < .001), but no significant change was observed in the blood donation or observation groups. Analysis between groups indicated that plasma donation had a larger treatment effect than blood donation, but both were significantly more efficacious than observation in reducing PFAS levels.

Conclusions and Relevance Plasma and blood donations caused greater reductions in serum PFAS levels than observation alone over a 12-month period. Further research is needed to evaluate the clinical implications of these findings.



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• After a year, levels of perfluorooctane sulfonate (PFOS) decreased by about 30% (eyeballing values from chart for this) with plasma donations every six weeks, and 10% with blood donation.
• Perfluorohexane sulfonic acid (PFHxS) decreased by about 28% with plasma donation, but did not decrease with blood donation.
• Perfluorooctanoic acid (PFOA) decreased by about 45% with plasma donation, but did not decrease with blood donation.

 

Four Cases of Pesticide Poisoning, Presenting as “ME,” Treated with a Choline and Ascorbic Acid Mixture
John Richardson

Journal Of Chronic Fatigue Syndrome Volume 6, 2000 - Issue 2

Abstract
Objectives: 1. To demonstrate in four patients, in whom the correct diagnosis of pesticide poisoning had been missed, the injustices inflicted on them when they are told ME does not exist. 2. To show how closely the features of such poisoning, especially by organochlorines, resemble those of the much more classic ME which is usually due, at least in the author's practice in the northern region of the UK, to persistent enteroviral infection. 3. To draw attention to a new and apparently successful form of treatment with an oral mixture of choline and ascorbic acid. 4. To suggest reasons why this treatment merits further scientific investigation.

Setting: A charity based private practice involved in the investigation of viral mediated disease.

Subjects: Four patients, two male and two female, each referred with a diagnosis of ME.

Intervention: a. Samples of blood were sent to Biolab Medical Unit where a variety of pesticide residues, including the very persistent organochlorines, were identified and progress in detoxification was monitored, b. All four cases were treated orally with a choline and ascorbic acid mixture.

Results: After a variable number of months, during the early phase of which the blood levels of some of the toxins rose, possibly due to mobilization from fatty stores, all symptoms cleared as blood levels fell.

Key Messages: The term ME comprises a number of clinical features, characterizing a patient who is ill. To refuse to recognize their existence does the patient much injustice.

Some cases of ME may be found to have pesticide poisoning. The possibility of it should always be borne in mind. The source may be either in the UK or abroad. A positive enquiry and a single blood test will provide a diagnosis.

Organochlorines may persist in the body for many years, as may the symptoms derived from them.

A detoxification program based on oral administration of a choline and ascorbic acid mixture has shown much promise and deserves verification of its value.

Conclusions: Amongst the group of clinical features known as ME, the possibility of pesticide poisoning should always be borne in mind. Treatment with choline and ascorbic acid mixture is worth trying, pending its more formal investigation.

The four cases, summarized by AI:

Study (Paywall)

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Book by the above author, John Richardson, available to borrow on Internet Archive:

Enteroviral and toxin mediated myalgic encephalomyelitis/chronic fatigue syndrome and other organ pathologies, 2001

 

MEpedia has some good information on Pesticide exposure link to ME/CFS.

 

American ME and CFS Society: What Causes ME/CFS?

"ENVIRONMENTAL CAUSES

• Organophosphates and other pesticides can trigger symptoms similar to ME/CFS
• Radiation exposure may be a catalyst for ME/CFS
• Toxins can cause mitochondrial impairment

Environmental toxins have frequently been implicated as possible causes of ME/CFS, particularly in patients with gradual onset. Dr. Majid Ali, a physician who believes that ME/CFS is caused by toxic overload, writes in his book, The Canary and Chronic Fatigue, that “chronic fatigue sufferers are human canaries—unique people who tolerate poorly the biologic stressors of the late 20th century.”

Dr. Martin Pall has noted that the symptoms of post-radiation syndrome are identical to those of ME/CFS. Alan Cocchetto, Medical Director of the National CFIDS Foundation, has identified some unique mitochondrial characteristics in his research that implicate low level radiation as the catalyst for some patients. As Dr. Pall’s NO/ONOO‾ model can also lead to mitochondrial defects, the two models may eventually prove to be similar, if not the same.

Pesticides are the primary focus of researchers investigating environmental causes of ME/CFS. A retrospective study conducted in Scotland, found that sheep farmers who had been exposed to organophosphates in sheep dips showed high prevalence of chronic fatigue and that higher chronic fatigue scores were associated with higher exposure to organophosphate pesticides.

Dunstan and colleagues found that serum levels of organochlorine (a chemical found in pesticides) was higher in ME/CFS than in controls. There were no significant differences in organochlorine levels between those ME/CFS patients with a history of toxic chemical exposure, and those without. The researchers concluded that the exclusion of patients from the CDC definition of ME/CFS on the basis of a history of exposure to toxic chemicals was not valid, and that low level organochlorine bioaccumulation might lead to the development of ME/CFS.

A third group of Scottish researchers led by Dr. Faisel Khan, found a link between ME/CFS, Gulf War Illness (GWI) and agricultural workers exposed to organophosphate pesticides. All three exhibited cholinergic abnormalities, however only the ME/CFS group showed abnormalities in the vascular system. They concluded that ME/CFS had a different etiology from either GWI or pesticide exposure.

Two later studies by the authors found that sensitivity to acetylcholine was restricted to those patients who fit descriptions for ME and post-viral fatigue syndromes, but not those for Gulf War Illness or for those exposed to organophosphate compounds, or those with fibromyalgia. (For recent developments see: Gulf War Illness: New Report Lauds Treatment Research, Confirms Toxic Causes.)

The authors were confident that the finding of increased sensitivity to acetylcholine in ME/CFS patients was “robust and unusual,” but did not conclude that pesticide exposure was causal.

Vaccinations have also been reported as triggers. In 1997, Doris M Jones MSc reported that among the 225 ME/CFS patients in her study group, 13% had received one or more vaccines in the month before ME problems developed. In a separate group of 55 subject, 16% had received one or more vaccines in the month before ME/CFS problems developed. There have been a number of studies implicating aluminum adjuvants (substances which are added to vaccines to increase their effectiveness) in the development of long-term neurological impairments. A particular concern is that even small amounts of adjuvant have the capacity to pass the blood-brain barrier."

 

The Canary and Chronic Fatigue
by Majid Ali, published 1994

Full scanned book available to borrow on Internet Archive.

 

Thank you for keeping it real @Jonathan Edwards
The last thing we need for this field is telling our doctors that pollution and environment is the cause of ME or suggesting to researchers that it is a good research lead. It would set us back yet again.

There is some humility in saying ‘we don’t know what causes you to not recover’ and yet please stop there and do not suggest that if you are less meat, no wheat, and avoided toxic products that everyone uses, you would have had a different outcome. We still don’t know what causes ME and we are even not sure yet whether it is one disease or several diseases.

 

I don't have an issue saying "we don’t know what causes you to not recover".

But I will largely have to disagree with the rest. Researchers are barely even looking at this, and for those that are, it is inherently extremely hard to study.

I don't know if the issue is that there's a sentiment that reducing environmental toxins is some new age mumbo jumbo akin to healing cancer with crystals and positive affirmations. Maybe it gets associated with influencers selling grass smoothies to reduce toxins in the body based on no science. We're breathing and eating low doses of thousands of different newly created chemicals for our entire lives, almost none of which have been thouroughly studied for long term effects like ME or many of the other chronic conditions that plague the world.

Just looking at the one description of the Scottish study above. You think it would be best to not pursue any more research even though they've shown a significant link between pesticides and something like ME and a 10,000 (!) times higher risk of depression? Or the two others linking pesticides with depression or GWI? Just stop there and don't even look at other populations or other pesticides to try to see if the above link is sound and if more cases of ME-like illness are caused by pesticides?

Is it not obvious that if a high dose of pesticides, or some other industrial chemical, is highly dangerous to the people that work with it, a low dose spreading to the entire world may also be dangerous to a large number of people? It's just incredibly hard, in comparison, to make the connection to a single chemical out of the thousands in our environment being inhaled/ingested for our entire lives, and there is no dramatic onset, like with acute exposure, to make it easy to point to anything.

I mean, plenty of people with ME have sensitivity and obviously increased symptoms to even tiny amounts of fragrances in laundry detergent, connections that likely were not easy for them to find, and researchers weren't exactly falling over themselves to prove it for them. How are they going to know whether or not they're also sensitive to some pollutant wafting into their bedroom 24/7? Or sensitive to something that takes years to build up in the body to cause symptoms? Researchers and clinicians are barely considering even just the chemicals that patients are saying they are sure make their ME symptoms worse.

Researchers should be exploring all available avenues, including genetics, immune dysfunction, viral persistence, microbiome, etc. But for environmental toxicity to virtually not even be mentioned in relation to ME or other chronic illness research is incredible.

 

HYPOTESIS: We underestimate the risk of chemicals in water and food in ME/CFS

Henrik Nielsen

EUROMENE Book of Abstracts, p. 10, March 2020

"When conventional organisations of farmers and industry inform that the use of pesticides, chemicals and heavy metal are safe, they make an error. It is a statement that pesticides, chemicals as well heavy metals enter nerve tissue and gut and no doubt interfere with health negatively. What we need is to show the exact mechanism/relationships between specific diseases and “poison” involved. This statement may not be an excuse for politicians not to handle now. Data collected over the past many years shows a growing support that healthcare problems are growing secondary to exposure worldwide to these elements. The Seveso disaster close to Milan in 1976 was one of the first accidents in industry which resulted in research in health risk secondary to chemicals. As a result, 2.5 kg dioxin was spread out in an area where many people lived, the understanding of this was not obvious, as information about chemicals used was not given prior to the two weeks had passed – after that the area was evacuated. A year later, 122 children were born with deformities, 450 children with chronic dermal diseases, and an increased occurrence of type 2 diabetes especially in women was observed. Dioxin is only one example how damage can involve living organisms – Danes are daily exposed to drinking water and food. In 2019, it was found that two in three tests in water to drink were positive for smaller cocktails of pesticides. Dependent on how the cocktails are mixed – they invade the human organs. A lab-study from 2017 illustrates the example of 338 pesticides’ penetration over membranes in the boiled egg model [1]. Today it is clearer that several diseases can result as a consequence of exposure to environmental factors – named trigger points. One factor of pesticides includes phthalate and chemicals in dress coats. Industrial air emission and proximity to emitters are associated with anti-citrullinated protein antibodies (ACPA) in a sample of 1586 unselected subjects [2]. In a controlled clinical study based on exposure to pesticides in tobacco field workers (n = 40) versus a control group in an office (n = 40), the groups were followed 360 hours in a period from June to September. All 80 tested subjects were non-smokers. In the exposed group blood concentration of aluminum, arsenic, chromium, copper, nickel, potassium, selenium and zinc were increased. Blood levels of antioxidants (e.g. B12–C vitamins) were increased but not sufficient to counterbalance the damage – mitochondrial damage/DNA damage [3]. From other designs GWI (Gulf War Veterans) [4], Alzheimer and Parkinson diseases [5], the evidence of pre- and post- natal exposures to environmental factors that predispose to the onset of neurodegenerative diseases later in life highlights the necessity to expand the research on identifying environmental risk factors to the development of neurodegenerative diseases (ME/CFS) – see reprogramming cells from Veterans [4].

References:
1. L. Chedik, D.Mias-Lucquin A. Bruyere, O. Fardel, Int. J. Environ. Res. Public Health, 14 (2017) 708.
2. S. Bernatsky, A. Smargiassy, L. Joseph, P. Awadalla, I. Colmegna, M. Hudson, M. J. Fritzler, Environ Res, 157
(2017) 60-63.
3 V. F. S. Kahl, V. Dhillon, M. Fenech, M. R. de Souza, F. N. da Silva, N. A. P. Marroni, E. A. Nunes, G.
Cerchiaro, T. Pedron, B. L. Batista, M. Cappetta, W. Mártinez-López, D. Simon, J. da Silva, Oxid Med Cell
Longev, 2018 Jun 3;2018:7017423.
4. L. Qiang, A.N.Rao, G. Mostoslavsky, M. F. James, N. Comfort, K. Sullivan, P. W. Baas, Neurology, 88
(2017)1968-1975.
5. M. Chin-Chan, J. Navarro-Yepes, B. Quintanilla-Vega, Front Cell Neurosci, 9 (2015) 124"

Link

 

Links between air pollution and COVID-19 in England
Marco Travaglio, Yizhou Yu, Rebeka Popovic, Liza Selley, Nuno Santos Leal, Luis Miguel Martins

Environmental Pollution
January 2021

"Abstract
In December 2019, a novel disease, coronavirus disease 19 (COVID-19), emerged in Wuhan, People’s Republic of China. COVID-19 is caused by a novel coronavirus (SARS-CoV-2) presumed to have jumped species from another mammal to humans. This virus has caused a rapidly spreading global pandemic. To date, over 300,000 cases of COVID-19 have been reported in England and over 40,000 patients have died. While progress has been achieved in managing this disease, the factors in addition to age that affect the severity and mortality of COVID-19 have not been clearly identified. Recent studies of COVID-19 in several countries identified links between air pollution and death rates. Here, we explored potential links between major fossil fuel-related air pollutants and SARS-CoV-2 mortality in England. We compared current SARS-CoV-2 cases and deaths from public databases to both regional and subregional air pollution data monitored at multiple sites across England. After controlling for population density, age and median income, we show positive relationships between air pollutant concentrations, particularly nitrogen oxides, and COVID-19 mortality and infectivity. Using detailed UK Biobank data, we further show that PM2.5 was a major contributor to COVID-19 cases in England, as an increase of 1 m3 in the long-term average of PM2.5 was associated with a 12% increase in COVID-19 cases. The relationship between air pollution and COVID-19 withstands variations in the temporal scale of assessments (single-year vs 5-year average) and remains significant after adjusting for socioeconomic, demographic and health-related variables. We conclude that a small increase in air pollution leads to a large increase in the COVID-19 infectivity and mortality rate in England. This study provides a framework to guide both health and emissions policies in countries affected by this pandemic."

Full text

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It seems premature for them to say they show that PM2.5 particles were a "major contributor to COVID" based on this study, although I've only skimmed the full text. Just with all the potential confounders, like maybe jobs in the more polluted areas tend to have people in closer contact. Or maybe there's more public transportation squeezing people together in those areas.

 

I think that, as you'd expect, there's a higher prevalence in health care and education. The (late) ME nurse Keith Anderson told me there was higher prevalence around estuaries, but I don't know what his source was.

You are right @Hutan, we know so little about the patient population.

 

I hear that. I'm not confident it is the case that spreading awareness and sharing research about this field is counter-productive, but I can maybe see an argument for that.

I'm too tired for trying to navigate the politics of research, though I get that it's a big factor in things like this. But I'm just frustrated because it's like there's a building with water all over the floor all the time and everyone is focusing on making clever systems to clean up the water or work around it, but no one cares to check if there's a leak somewhere.

Sure, those would be great, as would a biomarker. I can imagine researchers trying to compare rates of ME between the US and a tribal population in the Amazon rainforest would be extremely difficult with all the language, cultural, and practical challenges that would surely arise. If they could just draw some blood and send it to a lab, that'd make things much easier.

It's not just anecdotes though. There's one example of a solid lead in a post above, with the sheep dip causing ME. The next step should surely be to try to confirm or deny this study, right? Look for correlations with the same or similar chemicals in other populations. [Edit: Though looking more into that, even though news articles and the study refer to ME or CFS, the study says "It should be noted that the questionnaire provided an assessment of CF and not CFS". But even if the link is to CF instead, then pesticide links to CF should be further investigated.]

And I'm not just advocating for this for ME, but for all chronic illnesses - this research is lagging everywhere. We even have perfect examples of environmental toxins flying under the radar for years, causing illness in millions of people: things like lead, asbestos, mercury, radium, PCBs. It is not unscientific to think "I wonder if there are more examples of this clear issue that we haven't found yet. Maybe we should try harder to find them before a million more people have cancer or brain damage, and try to limit the suffering that will happen." It's unscientific to look at that and think we're now perfect and industry is only pumping out the safest of chemicals after learning its lessons. (I know/think you personally aren't calling me a Luddite, but that'd be my response to someone that does think that.)

Maybe that's the price we pay as society to have modern technology, where the powers that be know they can't possibly thoroughly test everything their population demands and some or many people will be harmed, but the risks and benefits are carefully weighed by government and industry (which I doubt). Even in that case, the risk should be part of public consciousness so that people are free to protect themselves or demand change. It seems like the majority of people don't even know or think about the possibility that the next lead or asbestos could be happening right now, in a thousand different ways.

But I get that people want a relatively easy fix. If the majority of the population only experiences mild health issues, yeah, why would they, for example, like being told they should upend their life and move to a rural town to avoid air pollution to calm their asthma if they have the alternative of pills and inhalers with minimal side effects, and science promising them ever-better medications.

 

I was recently thinking about a cat I had who was diagnosed with cat leukemia and eventually had to be put down. I'm very bad at remembering timelines, so I don't know if I adopted him before or after my precipitating infection (I inherited him from a friend), but it was around the same time. I also don't remember if he had a blood test to confirm the diagnosis.

When he became ill he stopped eating and spent all his time on lying on a shelf away from the light. At the end he was struggling to breathe.

I've become much more aware of transmission of infections between species because of Covid-19 and H5N1, so that's why I'm thinking about this, although it's probably most likely that his and my illnesses are unrelated.

(I miss him)